1
El papel de los sistemas
emocionales
Contenido
La organización del cerebro: tipos de procesos cerebrales .......................................................... 2
El Modelo de Pankseep de los tres procesos cerebrales .......................................................... 3
Los sistemas emocionales ............................................................................................................. 5
Sístema de búsqueda o exploración de lo desconocido ........................................................... 5
Sistema de deseo sexual (Lust): Combinación de deseo y placer. ............................................ 7
Sistema de cuidado o crianza (Care-especialmente en el educador) .................................... 14
Sistema de juego ..................................................................................................................... 19
Sistema de miedo .................................................................................................................... 25
Sistema de rabia o ira .............................................................................................................. 27
Sistema de pánico ................................................................................................................... 33
Regulación de los sistemas emocionales .................................................................................... 38
El Placer, el gran regulador. .................................................................................................... 41
Una neurobiología común para el placer y el dolor ................................................................ 48
Neuroquímica del amor .......................................................................................................... 49
Diferencias entre el enamoramiento infantil y adulto ............................................................ 50
Referencias y enlaces .................................................................................................................. 51
Anexos ......................................................................................................................................... 54
Anexo I..................................................................................................................................... 55
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La organización del cerebro: tipos de
procesos cerebrales
Una parte significativa de la comunidad científica actual comparte que los procesos
emocionales se organizan en el cerebro en forma de sistemas (Pankseep, Berridge y
Ledoux). A partir de esta premisa común y del reconocimiento de un núcleo pequeño
de emociones universales básicas, se discute la funcionalidad de cada uno de los
sistemas y los niveles cerebrales implicados. Desde la perspectiva de autores como
Ledoux o Pankseep, los sistemas emocionales universales serían compartidos por todos
los mamíferos y, en consecuencia, el estudio de los circuitos cerebrales y de la
neuroquímica asociada, así como de las alteraciones genéticas en animales de fácil
reproducción, como las ratas, permitiría extrapolarse a los seres humanos. Tal es el caso
del miedo, estudiado por Ledoux, que se puede condicionar sin la participación inicial
de la corteza cerebral y de la voluntad. Este planteamiento pretende conocer con
precisión la fisiología de los sistemas emocionales e investigar sus relaciones con
patologías fundamentales como la depresión o las fobias, y comprender procesos
afectivos, como el apego. Desde esta perspectiva, la investigación con animales puede
llevarnos a propuestas específicas a nivel neuroquímico o conductual que sirvan para
actuar sobre diferentes trastornos o patologías, incidiendo directamente sobre los
núcleos o vías neuronales, así como sobre los neurotransmisores, y los mecanismos
químicos subyacentes.
A su vez, esta línea de investigación se complementa con los estudios sobre el ADN y
las instrucciones genéticas que regulan la producción molecular asociada a la formación
y fisiología del sistema nervioso, lo que permite a su vez desarrollar terapias que
permiten regular, controlar o modificar la expresión del ADN o actuar químicamente o
por otros medios sobre las proteínas sintetizadas.
El enorme desarrollo que ha tenido en los últimos años la investigación genética y
cerebral no se podría haber producido sin la ayuda de la bioingenieria y la informática.
De esta manera, por ejemplo, disciplinas como la optogenética, que permite manipular a
voluntad la activación o inhibición de neuronas y circuitos nerviosos, introduciendo
genes específicos sensibles a la luz a nivel neuronal, se han podido desarrollar gracias a
los avances señalados. Estas técnicas se pueden aplicar a animales vivos, lo que permite
estudiar la estructura y la función cerebral al mismo tiempo, mientras el animal
desarrolla una conducta, sin tener que recurrir, como hasta ahora, a los estudios sobre
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los tejidos de los animales muertos. La posibilidad de conectar al cerebro,
microdispositivos electrónicos, incluídos microscopios, así como microcánulas y
microelecrodos, a los animales vivos, en su mayoría ratas, permite introducir con
precisión celular, sustancias en el cerebro, así como estimular eléctricamente y medir al
mismo tiempo los cambios químicos y eléctricos, registrándose y analizándose en los
ordenadores, mediante el software adecuado, los datos que nos proporcionan los
circuitos cerebrales o incluso las neuronas individualmente. De todos estos avances se
están beneficiando enormemente los estudios sobre los sistemas emocionales.
El Modelo de Pankseep de los tres procesos cerebrales
Teniendo en cuenta las consideraciones anteriores y que el Cerebro-Mente de los
mamíferos es un órgano muy complejo, necesitamos de alguna ayuda conceptual para el
estudio de los sistemas emocionales. De este modo, algunos autores, proponen
simplificaciones teóricas evolutivas, desde las que poder hacernos una idea global e
integrada.
Yo prefiero un concepto tripartito de las complejidades algo diferente, que no nos meta
en “problemas” neuroanatómicos (Pankseep,2014).
Siguiendo a Pankseep, que toma a su vez como referencia a MacLean (1970)
planteamos 3 tipos de procesos cerebrales que pueden participar en la explicación de los
sistemas emocionales:
Procesos-primarios, (Afectos primordiales básicos, sub-neocorticales), que como
resultado de la evolución proveen útiles vitales toscos pero eficaces, muchos de las
cuales típicamente reflejan “intenciones-en-acciones” intrínsecas —procesos
tradicionalmente tratados como incondicionados, “innatos” o “instintivos” y que han
engendrado tanto acalorado debate (los sustratos neurales generalmente corresponden a
los cerebros reptiliano y paleomamífero de MacLean). Se incluyen entre los procesos
primarios:
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Afectos emocionales (Sistemas de acción-emoción. Intenciones en acciones. Ej: El
dolor producido por una quemadura produce miedo al fuego; un pinchazo con una aguja
produce miedo a la aguja. Propuesta de Pankseep: Búsqueda, juego, lujuria, juego,
miedo, rabia y pánico.
Afectos Homeostáticos (Intraceptores cuerpo-cerebro: hambre, sed…)
Afectos sensoriales (Sensores exteroceptivos que disparan las sensaciones y los
sentimientos de placer y displacer. Ej el roce del alimento con la lengua).
Procesos-secundarios, (Emociones de proceso secundario, aprendizaje vía ganglios
basales) que reflejan las capacidades cerebrales básicas de aprender mediante
sensibilización-habituación, condicionamientos clásico y operante, (estos están
representados en todos los niveles de organización cerebral). Se incluyen entre los
procesos secundarios:
Condicionamiento clásico (Por ej, miedo, vía amígdala central y vasolateral)
Condicionamiento instrumental u operante. (Seeking vía Nucleus Accumbes)
Hábitos emocionales o conductuales (Ampliamente inconscientes- Estriado dorsal)
Procesos-terciarios, (Afectos terciarios y Funciones de la conciencia Neo-cortical), que
incluyen todos aquellos procesos “reflexivos” del Cerebro-Mente superior que
incluimos en conceptos tales como pensamiento, deliberación, planificación y las
formas superiores de la intencionalidad (esto es, intenciones-de-actuar), y de esto no
podemos tener mucho sin las funciones de aprendizaje general evolutivamente marcadas
de nuestras expansiones neocorticales. Se incluyen entre los procesos terciarios:
Funciones cognitivo ejecutivas. Pensamientos y planificación (Corteza Frontal).
Reflexiones emocionales y regulaciones emocionales (Regiones Medial Frontal)
“Free Will”. (Funciones de la más Alta Memoria de Trabajo-intención para actuar)
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Los sistemas emocionales
Las emociones básicas que Ekman (1972) descubrió como universales a través de
estudios transculturales de la percepción del rostro humano no son fenómenos o
reacciones simples, sino que están vinculadas a sistemas emocionales. Cada uno de
éstos presenta características neurológicas propias, tanto en circuitos neuronales, punto
emocionales específicos (por ej, Berridge la existencia de unos puntos calientes para el
placer, - hotspot-) como en neurotrasmisores, neuropéptidos o química hormonocerebral. Además, algunas emociones comparten en gran parte los circuitos y los
neuropéptidos, diferenciándose sólo en las concentraciones necesarias del neuropéptido
para provocar una reacción emocional u otra. Por ejemplo esto puede suceder entre el
placer y el miedo. A su vez otras emociones como la rabia, están muy vinculadas al
miedo y al dolor. En consecuencia cada emoción debe ser estudiada dentro de un
sistema y dicho sistema puede incluir uno o diferentes procesos. Por ejemplo para
Ledoux, el sistema de miedo es fundamentalmente secundario, no consciente y
adaptativo para la supervivencia; sus procesos neuroanatómicos residen en la amígdala
(Ledoux, 2014)i. A continuación describimos los tipos de sistemas emocionales,
empleando el sistema de clasificación de Pankseppii:
Sístema de búsqueda o exploración de lo desconocido
Según Panksepp es el más universal de los sistemas emocionales. El Sistema de
búsqueda fue expuesto por primera vez en 1954 por Milner. Él lo consideraba como un
sistema de búsqueda de la recompensa. Si estimulamos cerebralmente al animal, lo que
se produce es una actividad exploratoria o de búsqueda, sin que necesariamente se
satisfaga ninguna necesidad. El animal puede mantener las conductas de exploración
hasta que cae exhausto y se duerme, sin que necesariamente haya tenido que obtener
satisfacción alguna. Es el sistema fundamental del que están dotadas las mentes
creativas, siempre ávidas de acercarse a lo desconocido.
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El sistema de búsqueda opera según Panksepp (1998), desde el punto de vista
neurofuncional de la manera siguiente iii:
To be very specific regarding neurocircuitry for the SEEKING system, Panksepp refers to the
extended lateral hypothalamic corridor, which is part of the previously discussed medial
forebrain bundle (MFB), a prominent tract of nerve fibers, both ascending and descending,
within which is incorporated the mesolimbic and mesocortical dopamine pathways of the
SEEKING system. Although we have discussed the MFB previously, here again is the
illustration from the HOPES Brain Tutorial, a project of Stanford University (image links to
source). In real tissue, this MFB pathway appears as white matter (see Gray matter, white
matter, glial cells). It is this tiny pathway of a multitude of nerve fibers that motivates us via the
SEEKING system.
In locating the SEEKING system, Panksepp refers to the nucleus accumbens, which is part of
the corpus striata (basal ganglia). The lateral hypothalamic corridor, explains Panksepp,
"running from the ventral tegmental area (VTA) to the nucleus accumbens, is the area of the
brain where local application of electrical stimulation will promptly evoke the most energized
exploratory and search behaviors an animal is capable of exhibiting." The "corridor" to which
Panksepp refers is also called the mesolimbic pathway, first discussed in Dopamine action,
synthesis, and pathways.
If you are interested in obsessions and compulsions, it is important to remember that the
SEEKING system as a whole and the nucleus accumbens in particular play important roles in
generating these behaviors.
When the mesolimbic pathway from the dopamine-producing VTA to the nucleus
accumbens is stimulated, SEEKING behavior ensues. Panksepp writes: "For instance,
stimulated rats move about excitedly, sniffing vigorously, pausing at times to
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investigate various nooks and crannies of their environment. If one presents the animal
with a manipulandum, a lever that controls the onset of brain stimulation, it will readily
learn to press the lever and will eagerly continue to 'self-stimulate' for extended periods,
until physical exhaustion and collapse set in. The outward behavior of the animal
commonly appears as if it is trying to get something behind the lever."
Sistema de deseo sexual (Lust): Combinación de deseo y
placer.
Los animales tienen la necesidad de traspasar sus genes y dentro de éstos, los mamíferos
han desarrollado un poderoso sistema, diferenciado en machos y hembras, que permite
la supervivencia y el éxito de la especie. Las conductas sexuales de aproximación,
(gestos, miradas, sonidos, conductas de cortejo) modifican e incrementan el deseo
sexual, lo que incrementa los niveles hormonales y de determinados neuropéptidos,
(tetosterona y dopamina,). El contacto físico y la obtención de orgasmos suponen una
enorme descarga de opiáceos naturales y neurotransmisores. Finalmente, después del
orgasmo, se desarrollan las conductas que implican intimidad y fidelidad, necesarias
para el cuidado de la madre y de la prole, con cambios químicos asociados, como el
incremento de la oxitocina. El lector puede profundizar más adelante en el apartado
dedicado al placer y a la neuroquímica del amor.
La actividad sexual se apoya en los demás sistemas emocionales: búsqueda,
exploración, juego, miedo y pánico.
Si este sistema ha funcionado correctamente precisaremos del sistema de cuidado o
crianza.
The MATING System, the Brain, and Gender Determination
From the perspective of sociobiology, natural selection favors genes (including those
that code for neurocircuitry and neurochemicals) that increase chances for gene
duplication. One could say that the biological aim of living creatures is to organize in
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such a way as to duplicate their genes. In mammalian societies, care of the young is of
upmost importance. But mammals, depending on their environment, organize things
differently.
Jaak Panksepp points out in Affective Neuroscience: The Foundations of Human and
Animal Emotions (1998) that "among our brethren great apes" there is no single plan for
family structure." He writes: "Whereas gibbons appear to mate for life with a single
partner, gorillas prefer a harem-type family structure, orangutans tend to be social
isolates, with the sexes coming together mostly for copulatory purposes, while
chimpanzees are quite social and promiscuous, sharing partners rather indiscriminately."
The photograph above right is of two gibbons from Highland Farm Gibbons Sanctuary
(image links to source).
Regardless of family matters, certain things must get done to duplicate those genes.
When my husband was a young lad, his friend told him that there was something inside
a man that had to get inside a woman to make a baby. "So how does it get there," my
very analytical husband-to-be asked with disbelief, "fly through the air?"
Sex differences in brain anatomy:
From his neuroscientist point of view, Panksepp points out that due to the "branching of
control factors for brain and body organization, it is quite possible for a male-type body
to contain a female-type brain, and for a female-type body to contain a male-type
brain." But before we delve into issues of gender and sexuality, we will first discuss
brain anatomy and circuitry related to optimizing reproduction. While they share some
neurochemicals such as oxytocin, Panksepp explains that specific brain circuits and
chemistries that are distinct for males and females mediate sexual urges that foster
reproduction.
When fetal steroids masculinize the XY rat's brain, a specific area of the pre-optic area
(POA) is enlarged compared to females. (We will discuss more specifics about how the
mammalian brain is masculinized a little later in this section.) Panksepp explains that
this enlarged, masculinized area is called the sexually dimorphic nuclei of the preoptic
area (SDN-POA). In this case, the term "dimorphic" means a structure that occurs in
two different forms—the female form and the male form. Compared to the more robust
preoptic area in males, Panksepp explains that in females, "many neurons in this part of
the brain die during fetal development for lack of testosterone, or more precisely its
product estrogen, which is a powerful growth factor for these neurons."
When fetal steroids masculinize the XY human's brain, a specific area of the brain is
also enlarged compared to females, although the size difference is not as great as that
found in rats. This enlarged brain area is called the interstitial nuclei of anterior
hypothalamus (INAH). In the image below (links to source) from Neuroscience, Purves
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et al., editors, Sineuar Associates, Inc., the large vivid pink area represents the anterior
hypothalamus.
The enlarged pre-optic area (POA) of the male rat brain is an important part of what
here we will call MATING neurocircuitry. Panksepp writes: "Following lesions of the
POA, male rats that have had abundant sexual experience will seek access to receptive
females, even though they do not attempt to copulate with them. In other words, their
social memories, situated perhaps in the cingulate cortex, amygdala, and nearby areas of
the temporal lobes, are still capable of motivating social approach, although sexual
engagement is no longer initiated." Later, he adds: "Castrated male rats that have lost
their sexual ardor can be reinvigorated simply by placing testosterone directly into the
POA."
In Part 1 of MyBrainNotes.com, we discuss Paul MacLean's triune brain concept.
MacLean also played a role in delineating MATING neurocircuitry. Panksepp writes:
"Paul MacLean mapped out the monkey brain for sites from which genital arousal
(erections) could be evoked by localized ESB [electrical brain stimulation]. He
discovered a broad swath of tissue, in higher limbic areas, where sexual response could
be elicited. They included, prominently, areas such as the septal area, bed nucleus of the
stria terminalis [BNST], and preoptic areas, all of which converge through the anterior
hypothalamus into the medial forebrain bundle of the lateral hypothalamus."
There are other differences between the female brain and the masculinized male brain.
For example, growth in the masculinized corpus callosum, which connects the two
cerebral hemispheres, is reduced in males when compared to females. Panksepp points
out that androgen (testosterone is the primary androgen) and estrogen receptors are
concentrated in certain brain areas, "down to the lower reaches of the spinal cord, where
both male and female sexual reflexes are controlled." Panksepp reports that in the lower
spinal cord, the nucleus of the bulbocavernosus is distinctly larger in males than in
females.
As we discuss above, specialized neurochemicals combine with specialized
neurocircuitry and, as Panksepp puts it, "can trigger complex and coordinated sequences
of sexual behavior." He writes: "If one places a small, naturally occurring, nine-amino
acid peptide called vasotocin into the brains of male frogs and lizards, they begin to
exhibit courting sounds and sexual behaviors. Given the opportunity, males treated with
vasotocin mount and clasp females and copulate." The picture to the right (links to
source) of two green anoles mating naturally is courtesy of
winott@snakesandfrogs.com.
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In mammals, Panksepp explains that two neurochemicals very similar to the reptilian
vasotocin play a role in sexual behavior. These two mammalian neurochemicals are
vasopressin and oxytocin; they "assume key roles in controlling certain aspects of
sexual behaviors" and each "differs from vasotocin [the reptilian neurochemical] by
only one amino acid."
Panksepp emphasizes that vasopressin and oxytocin are not strictly male and female
neurochemicals. Both play a role in the reproductive and parental behavior of both
males and females. Vasopressin is more abundant in the male brain and has a primary
effect on male sexual and social behavior. Vasopressin mediates "many aspects of male
sexual persistence (including courtship, territorial marking, and intermale aggression)."
Panksepp elaborates on the male rat sex act:
the general male strategy (facilitated by testosterone) is to exhibit fairly persistent
searching for numerous sexual interactions … followed by the emission of vigorous …
50 KHz vocalizations … which, if the female does not object, culminate in …
copulatory behavior. … the male mounts the female from the rear, palpating her flanks
with his forepaws to arouse an arched-backed, rump-raised receptive posture called
lordosis. Whereupon, the male rat exhibits sets of rapid thrusting movements called
intromissions, which, if well guided, lead to entry of the penis into the vagina. After a
series of intromissions, the male ejaculates, which is accompanied by a "deep thrust,"
and then he pushes off, often falling over in the process. He then attends to personal
matters, with intense grooming of his genital area, with a shift to 22 KHz …
vocalizations.
Panksepp points out that, in the female brain, vasopressin energizes "some of the more
aggressive aspects of maternal behavior (i.e., protecting the young from harm)."
Oxytocin is more abundant in the female brain. Panksepp writes: "Animal research
indicates that both brain opioid and oxytocin circuits are activated by various
pleasurable pro-social activities, such as grooming, play, and sexual interchange."
Oxytocin mediates "female social and sexual responsivity (especially the tendency of
female rodents when mounted to exhibit lordosis…)," writes Panksepp. He explains that
sensitization of female sexual eagerness transpires in the ventromedial nucleus of the
hypothalamus and that damage to this area impairs responsivity. Panksepp writes:
The sex hormones that prepare the body for fertilization also dramatically change
neurochemical sensitivities in this part of the brain. … Hormone priming (just like
normal estrus) leads to a proliferation of oxytocin receptors in the medial hypothalamus,
as well as an expansion of the dendritic fields, which physically expand, reaching out
toward the incoming oxytocinergic nerve terminals arising from more rostral neurons.
This completes a circuit that sensitizes the lordosis reflex of the spinal cord (and
presumably prepares the female psychologically to interact seductively with males).
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Regarding the female rat's role in the sex act, Panksepp writes: "The most evident
behaviors in the rat are repeatedly running toward and away from the male, or past him
in a hopping, darting fashion with the head wiggling and many 50 KHz vocalizations."
In the male brain, oxytocin sustains "some of the gentler aspects of male behavior (e.g.,
the tendency of fathers to be nonaggressive and supportive toward their offspring)."
Oxytocin "also appears to help mediate the behavioral inhibition, or 'refractory
period,' that follows orgasm in males."
Gender determinants—the role of testosterone:
In Affective Neuroscience, Panksepp writes: "One is typically born either
genetically female (with the XX pattern of sex chromosomes) or
genetically male (with the XY pattern)." These sets of chromosomes are
not, however, the ultimate determination of gender. Panksepp says that
"masculinization results from the organizational effects of fetal
testosterone, which, in humans, occur during the second trimester of
pregnancy."
So what prompts fetal testosterone? "What the Y chromosome provides for
the male is testis determining factor (TDF)," explains Panksepp, "which
ultimately induces the male gonadal system to manufacture testosterone.
The XX pattern allows things to progress in the ongoing feminine manner,
unless some external source of testosterone (or, more accurately, one of its
metabolites) intervenes." The photograph to the left is of an X chromosome
and a Y chromosome and was taken with an electron microscope (image
links to source). This photograph is part of "Life in the Universe"
coursework. Nicholas M. Short, Sr. NASA, developed the coursework.
After fetal testosterone has been synthesized from cholesterol, via many
steps that include the intermediates progesterone and
dihydroepiandrosterone, it can be biochemically modified in two distinct
ways to imprint maleness onto the XY fetus. Panksepp explains that the
"timing and intensity" of these processes determine how the XY fetus's
brain and body development proceeds. The two processes to which
Panksepp refers are clarified below:
To organize the male body, the enzyme 5α-reductase assists in converting
testosterone into the steroid dihydrotestosterone (DHT)
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To organize the male brain, the enzyme aromatase assists in converting
testosterone into the steroid estrogen
These processes are confusing since most people associate estrogen
production strictly with being female when in reality it is estrogen that
organizes the male brain. Panksepp explains that "the XX sex chromosome
pattern informs the female body to manufacture proteins such as the
steroid-binding factor alpha-fetoprotein… ." This chemical "protects the
female fetus from being masculinized by the generally high levels of
maternal estrogens. If there is not enough of this fail-safe factor, or it the
maternal levels of estrogens are so high that they saturate the available
alpha-fetoprotein, the female will proceed toward a male pattern of
development—sometimes in both body and mind, sometimes in one but not
the other, depending on the hormonal details that have transpired."
The effects of maternal stress on gender:
Regarding development of the XY fetus and the two modifications to
testosterone that imprint maleness mentioned above, Panksepp notes that
the "products of testosterone metabolism are critical ingredients that dictate
whether a genetic male will continue along the male path in terms of body
and brain development, both before and after puberty." He explains that
"homosexuality and bisexuality are promoted if 'errors' occur in the various
control points of these biochemical processes … ." Regarding such errors,
Panksepp writes: "It has been repeatedly shown in animal models that
maternal stress can hinder the normal process of brain masculinization by
desynchronizing the underlying physiological processes… ."
In a normal litter from unstressed rat mothers, approximately eighty percent
of the male offspring will exhibit male-typical, sex-seeking behavior while
twenty percent remain asexual. Panksepp emphasizes that stress changes
these ratios. "When a pregnant rat is exposed to any of a variety of stressors
during the last trimester (third week) of the three-week gestation period,"
only about 20 percent of male offspring will exhibit male-typical, sexseeking behavior while sixty percent are either bisexual or homosexual.
The bisexual XY rats exhibit male behavior with a highly receptive female
and female behavior in response to a sex-seeking male. The homosexual
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XY rats exhibit lordosis when a sexually aroused male mounts them. As in
unstressed litters, the remaining twenty percent of rats born to stressed rat
moms are asexual. Panksepp does point out, however, that environment has
some effect on sexuality. He writes: "The male offspring of stressed
mothers exhibit more 'normal' sexual behavior if they are housed
continuously during adulthood with sexually experienced females."
The role of genetics and timing in determining gender:
In addition to the effects of stress on gender development, Panksepp
provides an example of how a genetically induced neurochemical
deficiency can affect gender, at least during childhood. Some babies born
in the Dominican Republic appear female at birth, although close
inspection would reveal some enlargement of what seems to be a clitoris.
Panksepp explains that in the womb, these XY children do secrete
testosterone at the usual time and since they have normal aromatase
activity, their testosterone is converted to estrogen. Accordingly, their
brains are fully organized as male. Because they are genetically deficient in
5α-reductase, however, testosterone is not converted to DHT so their
bodies do not appear male at birth. When such XY children "enter puberty
and begin to secrete testosterone," writes Panksepp, "they develop maletypical bodies—with an increase of body hair, deepening of the voice,
enlargement of the penis, and finally, the descent of the testes. Male-typical
sexual urges also begin to emerge. Thus, the boys' pubescent erotic desires
come to be directed toward females, even though they were reared as girls
throughout childhood!" These boys are called guevedoces, which means
"penis at 12," notes Panksepp.
"The hormones secreted at the onset of puberty," observes Panksepp,
activate "the latent male or female sexual proclivities that have remained
comparatively dormant within brain circuits since infancy." He writes:
"Thus, the brain substrates for sexuality that are organized by these early
hormonal experiences help determine what type of gender identities, erotic
desires, and sex behaviors individuals will exhibit at puberty, when the
elevations in hypothalamic gonadotrophic hormones and gonadal sex
steroids begin to 'activate' sexual tendencies."
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Mariateresa Molo et al., in "Characteristics of Brain Activity in Patients
With Gender Identity Disorder," provides support for the idea that an XY
fetus can end up with a female-type brain and that an XX fetus can end up
with a male-type brain. The researchers found bioelectrical similarities in
the brains of female controls and male-to-female transsexuals. Likewise,
they found similarities in the brains of male controls and female-to-male
transsexuals.
Books about gender:
David Bainbridge, The X in Sex: How the X Chromosome Controls our
Lives, Harvard University Press, Cambridge, 2003.
Simon LeVay, Gay, Straight, and the Reason Why: The Science of Sexual
Orientation, Oxford, 2010.
Sistema de cuidado o crianza (Care-especialmente en el
educador)
Según Pankseep, es probablemente una fuente primaria de la empatía.
Participan en él: la corteza cingulada, área septal, nucleos basales, amígdala y algunas
áreas del hipotálamo. Está íntimamente relacionado con el nivel de oxitocina. La
lactancia, las caricias, el lamido o las palabras amables de alguien querido, incrementan
el nivel de oxitocina. En el caso de las caricias o de las lamidas de las madres, caso de
las ratas, se ha demostrado que mejoran la resistencia al stress de las crías en la edad
adulta (McGowan y cols, 2011) . Las mujeres tienen un nivel medio superior a los
hombres.
Se puede activar con los llantos y gritos de la cría.
In Affective Neuroscience: The Foundations of Human and Animal
Emotions (1998), Jaak Panksepp proposes that nurturance in mammals
probably "arose from neurochemical processes that controlled mating and
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15
egg laying in reptiles." The precursor of mammalian oxytocin, the
neurochemical vasotocin, explains Panksepp, "controls sexual urges in
reptiles" and "helps deliver reptilian young into the world." Regarding
reptiles, Panksepp writes: "Although a number of species—for instance,
crocodiles—do exhibit some parental care, it is meager by mammalian
standards." He provides a delightful story to illustrate hands-off reptilian
parenting:
When a sea turtle, after thousands of miles of migration, lands on its
ancestral beach and begins to dig its nest, an ancient birthing system comes
into action. The hormone vasotocin is secreted from the posterior pituitary
to facilitate the delivery of the young. Vasotocin levels in the mother
turtle's blood begin to increase as she lands on the beach, rise further as she
digs a pit large enough to receive scores of eggs, and reach even higher
levels as she deposits one egg after the other. With her labors finished, she
covers the eggs, while circulating vasotocin diminishes to insignificant
levels… . Her maternal responsibilities fulfilled, she departs on another
long sea journey. Weeks later, the newly hatched turtles enter the world
and scurry independently to the sea without the watchful, caring eyes of
mother to guide or protect them.
As mammals evolved, vasotocin evolved into oxytocin and arginevasopressin (AVP), the neurochemicals so very important to mating
behavior. As we discuss in The MATING System, the Brain, and Gender
Determination, these two mammalian neurochemicals differ from
vasotocin, the reptilian neurochemical, by only one amino acid. Panksepp
points out that oxytocin, the same neurochemical which prompts
receptivity in female mammals—including the lordosis reflex in the rat—
also prepares "the mother's brain for nurturance." He writes: "The initial
clue that there is an intrinsic bodily signal to promote maternal behavior
was the fact that transfusion of blood from a female rat that had just given
birth could instigate maternal behaviors in a virgin female."
Maternal care, hormones, and brain anatomy:
In rats, Panksepp reports that a "heightened maternal desire corresponds to
the peak" of hormonal changes, "reaching an apex several hours before
birth." Rat mothers begin to build nests for their offspring during this time.
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16
Panksepp explains that "estrogen, which has remained at modest levels
throughout pregnancy, rapidly increases as parturition nears. Progesterone,
which has been high throughout pregnancy, begins to plummet. And, of
course, there is a precipitous rise in prolactin, which induces the mother's
acinar glandular tissues to manufacture milk." Panksepp writes: "Prolactin
may be the critical ingredient in sustaining the natural behavior sequence,
not only because brain injections of prolactin promote nurturance, but
females who are nonmaternal because they have been surgically deprived
of their pituitary glands do gradually become maternal when replacement
injections of prolactin are provided."
Regarding oxytocin, Panksepp notes that "during the last few days of
pregnancy and the first few days of lactation, there are remarkable
increases in oxytocin receptors in several brain areas, as well as increases
in the number of hypothalamic neurons that begin to manufacture this
neuropeptide." He writes: "During lactation, oxytocin cells begin to
communicate with each other directly via the development of gap junctions
between adjacent oxytocinergic neurons, allowing them to synchronize
their neural messages precisely." Regarding specific structures in the brain
where this activity takes place, Panksepp points out that "the greatest
oxytocin receptor proliferation is observed in the bed nucleus of the stria
terminalis (BNST); when that area is damaged, maternal behavior is
severely impaired." We discuss the stria terminalis in other sections of
MyBrainNotes.com but I will reiterate here the excellent description found
in MedlinePlus Dictionary. The stria terminalis is "a bundle of nerve fibers
that passes from the amygdala along the demarcation between the thalamus
and caudate nucleus mostly to the anterior part of the hypothalamus with a
few fibers crossing the anterior commissure to the amygdala on the
opposite side."
Panksepp notes that "lesions of the BNST and the nearby POA [preoptic
area within the hypothalamus] can eliminate essentially all aspects of
maternal behavior." The preoptic area lies in the same general subcortical
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17
area as the BNST; this area is outlined with a red circle in the MRI image
above left (links to source). Oxytocin prompts signaling in neurons that exit
"from the POA laterally and descend in the medial forebrain bundle, with
key terminals being in the VTA [ventral tegmental area]." The VTA is
located in the midbrain, very near to the BNST, as illustrated in the MRI
image above left. The illustration to the right shows the position of the
preoptic area within the hypothalamus. This image is from Endocrinology,
S.S. Nussey and S.A. Whitehead, obtained from the NCBI bookshelf (links
to source).
As we discuss in Dopamine action, synthesis, and pathways, neurons in the
VTA within the midbrain synthesize dopamine, which is essential to
motivated behavior. Panksepp writes: "It has been established that the
oxytocinergic synapses that terminate on dopamine cells on the VTA do, in
fact, promote maternal behavior." He explains that oxytocin injections into
the VTA "can induce maternal behavior… ."
Panksepp points out that "well-established maternal behavior no longer
requires brain oxytocin arousal; oxytocin blockade impairs maternal
behavior only if administered to mothers during the birth of their first litter
of pups. In animals that have been allowed to exhibit maternal behavior for
several days, oxytocin antagonists have no outward effect on maternal
competence." In other words, even when drugs block oxytocin, such action
does not block previous learning. In addition to neurons in the pre-optic
nucleus of the hypothalamus, neurons in the paraventricular nucleus (PVN)
of the hypothalamus also produce oxytocin. Panksepp writes: "PVN lesions
administered prior to parturition weaken subsequent maternal behavior, but
those administered after several days of normal maternal functioning do
not." His postulates that "a great deal of learning is probably controlled in
the higher reaches of CARE circuits such as the anterior cingulate cortex
and bed nucleus of the stria terminalis [BNST]."
Unfortunately, the circumstances within which human infants are born are
not always supportive of necessary learning curves and attachment.
Panksepp illustrates:
For instance, not too long ago in certain arctic aboriginal groups, such as
the Netsilik Eskimo of northern Canada, long-term social concerns often
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18
overrode short-term emotional ones. Female babies who had little hope of
finding an appropriate mate, because no male babies of comparable age had
been born in the tribe, would be left to die in the snow, with little outward
distress or remorse exhibited by the parents.
In addition to adverse cultural pressures in various human cultures, it is my
opinion that another anxiety-provoking circumstance—uncertain
paternity—can also affect a woman's attachment to her offspring. The fear
that the questionable paternity issue will be discovered can only lead to a
great deal of anxiety—the focus of which, of course, is the baby. I contend
this kind of situation happens much more often than we humans are willing
to admit.
Access to sex, male oxytocin, and reduced aggression:
Above, we discuss the neurochemical details of a mother's attachment to
offspring. But what about neurochemicals and paternal attachment?
Panksepp is clear on this: "Oxytocin administration reduces all forms of
aggression that have been studied." In rodents, Panksepp points out that
"free access to sexual gratification can lead to an enormous threefold
elevation in oxytocin levels in some parts of the male brain. Apparently,
sex promotes the synthesis of nurturant and antiaggressive
neurochemistries." Male rat behavior bears this out. Panksepp reports that
male rats will often "kill the young in a territory they have successfully
invaded." However, once they have mated with a female, most often any
rats born three weeks later are spared. This makes evolutionary sense since,
as Panksepp explains, for rats, "it typically takes three weeks from the time
of successful fertilization to the time of birth." In other words, the increased
oxytocin in male rats that have had sex makes the male rats more nurturing
and less aggressive. But how do researchers know it is the oxytocin that
promotes nurturing behaviors? In the laboratory, when a male rat is placed
into a new territory where there are young rats, he would be expected to kill
the rat babies. But when oxytocin is administered to the male rate in this
situation, Panksepp notes that the tendency to commit infanticide
"dramatically diminishes."
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Sistema de juego
Es un sistema que permite adquirir habilidades sociales y motrices que no son innatas.
Produce placer y está intimamente vinculado a la risa. El juego se produce muy
claramente en todos los mamíferos que requieren de complejas habilidades sociales y
destrezas motoras.
"To the best of our knowledge," writes Jaak Panksepp in Affective
Neuroscience: The Foundations of Human and Animal Emotions (1998), "a
basic urge to play exists among the young of most mammalian species…."
He recounts Jane Goodall's experience with chimpanzees: "A chimpanzee
infant has his first experience of social play from his mother as, very
gently, she tickles him with her fingers or with little nibbling, nuzzling
movements of her jaws. Initially these bouts are brief, but by the time the
infant is six months old and begins to respond to her with play face and
laughing, the bouts become longer."
Before initiating play, animals must be comfortable. "Indeed, when placed
in new environments, animals typically exhibit strong exploratory activity
with little tendency to play until they have familiarized themselves with the
new surroundings," writes Panksepp. "In all species that have been studied,
playfulness is inhibited by motivations such as hunger and negative
emotions, including loneliness, anger, and fear." Panksepp points out that
in "most primates, prior social isolation has a devastating effect on the urge
to play. After several days of isolation, young monkeys and chimps become
despondent and are likely to exhibit relatively little play when reunited. …"
He notes that playfulness returns "only when confidence has been
restored." Rodents respond differently to isolation. "Laboratory rats show a
greater emotional equanimity in coping with social isolation as compared
to many other mammals." writes Panksepp. "Prior social isolation
systematically increases roughhousing play in juvenile rats, while social
satiation systematically reduces it."
While hunger reduces play behavior in young rats, "a single meal brings
play right back to normal," reports Panksepp. "It may come as a surprise to
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20
some, but young rats given no other ludic [from ludare, meaning 'to play']
outlets love to be tickled by and play with a frisky human hand." He points
out that juvenile rats exhibit rough-and-tumble play behaviors "even if they
have been prevented from having any prior play experiences during earlier
phases of development." Panksepp explains that young rats start to play
around 17 days of age, and if denied social interaction throughout the early
phases of psychosocial development (e.g., from 15 to 25 days of age), "they
play vigorously as soon as they are given their very first opportunity."
Panksepp concludes that the impulse for rough-and-tumble play "is created
not from past experiences but from the spontaneous neural urges within the
brain."
The rough-and-tumble PLAY system "is important for learning various
emotional and cognitive skills," Panksepp emphasizes, "including
aspirations for social dominance and cooperation, which influence behavior
with different intensities throughout the life span of each animal." He
explains that "play may allow young animals to be effectively assimilated
into the structures of their society. This requires knowing who they can
bully, and who can bully them. One must also identify individuals with
whom one can develop cooperative relationships, and those whom one
should avoid." Panksepp points out that "the most vigorous play occurs in
the context of preexisting social bonds." In contrast, he says that if "one
animal becomes a 'bully' and aspires to end up on top all the time, playful
activity gradually diminishes and the less successful animal begins to
ignore the winner."
"Play probably allows animals to develop effective courting skills and
parenting skills," writes Panksepp, "as well as increasing their effectiveness
in various aspects of aggression, including knowledge about how to accept
defeat gracefully." He points out that "PLAY circuitry allows other
emotional operating systems, especially social ones, to be exercised in the
relative safety of one's home environment. Thus, in the midst of play, an
animal may gradually reach a point where true anger, fear, separation
distress, or sexuality is aroused." Panksepp notes, however, that serious
aggressive postures and sexual-type behaviors are rarely seen in playfighting. During the later stages of juvenile life, because of their larger size
and stronger competitive urges, more mature male animals may appear to
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21
play more vigorously than their smaller companions. This difference,
Panksepp explains, may in part reflect the drive to attain male dominance.
He writes: "It is certainly possibly that PLAY systems contribute to social
dominance urges, which may help explain our love of rough professional
sports, where such issues are paramount in the minds of players and
spectators alike."
Regarding the nonsocial functions of PLAY neurocircuitry, Panksepp
points out that play increases physical fitness, skillful tool use, and the
ability to innovate and think creatively. Young predators learn to hunt and
prey species learn how to avoid predators. He writes: "Indeed, perhaps play
even allows animals to hone deceptive skills, and thus in humans may
refine the ability to create false impressions."
The brain's PLAY neurocircuitry:
PLAY neurocircuitry appears to be "intimately linked to somatosensory
information processing within the midbrain, thalamus, and cortex,"
explains Panksepp. John A. Beal, Department of Cellular Biology and
Anatomy, Louisiana State University, provides the image below. I have
added labeling for these three areas of the brain. We discuss sensory
information processing in Part 1 of MyBrainNotes.com in The brain's
motor and somatosensory cortical maps.
PLAY neurocircuitry certainly helps young animals learn to interact with
their environment since somatosensory information is obtained from the
sense organs, such as the eyes and ears. Touch is also a form of
somatosensory information. Generally speaking, somatosensory
neurosignaling conveys information about the state of the body and
immediate environment, such as body position and ambient temperature.
Within the thalami, Panksepp notes that somatosensory information is
projected in two directions—up to the parietal cortex that processes bodily
sensations and into nonspecific thalamic nuclei that elaborate a playful
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22
motivational state. He points out that bilateral damage to thalamic areas
involved in PLAY circuitry reduces both pinning and dorsal contacts and
that "lesioned animals are no longer motivated to play." Panksepp reports
that in such lesioned animals, "other relatively complex motivated
behaviors, such as food seeking (foraging), are not diminished." John A.
Beal, Department of Cellular Biology and Anatomy, Louisiana State
University, provides the image above (links to source).
Panksepp emphasizes that PLAY behavior is an "endogenous urge" within
the brain and does not necessarily rely on somatosensory input. In rats,
"neither vision nor olfactory senses (including vibrissae) are necessary for
the generation of normal play." He points out that the "auditory system
contributes positively to play to some extent, since deafened animals play
slightly less, and rats do emit many 50-KHz laughter-type chirps both
during play and in anticipation of play." Panksepp explains that touch is the
sensory system that helps most in instigating and sustaining normal play.
Regarding experiments to test the importance of touch in generating PLAY
behavior, Panksepp writes: "Local anesthetization of the neck and shoulder
area is highly effective in reducing the level of playful pinning in young
rats even though the motivation for play, as measured by dorsal contacts, is
not reduced." Citing laboratory evidence, Panksepp concludes that "rats
have specialized skin zones that send play signals into the nervous system
when they are touched. In other words, mammals appear to have 'play skin,'
or 'tickle skin,' with specialized receptors sending information to specific
parts of the brain that communicate playful intentions between animals."
In animals that have had their cortex removed, "play solicitations and
overall roughhousing, as monitored by direct activity measures, remain
intact," writes Panksepp, although pinning behavior is reduced by about
half. "It seems clear that play has powerful effects on the cortex." Panksepp
concludes that juvenile play "involves programming various cortical
functions." He writes: "In a sense, the cortex may be the playground of the
mind, and PLAY circuits may be a major coordinator of activities on the
field of play."
Laughter and the brain:
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23
Panksepp asserts that "the hallmark of PLAY circuitry in action for humans
is laughter, a projectile respiratory movement with no apparent function,
except perhaps to signal to others one's social mood and sense of carefree
camaraderie." (Photo courtesy of David Shankbone.)
"Laughter," Panksepp explains "is not learned by imitation, since blind and
deaf children laugh readily." Ethologists consider genuine laughter to be
innate and primal. The social smile is more contrived. In Part 1 of
MyBrainNotes.com, we discuss the emotional versus the social smile in
The anterior cingulate cortex–emotion, attention, and working memory.
Panksepp notes that "an openmouthed display characterizes the most
intense forms of human laughter, and similar gestures are used as signals
for play readiness in other species such as chimpanzees and dogs." He adds
that chimpanzees' reunion rituals, "especially after long separations, are
typically characterized by a lot of hooting, howling, and touching."
Other evidence indicating that specific neurocircuitry in the brain generates
laughter is that "amylotrophic lateral sclerosis (ALS), a demyelinating
disease that affects the brain stem," according to Panksepp, "can release
impulsive laughter." He also points to "gelastic epilepsy, which is
accompanied by bouts of laughter."
ADHD and PLAY neurocircuitry:
Previously, in Attention, Learning, and Memory: The VIGILANCE
System, we learned that in ADHD, due to low levels of norepinephrine and
perhaps, dopamine, the prefrontal cortex fails to adequately inhibit
inappropriate impulses or distractions. Panksepp postulates that "many
children diagnosed with ADHD may, in fact, be exhibiting heightened play
tendencies." He writes:
Their hyperactivity, impulsiveness, and rapid shifting from one activity to
another may be partly due to their unconstrained and unfocused playful
tendencies. Indeed, the medications that are used to treat the disorder—
psychostimulants such as methylphenidate (i.e., Ritalin) and
amphetamines—are all very effective in reducing playfulness in animals.
Moreover, parents of hyperkinetic children often complain that one of the
undesirable side effects of such medications is the reduced playfulness of
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24
their children. Obviously, parents value these childlike characteristics and
are typically disturbed when the children's natural playfulness is
pharmacologically diminished.
Autism, opioids, and PLAY neurocircuitry:
"Virtually all investigators now agree that autism is a neurobiological
disorder," writes Panksepp in Affective Neuroscience. He explains that
compared to normal brain development, people with autism have "an
undersized cerebellum and brain stem, and a larger than normal cerebrum,"
along with "too many densely packed small neurons within parts of the
limbic system, suggesting that selective cell death, a natural process of the
developing brain called apoptosis, has not progressed normally." The result
is that in autistic individuals, subcortical or so-called limbic structures do
not interconnect with the rest of the brain as well as they normally would.
Panksepp quotes Leo Kanner, who in 1943 proposed that autistic children
"have come into the world with an innate inability to form the usual,
biologically provided affective contact with people." Panksepp reports that
the "current theoretical perspective is that these children do not develop a
'theory of mind,' which refers to the ability of most children past the age of
2 to begin recognizing the types of thoughts and feelings that go on in the
minds of others."
The motivation for rough-and-tumble PLAY, Panksepp points out, "is
practically the only social desire that autistic kids exhibit at a relatively
high level, but not with the reciprocating give and take and fantasy
structures of normal childhood play." He notes that rats treated with low
doses of opioids, like autistic children, do not exhibit a high desire for
social companionship except for rough-and-tumble play. Panksepp
proposes that "autistic children may have been exposed to excessive levels
of endogenous opioids, or related molecules, during early development."
He writes:
Moreover, they may continue to experience excessive opioid activity
within certain circuits of their brains as they mature. This could explain
their pain insensitivity and consequent tendency to exhibit self-injurious
behavior, as well as many other symptoms ranging from stereotypies to
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25
social aloofness. Because of these considerations, it has been suggested that
some benefits may be brought to these children by the administration of
opiate receptor blocking agents such as naltrexone.
Naltrexone may improve the lives of those autistic children "who have high
circulating levels of opioids in the brain, a condition that has been
demonstrated in about half of all autistic children who have been tested,"
explains Panksepp. "Moderate doses of naltrexone can reduce some of the
active symptoms of autism such as overactivity, stereotypies, and selfinjurious behaviors, and in low infrequent doses, it can promote social
activities."
Sistema de miedo
El miedo según Le Doux es fundamentalmente un sistema de proceso secundario, no
consciente que opera como una respuesta condicionada ante las amenazas. Tiene una
alto valor adaptativo para la supervivencia y por lo tanto, no precisa ser consciente. Hay
que diferenciarlo conceptualmente según Ledoux (2014), del miedo consciente.
Fear conditioning thus became a process that is carried out by
cells, synapses, and molecules in specific circuits of the nervous
system. As such, fear conditioning is explainable solely in terms
of associations created and stored via cellular, synaptic, and
molecular plasticity mechanisms in amygdala circuits. When the
CS later occurs, it activates the association and leads to the expression
of species-typical defensive responses that prepare the
organism to cope with the danger signaled by the CS. There is no need for conscious feelings of fear to intervene.
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26
Research on patients with brain damage revealed that fear
conditioning creates implicit (nonconscious) memories that are distinct from explicit/declarative (conscious) memory
La amígdala es el órgano más estudiado (Ledoux) del sistema de miedo defensivo pero
intervienen también otras zonas mesolímbicas y de la corteza prefrontal. A su vez, la
amígdala se subdivide en varias estructuras. Se interrelaciona intensamente con los
circuitos del placer (Berridge). A continuación Ledoux se describe la estructura y el
funcionamiento de la amígdala en un proceso de condicionamiento clásico defensivo
por miedo.
The lateral nucleus of the amygdala (LA) receives sensory inputs about the CS and US. Before training, the CS only
weakly activates LA neurons (Le doux, 2014).
The neural circuits and cellular, synaptic, and molecular
mechanisms underlying the acquisition and expression of conditioned
fear responses have been characterized in detail (4, 5,
53, 80–82). (For a different perspective on the circuitry, see refs.
49 and 83.) The lateral nucleus of the amygdala (LA) receives
sensory inputs about the CS and US. Before training, the CS only
weakly activates LA neurons. After the CS is paired with the US,
the ability of the CS to activate the LA increases. When the CS
later occurs alone, CS activation of the LA leads to neural activity
that propagates through amygdala circuits to the central
nucleus (CeA). Output connections of CeA then result in the
expression of defensive behavior and physiological responses, as
well changes brain arousal. Plasticity also occurs in the central
nucleus of the amygdala (84–86) and in CS sensory processing areas (87). At the cellular and molecular levels, fear
conditioning
occurs when LA neurons that process the CS are weakly activated
at the same time that the US strongly depolarizes the
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27
neurons (5, 53, 80, 81, 88, 89). This results in an increase in the
strength of the synapses that process the CS, allowing it to more
effectively activate amygdala circuits. Molecular mechanisms
engaged result in gene expression and protein synthesis, stabilizing
temporary changes in synaptic strength and creating longterm
memories. Many of the molecular findings were pursued
following leads from invertebrate work (14, 77, 90).
Los estudios sobre la amígdala y sus relaciones con la corteza prefrontal, nos ponen de
manifiesto (Ledoux) que las conexiones entre el cortex y la amígdala son más débiles
que las que se producen entre la amígdala y el resto del cerebro, lo que podría explicar
la dificultad de controlar los estados emocionales agresivos, una vez que éstos se han
desencadenado. La estimulación de la amígdala a través de estímulos visuales
desencadena reacciones de miedo, ansiedad o pánico que deberán ser reguladas por la
corteza prefrontal. A su vez, los estados emocionales generados en la amígdala están
vinculados neuronalmente con el hipocampo y son muy relevantes en la formación de
memorias.
.
Sistema de rabia o ira
http://mybrainnotes.com/brain-rage-violence.html
Es un sistema que se activa en escenarios naturales en situaciones extremas. Por
ejemplo en la lucha por la caza, o contra los enemigos o depredadores. Es un sistema de
apariencia negativa pero indispensable para la supervivencia.
When we think of rage, we often think of crime, and then guilt. In doing
this, we fail to recognize that rage is an innate emotional system in the
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28
human brain that contributes to our survival. Stimulating specific
neurocircuitry evokes rage in laboratory animals. Physical brain damage
and seizures can certainly affect how this innate neurocircuitry operates
and sometimes makes rage neurocircuitry more responsive, more
automatic. Moreover, evidence indicates that extremely negative
experiences can result in physiological changes in the brain that may
predispose one to bouts of rage.
(1998), Dorothy Otnow Lewis describes
The lesions between the cortex of the frontal lobes and the rest of the
central nervous system, between the self-reflective portions and the more
instinctual portions of the brain, also contributed to Lucky's episodic
violence. When the cortex of a cat is separated surgically from the rest of
the brain, leaving only the lower centers of the brain intact, the cat may at
first glance appear normal. The decorticate animal, when stimulated,
becomes ferocious, directing its attack at anything it perceives as
threatening or uncomfortable.
Regarding how negative experience affects the brain, Lewis writes:
What fascinates me most is the fact that brain concentrations of substances
like serotonin are not immutable. They are not simply genetic givens—
experience affects them. Certain kinds of stressors can decrease brain
serotonin levels and thereby change behavior. For example, if you isolate
animals at crucial developmental stages, if you keep them caged all alone,
their serotonin drops. What is more, when you then release them and put
them in contact with other animals, they are fiercely aggressive. Pain and
fear also reduce serotonin levels and promote aggression.
Rage, predatory, and other aggressions defined:
It seems that aggression, in its varied forms, arises from very different
neural circuits in the brain. In Affective Neuroscience: The Foundations of
Human and Animal Emotions (1998), Jaak Panksepp explains that
scientists applying electrical stimulation to "slightly different brain zones"
in laboratory animals evoke three distinct kinds of aggression. 1) predatory
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29
aggression, 2) rage-like aggression, and 3) inter-male aggression or
dominance aggression. Panksepp points out that "prolonged social isolation
or hunger may increase all forms of aggression, while high brain serotonin
activity may reduce them all."
Circuitry that prompts aggression is quite specific. Panksepp explains that
quiet-biting attack is typically evoked during electrical stimulation of the
dorsolateral hypothalamus while rage-driven aggression is typically evoked
during electrical stimulation of the ventrolateral and medial hypothalamus.
Electrical stimulation to SEEKING system locations in rats and cats
prompt different behaviors. Panksepp writes: "The species-typical
expressions of this system lead to foraging in some species and predatory
stalking in others." Stimulating this system in cats results in predatory
stalking and quiet-biting attack. "Obviously, this is a reasonable speciestypical SEEKING behavior for a carnivorous animal that subsists at the top
of the food chain."
Panksepp points out that when scientists stimulate specific circuits for ragedriven aggression in humans, the subjects report "experiencing a feeling of
intense rage." When rats are stimulated in specific RAGE neurocircuits,
they will attempt escape. Panksepp explains that most animals have
"unpleasant affective experiences" during electrical stimulation to RAGE
neurocircuits in their brain. He observes that such animals "exhibit
piloerection, autonomic arousal, hissing, and growling," and readily learn
to turn the stimulation off. He points out that these animals direct their
anger towards anything in their environment perceived as a threat, even
members of their own species.
In addition to innate circuitry for predation, rage, and dominance, Panksepp
discusses how animals develop a kind of "defensive" aggression which
"emerges largely from a dynamic intermixture of RAGE and FEAR
systems." He also draws attention to innate "appeasement" behaviors." An
animal that lies on it's back and exposes vulnerable parts like the belly and
neck can often reduce aggression by others of the same species. Sometimes
the appeasement signal is vocal. Panksepp writes: "Defeated rats often emit
long 22 Khz vocalizations."
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Panksepp also categorizes infanticide as a form of aggression although
pinpointing specific circuitry for this kind of behavior is not so easy. In the
animal world, especially including rats, it seems that males sometimes kill
the offspring of another male in order to stop lactation in the female
mother, restoring her reproductive abilities. The new male is thus able to
more quickly mate and produce his own offspring. "Considering that
female rats have a three-week gestational period," Panksepp writes, "it was
anticipated that the pup-killing tendencies of males might diminish
approximately three weeks after mating, at about the time their own
offspring might be born." He explains that research in the laboratory
indicates that this is exactly what happens. Panksepp points out two other
motivators of infanticide: "A mother may kill and consume some of her
own offspring if food is scarce, even though such killing can also occur for
more subtle 'political' reasons. Perhaps the most famous perpetrators of
such acts were the cruel female chimpanzees, Passion and her daughter
Pom, who killed off at least three and probably more of the young infants
of other females in the group that Jane Goodal studied for many years."
A very interesting observation that Panksepp makes relates to genetic
transmission of aggression. He points out that "genetic selection
experiments in both male and female rodents indicate that one can
markedly potentiate aggressiveness through selective breeding within a half
dozen generations, and that breeding for aggression is as effective in
females as in males."
The brain's RAGE neurocircuitry:
In Affective Neuroscience, Panksepp points to the work of Walter Hess
during the 1930s in determining that electrical stimulation to certain brain
areas can produce rage behavior in animals. Hess won the Nobel Prize in
1949. Panksepp writes: "It has long been known that one can enrage both
animals and humans by stimulating very specific parts of the brain, which
parallel the trajectory of the FEAR system." He adds: "Brain tumors that
irritate the circuit can cause pathological rage, while damage to the system
can promote serenity."
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Panksepp writes: "The
core of the RAGE system
runs from medial
amygdaloid areas
downward, largely via the
stria terminalis [a bundle
of nerve fibers] to the
medial hypothalamus, and
from there to specific
locations within the PAG
[periaqueductal gray] of
the midbrain."
In the illustration to the
left (links to source), the
amygdala is labeled on the
right and the thin stringlike stria terminalis, also
labeled on the right, links the amygdala to the hypothalamus, which lies
hidden beneath the thalamus in this illustration. Although not labeled, the
periaqueductal gray lies in the yellow center area that represents the
midbrain.
Regarding the kinds of stimuli that can access RAGE circuitry, Panksepp
points to such things as body surface irritation or when one does not
receive an expected reward. He explains that the most common triggers of
rage "are the irritations and frustrations that arise from events that restrict
freedom of action or access to resources." He points out that "a human baby
typically becomes enraged if its freedom of action is restricted simply by
holding its arms to its sides." Activation of RAGE circuits is "accompanied
by an invigoration of the musculature, with corresponding increases in
autonomic indices such as heart rate, blood pressure, and muscular blood
flow." According to Panksepp, the phrase "getting hot under the collar," is
accurate in that body temperature also increases during rage.
In the image below left, the medial hypothalamus is labeled in red lettering.
This image is from S.S. Nussey and S.A. Whitehead, Endocrinology, NCBI
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bookshelf (image links to source). For some perspective, the image below
right depicts the location and relative size of the hypothalamus as a whole
(image links to source).
RAGE circuitry is organized hierarchically. Lesions of higher areas such as
the amygdalae do not diminish responses from lower areas, while damage
to lower areas such as the medial hypothalami and periaqueductal gray
zones dramatically diminishes rage evoked from the amygdalae.
The image below (links to source) illustrates the position of the
periaqueductal gray of the midbrain and is taken from professor Robert
Lynch's course, "Territoriality and Aggressive Behavior," at the University
of Colorado at Boulder.
According to Panksepp, the following areas provide input to the
periaqueductal gray (PAG), a sort of primary generator for RAGE circuitry.
Panksepp emphasizes that most of these connections are reciprocating twoway circuits.
Areas of the frontal cortex containing reward-relevance neurons influence
RAGE circuitry.
Cortical areas called frontal eye fields, which help direct eye movements to
especially prominent objects in the environment, influence RAGE circuitry.
The orbitoinsular cortex, especially the insular area—where a multitude of
senses converge including pain and perhaps hearing—may provide specific
sounds direct access to RAGE circuitry. In humans, these sounds may
include, for example, an angry voice.
The medial hypothalamus provides powerful input related to energy (food)
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requirements and sexual matters thus influencing RAGE circuitry activated
in pursuit of such resources.
A lower area, the vestibular complex, may help enrage animals when their
bodily orientation is disturbed.
Cell groups such as the norepinephrine-producing loci coerulei and
serotonin-producing raphe nuclei, which exert modulatory control over all
behaviors, also influence RAGE circuits.
The nucleus of the solitary tract, which collects information via the vagus
nerve that is probably related to processes such as heart rate and blood
pressure, inputs to RAGE circuitry.
Sistema de pánico
Se puede desencadenar ante la separación de la figura de apego. Puede producirse
pérdida del apetito, sueño, irritabilidad y depresión. El neuromodulador principal es el
glutamato. Se ha estudiado a través de las vocalizaciones que realiza la cría cuando la
madre se separa de ella. También intervienen la noradrenalina, la serotonina y el factor
de liberación de la corticotropina (Panksepp, 2006).
Es un sistema diferente al del miedo. Implica una elevada ansiedad permanente y según
Pankseep es el fundamento de la depresión.
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Although they surely interact in some way, in Affective Neuroscience: The
Foundations of Human and Animal Emotions (1998), Jaak Panksepp
explains that "as indexed by measures of separation calls in species as
diverse as primates, rodents, and birds," PANIC/LOSS neurocircuitry is
clearly distinct from FEAR neurocircuitry. Electrical stimulation to very
specific brain areas, that we will refer to in this discussion as PANIC/LOSS
neurocircuitry, produces the separation calls to which Panksepp refers.
Although he considered both "sorrow" and "distress" as labels, he decided
to call the neurocircuitry that generates feelings of loneliness, grief, and
separation distress—as well as panic attacks in humans—the PANIC
system. I have added "LOSS" to Panksepp's "PANIC" to draw attention to
some of his observations that I find particularly meaningful.
The brain's PANIC/LOSS system and attachment:
Panksepp emphasizes that the PANIC/LOSS system "is especially
important in the elaboration of social emotional processes related to
attachment." He cites research that points to early childhood loss as a major
risk factor for future depression and panic attacks. He proposes that one
may be more vulnerable to depression and panic attacks "because of
permanent developmental modification of the emotional substrates of
separation distress." Indeed, in "Life Events Preceding the Onset of Panic
Disorder" (1985) Faravelli writes that panic patients were more likely to
have "underwent a major life event (death or severe illness, either personal
or of a cohabiting relative) in the two months preceding the onset of
symptoms."
Panksepp explains that "especially in intense forms such as grief,"
activation of PANIC/LOSS neurocircuitry "is accompanied by feelings of
weakness and depressive lassitude, with autonomic symptoms of a
parasympathetic nature, such as strong urges to cry, often accompanied by
tightness in the chest and the feeling of having a lump in the throat."
Panksepp explains: "To be a mammal is to be born socially dependent."
When "young animals are socially isolated, they typically lose weight even
if they have free access to lots of food. When the young are reunited with
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their kin, and a mood of apparent contentment is reestablished, appetite
returns."
"Brain evolution has provided safeguards to assure that parents (usually the
mother) take care of the offspring," writes Panksepp, "and the offspring
have powerful emotional systems to indicate that they are in need of care
(as reflected in crying or, as scientists prefer to say, separation calls)."
Regarding such vocalizations, Panksepp points out that "specific locations
in the auditory system, in both the inferior colliculi and the medial
geniculate nuclei, are highly tuned to receive and process these primal
communications." Panksepp provides a vivid example of the mother-infant
bond in the animal world:
The life of a young sea otter is completely dependent on the care provided
by its mother. After his sexual contribution, the father pays little heed to his
young. It is the mother's job to be both caretaker and food provider, as
often as not, on the open sea. The pup's life revolves around maternal
devotion. When she dives beneath the dark surface of the water for food,
being absent from her infant's side for many minutes at a stretch, the young
otter begins to cry and swim about in an agitated state. If it were not for
those calls of distress among the rising and falling waves, young otters
might be lost forever. Their security and future are unequivocally linked to
the audiovocal thread of attachment that joins them to their mothers. It is
the same for all mammals. At the outset, we are utterly dependent creatures
whose survival is founded on the quality of our social bonds—one of the
remaining great mysteries, and gifts, of nature.
The PANIC/LOSS neurocircuitry that prompts separation distress
"probably evolved from more ancient pain mechanisms of the brain,"
concludes Panksepp. He proposes that "social attachments emerge, in part,
from environmental events activating brain chemistries that can reduce
arousal in these [PANIC/LOSS] distress circuits."
The brain's PANIC/LOSS neurocircuitry:
In the laboratory, opioids were the first neurochemical discovered to
"powerfully reduce separation distress," notes Panksepp And what in our
environment stimulates opioid release naturally in the brain? Panksepp
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36
writes: "Love is, in part, the neurochemically based positive feeling that
negates those negative feelings." More definitively, he points out that
"neural circuits mediating separation distress are under the control of brain
opioids… ." The role of opiates in decreasing activity in PANIC/LOSS
neurocircuits also helps distinguish PANIC/LOSS circuitry from FEAR
circuitry. Panksepp explains that "opiates are very effective in reducing
separation distress but not fearful behaviors."
An important component of PANIC/LOSS neurocircuitry is the bed
nucleus of the stria terminalis. According to MedlinePlus Dictionary, the
stria terminalis is "a bundle of nerve fibers that passes from the amygdala
along the demarcation between the thalamus and caudate nucleus mostly to
the anterior part of the hypothalamus with a few fibers crossing the anterior
commissure to the amygdala on the opposite side." In the illustration below
left, the stria terminalis links to the hypothalamus which is hidden beneath
the thalamus.
The illustration above right shows the position of the preoptic area within
the hypothalamus. This image is from S.S. Nussey and S.A. Whitehead,
Endocrinology, from the NCBI bookshelf (links to source). Regarding
neural specifics for PANIC/LOSS neurocircuitry, Panksepp notes that there
is a high density of active distress-vocalization sites "in the ventral septal
area, the preoptic area [within the hypothalamus], and many sites in the bed
nucleus of the stria terminalis [BNST] (areas that figure heavily in sexual
and maternal behaviors)."
The red circle on the image to the right (image links to source) indicates the
general area within which the ventral septal area, preoptic area of the
hypothalamus, and bed nucleus of the stria terminalis are nestled.
From the amygdaloid, hypothalamic, and BNST areas, PANIC/LOSS
neurocircuitry runs "down through the dorsomedical thalamus to the
vicinity of the PAG [periaqueductal gray in the midbrain]," explains
Panksepp. Within the periaqueductal gray area, Panksepp notes that
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37
PANIC/LOSS neurocircuitry appears to arise from areas "very close to
where one can generate physical pain responses." He writes:
"Anatomically, it almost seems that separation has emerged from more
basic pain systems during brain evolution… ."
As it does in other emotional neurocircuits, Panksepp points out that
glutamate, an excitatory neurotransmitter, is probably the neurochemical
that activates PANIC/LOSS neurocircuitry, thus generating distress
vocalizations in young animals. In the laboratory, activating receptors for
glutamate and corticotrophin releasing hormone (CRH) can dramatically
increase distress vocalizations, even in the presence of other animals. In
Part 1 of MyBrainNotes.com, we discuss the role of CRH in triggering the
fight-or-flight response of the sympathetic nervous system, a component of
the autonomic nervous system (see ANS—the autonomic nervous system).
Panksepp emphasizes that CRH "arising from the paraventricular nucleus
of the hypothalamus ... accompanies virtually all emotions and many
psychiatric disturbances, especially depression." He points out that
blocking receptors for glutamate and CRH dramatically decreases such
vocalizations, even those induced by electrical brain stimulation.
Administration of opioids, oxytocin, and prolactin decreases activity in
PANIC/LOSS neurocircuitry. Drugs that block transmission of glutamate
and corticotrophin releasing hormone (CRH) also decrease PANIC/LOSS
activity.
Depression and PANIC/LOSS neurocircuitry:
Panksepp asserts that "the major life factor in humans that precipitates
depression is social loss." He explains that "the cascade of events during
the initial protest phase of separation [marked by separation calls or crying]
appears to establish the brain conditions for the subsequent despair phase
[depression]." More specifically, he explains that when the stress response
is activated, "a depletion of brain norepinephrine, serotonin, and certain
dopamine reserves" follows. Panksepp points out that activity in
PANIC/LOSS neurocircuitry is attenuated with tricyclic antidepressants
such as imipramine and chlorimipramine. These antidepressants have no
clear effect on FEAR-induced anxiety but have been "found to exert clear
antipanic effects in humans and to also reduce separation distress in
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animals." Panksepp notes the interesting fact that although they experience
far fewer panic attacks, people whose panic attacks have been attenuated
with tricyclic antidepressants often still fear that the attacks will occur.
Regulación de los sistemas emocionales
Como veremos a continuación, las emociones las puedo provocar, inhibir o alterar de
muchas maneras, dado que los procesos primarios, secundarios y terciarios (Pankseep)
están interconectados. Puedo intervenir de distintas maneras
Modificación cognitiva: Comprensión de la situación, análisis, cambio de actitudes,
planificación futura y mejora de las expectativas. Este proceso modifica la fisiología del
S. Nervioso. Es fundamentalmente un proceso mental terciario.
Modificación de contexto: Ubico al sujeto en un contexto placentero favorable, (lugar,
alimentación, sueño, temperatura, ruido, sexualidad, juego, entorno natural, música...).
Estoy regulando el placer y evitando el displacer. Se produce también una modificación
del S.N. Proceso mental fundamentalmente primario y secundario.
Modificación de los vínculos afectivos, la interacción social y las relaciones sociales: A
este nivel actúo sobre las relaciones de apego, amistad, enamoramiento y otras de
naturaleza social (laborales, ocio, vecinales, participación social).
Modificación conductual: programas de condicionamientos asociados al
placer/displacer, aprendizaje por observación. Generación de hábitos sanos. Enseñanza
del placer y del displacer. Educación emocional. Estaríamos en el caso de las
emociones aprendidas. En este caso y siguiendo los principios del condicionamiento
clásico podemos estudiar las situaciones placenteras asociadas a determinados estímulos
condicionados e incondicionados. Nos encontramos con emociones generadas en
situaciones de aprendizaje observacional, por modelado u otras metodologías. Por ej:
Práctica del Yoga, Taichi, meditación, baile, educación emocional.
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Modificación neurológica: Estimulación eléctrica o química.
Farmacología.
Modificación química sobre el deseo: Introduciendo sustancias químicas en el
organismo o generando situaciones carenciales (alimento, sal, agua) puedo provocar un
exceso o déficit en la concentración de sustancias químicas que alteran la homeostasis
cerebral. Esto conlleva modificaciones en la valencia (saliencia) del deseo, y puede
modificar e incluso invertir el deseo (Berridge, 2013: caso del déficit salino en ratas),
alterándose los niveles de dopamina, neurotransmisor responsable del mantenimiento
del deseo. Estos cambios son independientes de los aprendizajes previos e incluso
pueden ir en contra de ellos, como Berridge ha demostrado en estudios con ratas a
través del condicionamiento clásico. Según Berridge se producen alteraciones
mesolímbicas de los circuitos del placer que son independientes del aprendizaje
anterior. Las estructuras principales del circuito neuronal del placer son: Nucleus
accumbes, ventral pallidum, parabrachial nucleus y cortex orbitofrontal, situándose los
puntos hedónicos “calientes” en los tres primeros. Se considera que la estimulación de
estos puntos tiene un papel predominante en los mecanismos del placer. Según la Teoría
de Berridge en el placer hay dos procesos distintos y complementarios: El primero es el
del deseo, regulado por la dopamina, sus estimulantes, simuladores e inhibidores. Y el
segundo es el de la acción de los opiáceos que producen placer directo. De este modo,
por ejemplo, los adictos pueden desear mucho consumir una droga aunque ésta no les
produzca un efecto placentero. Este fenómeno se produce en todo tipo de ludopatías y
dependencias psicológicas.
La inhibición con Gaba del nucleus accumbes produce según el caso, un incremento del
apetito y o de las conductas de temor.
Modificación química sobre el producto: Otra posibilidad más común consiste en
introducir opiáceos o sustancias que simulan, potencian o inhiben a los naturales, caso
de la cocaína, la morfina, el cannabis o la marihuana.
La acción combinada de la estimulación química, por ejemplo, en puntos calientes
(hostpot), con los estímulos condicionados e incondicionados (acción externa), produce
un efecto enorme sobre la sensación de placer.
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Modificación epigenética:
Debemos partir de la idea previa de que ante un estímulo amenazador o estresor, el
hipocampo actúa sobre el hipotálamo generando la descarga del factor de liberación de
la corticotropina (CRF) sobre la hipófisis anterior, que a su vez, sintetiza y libera
adrenocorticotropina (ACTH) sobre la corteza suprarrenal. Esta libera distintos
glucorticoides, como el cortisol que cumplen una función de mantenimiento de la
respuesta al stress. El cortisol liberado en sangre será capturado por los receptores del
hipocampo hasta un determinado umbral en el número de receptores.
Teniendo en cuenta el mecanismo anterior se ha detectado un gen cuya expresión afecta
a la estructura y/o función de un sistema emocional asociado al miedo, pánico y stress
en general. Es el caso de las ratas lamidas (Weaver, Meaney y Szyf, 2006) que se ven
afectadas positivamente por la expresión genética de receptores glucocorticoides del
hipocampo. De esta manera, en las ratas lamidas hay un mayor número de receptores. A
mayor número de éstos, mayor capacidad de recepción de glucocorticoides como el
cortisol, que cumple una importante función en el mantenimiento de la respuesta al
stress, incrementando la glucosa en sangre, la metabolización de grasas e hidratos de
carbono. Los receptores intervienen en un mecanismo de retroalimentación negativa, de
tal manera que a mayor número de ellos, mayor incremento de la retroalimentación
negativa. Cuando el nivel de los receptores de glucocorticoides, llega a un determinado
umbral, el hipocampo inhibe la liberación de corticotropina (CRF) sobre la hipófisis
anterior, lo que a su vez inhibe la produción de adrenocorticotropina (ACTH) sobre la
corteza suprarrenal, lo que a su vez conlleva que no se produzcan glucocorticoides,
como el cortisol, disminuyendo la respuesta al estímulo estresante. Ahora bien, si no
hay suficiente número de receptores de glucorticoides, como en el caso de las ratas
no lamidas, no se inhibirá tan rápidamente la producción de corticotropina en la
hipófisis y, por lo tanto, se seguirá produciendo cortisol u otros glucocorticoides.
En este último caso las consecuencias del stress se mantendrán durante más tiempo,
manteniendo al individuo en estado de alerta. El estrés es una reacción normal ante un
estímulo o situación amenazante, pero su permanencia en el tiempo, una vez que ha
desaparecido o atenuado la causa, tiene indudables consecuencias negativas.
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El Placer, el gran regulador.
Tal como planteó Freud, el placer es un gran regulador de la conducta; posiblemente,
como planteaba en su teoría, el más primigenio de todos los mecanismos reguladores de
la conducta.
En la actualidad los estudios neurocientíficos nos enseñan que podemos descomponerlo,
como ya citamos anteriormente, en deseo de obtener placer y en placer en sí mismo
(wanting and liking). Ambos mecanismos están regulados por neuropéptidos
(dopamina, opioides..) y se producen dentro de circuitos cerebrales específicos
(Berridge, 2013).
En los centros hedónicos, uno de los neurotransmisores que se libera ante un estímulo
placentero, por ejemplo el olor o la visión de un chocolate, es la encefalina, que coopera, a su
vez, para que se pueda liberar otro neurotransmisor en las neuronas postsinápticas vecinas, la
anandamida. Al difundirse este nuevo neurotransmisor desde su lugar de liberación,
interacciona con receptores ubicados en la primera neurona que había liberado encefalinas
aumentando la liberación de éstas. Creándose así un ciclo de retroalimentación positivo que
permite intensificar el placer percibido.
Las encefalinas y endorfinas, que son péptidos opioides endógenos ubicados en el
cerebro, también se producen en la glándula pituitaria y son liberados como hormonas.
Tienen acción analgésica y gran afinidad con los receptores de la morfina; regulan el
dolor y la nocicepción corporal.
Circuitos sobre el deseo y el placer
Los esquemas y dibujos que se exponen a continuación explican los circuitos
fundamentales que relacionan deseo, placer y aprendizaje (Berridge, 2013),
especificando las partes específicas de la región mesolímbica del cerebro y los
neuropéptidos empleados, entre los cuales se hace especial referencia al incremento del
deseo a través del incremento de los niveles de dopamina. Dentro de los circuitos, juega
un papel fundamental la activación o inhibición de los puntos calientes (hostspot) que
permiten incrementar la sensación de placer cuando se activan sincrónicamente.
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Una neurobiología común para el placer y el dolor
Siri Leknes and Irene Tracey
La amplificación del placer y la evitación del displacer
Cuando inyectamos un opiáceo, por ej, un agonista de la morfina, se incrementa el
placer que nos produce un rostro que nos agrada (estamos más tiempo viéndolo), bien
porque nos guste más o porque deseemos verlo más. Sin embargo, en este mismo caso,
tratamos también de evitar más rápidamente un rostro que no nos guste. Estos
resultados se encontraron en un experimento donde los hombres podían mantener o
eliminar un rostro de mujer atractiva o no atractiva. Conclusión. Si introducimos una
sustancia placentera, que incremente los opiáceos naturales del organismo, por ej, el
chocolate, podemos incrementar el deseo, (wanting) o el placer sexual (liking).
Los beneficios del dolor (Siri Leknes&Brock Bastian, 2014)
The International Association for the Study of Pain (IASP). Según la IASP se define
dolor como:
“an unpleasant sensory and emotional experience associated with actual or
potential tissue damage or described in terms of such damage.”
La definición anterior presenta limitaciones a su validez psicológica, debido a que:
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El ser humano puede profundizar en el dolor como por ejemplo sucede en los castigos o
en los deportes más extremos o duros.
Hay evidencia de una serie de mecanismos implicados en los beneficios putativos del
dolor, como es el caso del incremento de la atención. En otros casos, como en el placer
producido por el consumo de especias altamente irritantes en la comida, los sujetos
encuentran en ello un efecto placentero. En ocasiones una experiencia aversiva,
contrastada con otra que no lo es, se convierte en beneficiosa para el sujeto, como por
ejemplo, un masaje después de un ejercicio físico doloroso. A su vez, otros beneficios
potenciales derivan de la inhibición de otras experiencias dolorosas que pasan a un
segundo plano, como sucede cuando un dolor secundario pasa inadvertido ante el
producido por una lesión principal. También se puede obtener un mayor grado de
empatía y soporte social.
Neuroquímica del amor
Según Helen Fisher el amor es una combinación de lujuria, amor romántico y apego.
Pasemos a esbozar inicialmente, el primer componente: la lujuria.
La lujuria según diferentes autores es el pilar básico para el amor. El sistema emocional
sexual tiene dos componentes fundamentales: El deseo sexual (modificado
especialmente por los niveles de dopamina) y el placer sexual (desencadena la
producción de opiáceos naturales). Ambos son producidos fundamentalmente por los
efectos en el organismo de los elementos siguientes: lenguaje erótico (palabras y
paralenguaje), comunicación no verbal erótica (gestos, miradas, sonrisas),
condicionamientos pavlovianos eróticos (objetos, ropa, semidesnudos, visión de zonas
corporales), placer sensorial (vista, olfato, gusto..; incluíria las imágenes, los besos,
chupadas, lamidas, caricias, mordiscos, susurros, aromas, olores), orgasmos (placer en
sí mismo que se podría considerar como una modalidad muy especializada de placer
sensorial, fundamentalmente de carácter incondicionado pero, tal vez también, de
carácter condicionado primario).
En resumen, la actividad sexual puede estar destinada a incrementar el deseo sexual
(modificando lo niveles de dopamina) o a producir placer en sí mismo. Desde un punto
de vista cultural, la estimulación y el control del deseo sexual se ha convertido en un
patrón cultural central en la mayoría de las sociedades.
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Tal como indícabamos, para Helen Fisher, el amor es una combinación de lujuria, amor
romántico y apego. Es un sistema cerebral que una vez activado desencadena un
conjunto de reacciones neuroquímicas con finalidades adaptativas: la reproducción y el
mantenimiento de la pareja durante unos pocos años, básicamente los que se necesitan
para el cuidado de la cría. Para ella, el amor intenso es una respuesta de estrés que
activa la amígdala, lo que provoca una reacción de alerta e incluso activa el sistema de
pánico, lo que vuelve ciegos a los sujetos. Se activan también los centros de
recompensa, especialmente el Nucleo Accumbes, donde Berridge sitúa los principales
puntos calientes del placer que actúan coordinadamente con otros puntos extendidos en
la zona mesolímbica y probablemente en la corteza cerebral. Se produce también la
activación del hipotálamo lo que produce la acción de endorfinas y un decrecimiento de
los niveles de serotonina. El hipotálamo provoca la producción de cortisol lo que reduce
el campo visual del sujeto. Además incrementa la producción de tetosterona en las
mujeres y lo disminuye en los hombres, lo que hace que nos sintamos muy próximos al
otro género. Antes del orgasmo hay una gran producción de dopamina lo que conlleva
el incremento del deseo del otro y en el momento del orgasmo se produce un “pico” de
noradrenalina, vasopresina y oxitocina, lo que conlleva un elevado placer y el deseo de
unión con el otro. La oxitocina ayudaría a mantener el vínculo para el cuidado de las
crías. No obstante la oxitocina también se produce con el trato amable, el contacto físico
(lamidas, caricias y abrazos) y el diálogo con personas queridas como demuestran
varios autores (Pankseep). Además de estos mecanismos neuroquímicos intervienen
otros, como la adrenalina, la fenil-etil-amina (FEA) y las feromonas, que regulan el
deseo sexual y el amor romántico y que podemos consultar en el anexo I.
Fisher está muy preocupada con el empleo permanente de antidepresivos, porque estos
incrementan la producción de la serotonina, que inhibe la producción de dopamina, lo
que conlleva la desaparición del deseo sexual y en consecuencia del orgasmo. Sin
orgasmos, disminuye la producción de oxitocina lo que debilita el vínculo de las
relaciones de pareja. Por lo tanto, desde el punto de vista neuroquímico, los orgasmos
facilitarían la construcción y el mantenimiento del apego entre adultos.
Para el análisis del apego, remitimos al lector a la teoría de Bowlby. En cuanto al amor
romántico lo consideramos una construcción cultural sujeta a los discursos de cada
cultura.
Diferencias entre el enamoramiento infantil y adulto
Recopilación de textos: José Luis Prieto
50
Si seguimos el modelo de Fisher, el niño y el adulto comparten gran parte de la lujuria,
el amor romántico y, muy especialmente, el apego. Las diferencias en relación a la
lujuria estarían en el deseo sexual y la conducta sexual. Si el placer sexual lo
descomponemos en los componentes que hemos enunciados anteriormente, sólo el
placer ante el coito, sería distinto que en el caso de los adultos. Incluso es posible que
éste último lo sea sólo por razones culturales. La madre o el padre en la medida que
intuyen el deseo sexual del niño/a van retirándose de la relación “amorosa corporal” y
obligan a que el niño renuncie, algo que ya Freud analizó en el Complejo de Edipo. Esto
es especialmente relevante en la adolescencia. También podemos encontrar diferencias
en el grado de concentración de tetosterona que es mucho más bajo en el niño que en el
adolescente o el adulto. El adolescente hace un intento de acercamiento hacia la madre y
quizás hacia la hermana, pero éstas le rechazan, lo que le lleva a la búsqueda de una
mujer o un hombre externo al núcleo familiar. En resumen, el deseo y el placer sexual
se desplaza de las figuras parentales hacia figuras externas a las familiares. Esto tiene un
indudable valor adaptativo de cara a la especie.
Cuestiones
Hasta ahora nos hemos situado fundamentalmente en la zona mesolímbica, tal vez el
Ello de Freud. Pero qué pasa con el principio de realidad, con el Yo, con la corteza
cerebral. La mayor parte de las conductas no están orientadas de forma inmediata al
placer. Las funciones de la conciencia y por lo tanto de la corteza cerebral no están nada
claras en la actualidad. Es evidente que participan en los procesos emocionales, aunque
más tardíamente que las zonas mesolímbicas. No obstante, es preciso que la
investigación avance en este sentido, para poder explicar cómo regulamos de forma
consciente nuestros sistemas emocionales.
Referencias y enlaces
En la presentación de referencias se ha optado por incluir todas las fuentes utilizadas en cada
sistema emocional y en cada autor, incluendo referencias bibliográficas y enlaces. De este modo
el lector podrá consultar con mayor facilidad las fuentes de cada materia.
I.Bartal
Empatia
Recopilación de textos: José Luis Prieto
51
Bartal, I(2011). Empathy and Pro-Social Behavior in Rats, Science 334, 1427.
Enlace:
http://www.sciencemag.org/content/334/6061/1427.abstract?ijkey=a4cdecd3caaca20c6296b9ba
3422aa5c201fb9ff&keytype2=tf_ipsecsha
K.Berridge.
El placer
Affective Neuroscience & Biopsychology Lab . University of Michigan Psychology
Department. Biopsychology Program.
Berridge, K.C & Kringelbach, (2013). M.L. Neuroscience of affect: brain mechanisms of
pleasure and displeasure. Current Opinion in Neurobiology. 23: 294-303,.
Enlace: http://www-personal.umich.edu/~berridge/
Virginia Campbell Podcast
Brain Science Podcast
Enlace: http://brainsciencepodcast.com/
Hellen Fisher
Neuroquímica del amor
Fisher, H. (2004). ¿Por qué amamos?. Naturaleza y química del amor romántico. Madrid.
Santillana
Enlace: http://www.slideshare.net/ZUNAC/fisher-helen-porque-amamos
Vídeo 1: Helen Fisher: ¿Por qué amamos y engañamos?
https://www.youtube.com/watch?v=CgVIPVODTXA
Vídeo 2: Neuroquimica: Cerebro enamorado (Helen Fisher)
http://www.dailymotion.com/video/xoy8v9_neuroquimica-cerebro-enamorado-helen-fisher_school
Recopilación de textos: José Luis Prieto
52
Siri Graff Leknes
Placer y Dolor
UIO, Department of Psychology
Leknes S, Bastian B (2014). The benefits of pain. Review of Philosophy and Psychology
(Special issue on Pain and Pleasure): 57-70
Enlace: http://www.sv.uio.no/psi/english/people/aca/sirigra/
Joseph Ledoux. Ledoux Lab. Center
El miedo
Ledoux, J. (2014) Coming to terms with fear. Center for Neural Science and Department of
Psychology, New York University, New York.
LeDoux JE. (2012) Rethinking the Emotional Brain. Neuron, Volume 73, Issue 4, Pages 653676,
Enlace: http://www.cns.nyu.edu/ledoux/
Jaak Panksepp, Ph.D.
Sistemas emocionales
Campbell, G. (Interviewer). & Panksepp, J. (Interviwee). (2014) Retrieve from Brain Science Podcast.
Episode #91.
Enlace: http://brainsciencepodcast.com/bsp/the-origin-of-emotions-with-jaak-panksepp-bsp-91.html
Washington State University. Neuroscience Program, Integrative Physiology and neuroscience
Enlaces
http://www.sciencemag.org/content/334/6061/1358.full?ijkey=IVBCV.ahM1.s.&keytype=ref&siteid=sci
#xref-ref-3-1
http://ipn.vetmed.wsu.edu/people/faculty-ipn/pankseep-j
http://mybrainnotes.com/brain-ocd-dopamine.html
Panksepp, J. (2011). Empathy and the Laws of Affect. Science, 334, 1358-1359.
Recopilación de textos: José Luis Prieto
53
Panksepp, J. (2010) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181986/
Luiz Pessoa and Ralph Adolphs
Procesamiento emocional
Pessoa, L. & Adolphs, R.(2010). Emotion processing and the amygdala: from a ‘low road’ to ‘many
roads’ of evaluating biological significance. Nat Rev Neurosci. 11(11), 773-783
Enlace: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025529/
Otros autores
Apego
Barg, G (2011) Bases neurobiológicas del apego. Revisión temática. Cienc.
Psicol. vol.5 no.1 Montevideo.
Weaver, I. C. G., Meaney, M. J., & Szyf, M. (2006) in the offspring that are reversible in
adulthood. Proceedings of the National Academy of Sciences of the United States of America,
103(9), 3480-5.
Anexos
Recopilación de textos: José Luis Prieto
54
Anexo I
NEUROQUÍMICA DEL AMOR
* Por Virginia Gudiño
Las conductas de afiliación y apego social son comportamientos
esenciales en las relaciones humanas, pero recién comienzan a
conocerse los circuitos cerebrales que regulan su complejidad. La
evolución realizó ciertos trucos neurales y utilizó los mismos recursos
que usó para mantener unidos a madres e hijos, reciclándolos para
lograr el mismo efecto con las parejas.
¨Etapas o Estados¨ del Amor
Los mamíferos y aves han desarrollado tres sistemas cerebrales de motivación-emoción que
actúan en serie:
¿ Cómo reacciona nuestro cuerpo?
Fisiológicamente hay reacciones como: sudoración, taquicardia, indecisión, enfoque
exclusivo y distorsión de la naturaleza del estímulo mismo. El iniciador de estos procesos, es
un ¨chispazo¨ hormonal. En esta situación nuestro cuerpo produce una inundación de
sustancias endógenas, llamadas neurotransmisores (comunican a las células nerviosas entre
sí).
Al encontrarnos con una persona deseada, nuestro organismo recibe una señal que no tarda
en manifestarse. El hipotálamo, a través del sistema nervioso, emite mensajes que, captados
por las glándulas suprarrenales, segregarán un mayor cantidad de adrenalina y noradrenalina
(neurotransmisores).
Consecuentemente, el corazón comenzará a latir con una mayor velocidad (unas 130
pulsaciones por minuto), aumenta la presión arterial máxima (sistólica), se liberan grasas y
azúcares que aumenta la capacidad muscular y se produce una cantidad de mayor de glóbulos
rojos con el objeto de mejorar el transporte de oxígeno a través del torrente sanguíneo.
Enamoramiento

Estado alterado,
transitorio, de la
conciencia.

Proceso que hace
emerger el amor

Enamorarse está entre los
comportamientos humanos
más irracionales.
 Con el tiempo, hay
sentimientos más ¨reales¨,
Recopilación de textos: José Luis Prieto

Los circuitos
del cerebro
quedan
intactos hasta
que un nuevo
amor se cruce
55
romántico.

por tanto, puede que ese
amor perdure o bien que se
busque a otra persona con la
esperanza de encontrar a la
adecuada.
por el camino
Sume al que lo siente
en algo que parece una
enfermedad mental –
mezcla de manía,
demencia y obsesión–
que podría ser
confundido con una
psicosis.
Se activan 12 áreas en el cerebro cuando nos enamoramos
La Dra Stephanie Ortique, profesora de la Universidad de Syracuse en Nueva York, ha llegado
a la conclusión de que enamorarse puede provocar la misma respuesta eufórica que
provocan las drogas ilícitas en el cerebro y que, asimismo, se activan varias zonas
cerebrales, incluyendo aquellas vinculadas con funciones cognitivas sofisticadas.
En este estudio, que fuera publicado por el Journal of Sexual Medicine, la investigadora y su
equipo analizaron otros estudios llevados a cabo en el pasado sobre cómo responde el
cerebro al concepto del amor.
El resultado alcanzado fue que cuando una persona se enamora se activan 12 áreas
cerebrales para liberar compuestos químicos como la dopamina, la oxitocina y la adrenalina
y, es la activación de ciertas zonas cerebrales lo que genera un estímulo en el corazón y el
sentimiento de ¨mariposas en el estómago¨, pero también se activan áreas cognitivas más
complejas como las encargadas de la representación mental y la autoimagen corporal, así que
¨el amor es un proceso más complicado que la adicción a las drogas. ¨
Si reducimos el Amor a sustancias químicas ...
La Dra. Helen Fisher, autora del libro The Anatomy of Love, divide en tres las etapas del
amor romántico:
1- El Deseo o la Lujuria:
 Predomina la testosterona: prima el deseo de sexo, dado
que, los niveles altos de esta hormona van de la mano con
la pulsión sexual.

Se produce un pico de adrenalina, lo que incrementa la
presión sanguínea (provoca los rubores de las primeras
etapas del enamoramiento), aceleración del ritmo cardíaco
y sudoración en la palma de las manos.

Hay una elevación de la noradrenalina, lo que lleva a la
excitación sexual y “elevación” del humor, con
sentimientos de seguridad y gusto al compartir momentos
con la persona que consideramos especial.
Cuando alguien está en las garras de este amor romántico es irracional, va al gimnasio a las
seis de la mañana... ¿Por qué? Porque él, o ella, está ahí. ‘Esta compulsión hacia el amor
romántico puede ser más fuerte todavía que las propias ansias de vivir’, dice la doctora Helen
Fisher, antropóloga de la Universidad Rutgers y coautora del análisis.
2- Atracción

Predominan la feniletilamina (FEA), la dopamina, la norepinefrina y la oxitocina.
 Baja la Serotina, estando así en la etapa de euforia y de romance.

La FEA (estimulante natural conocido como “molécula del Amor”) inicia una reacción
Recopilación de textos: José Luis Prieto
56
química en cadena en el cerebro. Estimula la secreción de dopamina y luego ésta
inducirá a la de oxitocina.

La dopamina afecta procesos cerebrales que controlan el movimiento, la respuesta
emocional y la capacidad de experimentar dolor o placer. También Induce un proceso
de aprendizaje positivo en el cerebro, transformando el simple deseo con fines
sexuales en algo mucho más profundo, dando asi inicio a las relaciones.
 La oxitocina, es el “el químico de los mimos”.
Cuando el cuerpo entra en contacto con las feromonas (sustancias
químicas que nuestro organismo produce y que tienen como única
misión afectar nuestro comportamiento sexual y atraer al sexo
opuesto) nuestro proceder se altera y nuestras percepciones se
tornan totalmente idiosincrásicas e impredecibles. Estamos
enamorados (Véase: Sex, Time and Power: How Women’s Sexuality
Shaped Human Evolution por L. Shlain).
El amor romántico es "creado" por una endorfina, la fenil-etil-amina (FEA), que produce
sensaciones de satisfacción y armonía ante el estímulo que la desencadena, y nos produce
una sensación de bienestar asociada a una cierta persona.
En efecto, el idilio romántico coincide con estos factores químicos que dan lugar a las
sensación tan especial de ¨estar enamorado¨. Esta es la razón por la cual, los enamorados
pueden permanecer largas horas conversando, haciendo el amor o simplemente 'estando
juntos' sin sentir cansancio uno del otro.
Y en esta misma línea, se ha observado que las personas que
vivieron una desilusión amorosa, buscarían compensar la
disminución de feniletilamina (FEA) a través del consumo de
chocolate (golosina especialmente rica en esta sustancia).
La función de la fenil-etil-amina (FEA) es la de garantizar la armonía y la tolerancia hacia
una posible unión reproductora, destinada a persistir como relación amorosa por unos 3 ó 4
años.
3) Vínculo:



Predominan la oxitocina, la vasopresina y la serotonina, evolucionado así hacia una
relación apacible, duradera y segura.
La oxitocina es la responsable del nacimiento de lazos afectivos en una pareja. En
las mujeres, es liberada principalmente durante el parto (contracción del músculo
uterino), el amamantamiento y los orgasmos (contracciones musculares). En los
hombres: propicia la erección y acelera el impulso eyaculatorio.
La vasopresina, tambien llamada “hormona monogámica”, es liberada durante la
actividad sexual . Incrementa los niveles de agresión y acompañada de la oxitocina,
induce el sueño.
La oxitocina aumenta la confianza entre las personas y ayuda a
forjar lazos permanentes entre los amantes, tras la primera oleada
de emoción. Reduce la actividad de la parte del cerebro donde se
detecta el temor, facilitando el unirse a una persona.
¿Cómo revitalizar una relación?
Recopilación de textos: José Luis Prieto
57
Los científicos creen saber cómo mantener fluidos los circuitos
amorosos. Se puede estimular el amor romántico mediante
sustancias químicas, a través de gestos como abrazos, besos y otras
formas de contacto íntimo. Si uno quiere realmente revigorizar una
relación, se deben hacer las cosas que estimulan la producción de
estas moléculas y dejarlas que alimenten sus emociones.
"Mi esposa me dice que las flores la estimulan"…"No sé si es así, a un científico le cuesta ver
cómo pueden estimular los circuitos, pero sé que parecen tener efecto. Y la ausencia de ellas
también tiene un efecto". (Larry Young, del centro de investigaciones Yerkes de la Universidad
Emory de Atlanta).
Hoy, conocer aspectos científicos relevantes en ese sentido, nos posibilita comprender estos
procesos, pero lo más importante es la aplicación práctica que le damos a la ¨nueva¨
información que tenemos, pues de nuestras acciones y del compromiso que ejercitemos
dependerá el que podamos consolidar o no, una vida compartida gratificante.
Toda relación podría considerarse un desafío, una construcción a la
cual dar forma y en la que intervienen multiplicidad de factores
(neurobiológicos, psicológicos, culturales, experiencias de vida,
etc)de cada una de las personas involucradas. Un desafío que vale la
pena afrontar, si de ello depende el poder crear y fortalecer
relaciones duraderas y felices.
Artículos Relacionados:
¿Qué es el Amor?
i
ii
iii
http://mybrainnotes.com/brain-ocd-dopamine.html
Recopilación de textos: José Luis Prieto