PSYC 302: Biopsychology
11/27/07Announcements:
1. Review Session today.
2. Final exam next Tues (12/4).
Substance Abuse and Addiction
Reward pathway-- Dopaminergic neurons have their cell bodies in the ventral
tegmental area (VTA), and their axons extend into various brain areas, including the
nucleus accumbens.
The nucleus accumbens is part of a structure called the striatum that includes the
caudate nucleus and putamen. Although it's a small structure, it's a very important
"pleasure center."
Olds & Milner- stuck an electrode accidentally in a rat's nucleus accumbens and they
found that the rat would forego sleep and food to self-stimulate.
Alcohol-- From a psychopharmacological perspective, alcohol inhibits the flow of
sodium ions into neurons, making it a CNS depressant. Decreases serotonin
(excitatory) activity and facilitates response by the GABA (inhibitory) receptors. It
blocks glutamate (excitatory) receptors and increases dopamine (excitatory; key to the
reward pathway) activity.
Type I vs Type II- Type I is late onset, and so it appears to be less genetic in basis, and
less severe than Type II, which is largely genetic.
Type II alcoholism has greater concordance in monozygotic vs. dizygotic twins. Plus,
there is a strong correlation between the occurrence of Typ II alcoholism in biological
fathers and sons, even when the son is adopted and raised in a non-alcoholic family.
One of the treatments for alcoholism is antabuse, which has a low adherence rate. The
drug causes the user to become severely nauseated when they drink alcohol.
Alcohol metabolism: alcohol ---> acetaldehyde ---> acetic acid
Acetaldehyde is very toxic and causes nausea and vomiting.
Methadone in the treatment of heroin addiction:
Methadone is just a substitute opiate for heroin. When taken orally, it crosses the
blood-brain barrier much more slowly than heroin, and so it produces its effects more
slowly, including withdrawal, and it's far less addictive. BUT if you inject methadone, it
becomes pretty similar to heroin in its effects.
Solution: Mix naloxone with methadone. Naloxone is an antagonist that blocks opiate
receptors. But when it's taken orally, it's broken down in the stomach and rendered
ineffective. If it's taken in any other way, it blocks the effects of methadone or any other
opiate.
DEPRESSION
Is there a genetic component?
There are two genes implicated in depression: One gene results in lowered serotonin
production and the other gene increases the efficiency of serotonin reuptake.
What are anatomical/structural differences in the brains of depressed individuals?
Depressed people have less activity in the LEFT prefrontal cortex and more in the
RIGHT.
Drug treatments:
1. tricyclics (e.g. Tofranil)-- prevents the presynaptic neuron from reuptaking serotonin,
dopamine and norepinephrine.
2. selective serotonin reuptake inhibitors (SSRIs; e.g., Paxil, Zoloft, Prozac)-- they
block the reuptake of serotonin but not of other monoamines.
3. Monoamine oxidase inhibitors- Monoamines are a class of neurotransmitters that
includes dopamine, serotonin, epinephrine, and norepinephrine. Monoamine oxidase
(MAO) is an enzyme that breaks down these neurotransmitters. By blocking MAO, you
leave the neurotransmitters in the synapse longer so that they exert a greater effect.
4. atypical antidepressants (Wellbutrine) inhibits dopamine and norepinephrine
reuptake
Comparing different treatments for depression, we see the following efficacy rates:
Antidepressants- 50-60%
Psychotherapy- 50-60%
Placebo- 30%
Electroconvulsive therapy (ECT; as seen in "Ordinary People" and "One Flew Over the
Cuckoo's Nest"). Nobody knows exactly why it works. It has certain side effects,
including memory loss, which can be minimized by administering the current only to the
right hemisphere), and it has a high relapse rate.
Depressed people have sleep maintenance insomnia (trouble getting back to sleep
when they awaken) and enter REM more quickly. This suggests that they are "phase
advanced", that their sleep-waking cycle has shifted so that their body temperature
starts to decrease earlier in the day.
In some cases, if you keep the patient awake for an entire night, their sleep-waking
cycle will return to normal and depression symptoms will decrease.
Seasonal Affective Disorder (SAD)- phase delay in the sleep-waking cycle, meaning
that sleep occurs later and temperature rhythms are altered so that temperature
decreases happen later, as well. Bright full-spectrum light.
Bipolar disorders- manic and depressive episodes
Bipolar I-- The manic episodes are more severe, and can include restlessness,
excitement, rambling thought, loss of inhibitions
Bipolar II- much milder manic phases (hypomania), which include agitation and anxiety
Treatments for bipolar:
Lithium, carbamazepine (Depakote) and Valproate-- all block the synthesis of
arachidonic acid (a precursor of cannabinoids in the brain), which is produced when the
brain is inflamed. Lithium does not increase GABA activity, but the other two do. Since
GABA is inhibitory, we assume that these drugs reduce manic symptoms by inhibiting
brain activity. Valproate stimulates growth of axons and dendrites.
Schizophrenia
Acute-- sudden onset, good prospects of recovery ("Eden Express" by Mark Vonnegut)
Chronic-- gradual onset, long-term course, harder to treat
Two classes of symptoms of schizophrenia:
1. Positive symptoms-- Psychotic cluster (delusions, hallucinations); disorganized
cluster-- inappropriate behavior, emotional displays, bizarre behavior, thought disorder)
2. Negative symptoms-- flat affect, weak social interactions, problems with speech and
working memory
Is schizophrenia genetic? There is evidence for and against:
FOR: greater concordance in dizygotic twins than in other siblings
AGAINST: The concordance rate for monozygotic twins is only 50%
Neurodevelopmental hypothesis-- Brain abnormalities that occur in prenatal or neonatal
development. Evidence for this hypothesis:
1. A number of different neonatal complications have been linked to schizophrenia.
2. Schizophrenics show certain brain abnormalities
a) decreased volume in the left temporar and frontal cortex
b) larger ventricles
c) smaller cell bodies, especially in the neurons of the hippocampus and right prefrontal
cortex
d) unlike most people, who have a larger planum temporale in the left hemisphere,
schizophrenics have a larger right p.t.
e) lower than normal left hemisphere activity
3. abnormalities in development have been shown to impair behavior in adulthood
People born in winter have a slightly higher risk of schizophrenia. Why?
Possibilities: more complications in delivery in the winter time, influenza and other
viruses occur most often in the winter
Treatment
Antipsychotic drugs (neuroleptics):
1. Phenothiazines --chlorpromazine (Thorazine)
2. Butyrophenones-- Haldol
Block dopamine synapses.
Dopamine hypothesis-- Schizophrenics have higher-than-normal dopamine activity
Evidence in support of this hypothesis:
1. Drugs that block dopamine receptors reduce schizophrenic symptoms.
2. Repeated doses of amphetamines or cocaine can produce similar symptoms
(stimulant-induced psychosis)
Glutamate hypothesis-- Schizophrenics have lower-than-normal glutamate activity.
Evidence in support of this hypothesis:
1. Brain imaging data have shown that schizophrenics have lower-than-normal
glutamate levels in their brain, especially in the prefronal cortex and hippocampus.
2. PCP, which inhibits glutamate receptors, produces symptoms similar to
schizophrenia, including hallucinations, thought disorder, and memory loss.
REVIEW
III-3f
genetics-- there is greater concordance in monozygotic vs. dizygotic twins, and greater
concordance in blood siblings than in adopted siblings
hormones-- there is no correlation between levels of sex hormones in adults and sexual
orientation, but there is evidence that males who are exposed to less testosterone
levels early in life show more interest in other males, and that females exposed to
higher levels of testosterone show interest in other females.
prenatal environment-- mothers of homosexual sons recalled higher than average levels
of stressful experiences during pregnancy; homosexual men tend to have older
brothers.
brain anatomy-- homosexual men have a larger anterior commissure than heterosexual
men, which is closer in size to that of a woman; the SCN is larger for homosexual vs
heterosexual men; and a part of the hypothalamus (the dimorphic nucleus) is smaller in
homosexual men, closer in size to that of a woman.
III-13a
Kanzi & Malika:
1. understand more than they can produce
2. use symbols to name and describe objects even when those objects are not present
3. request items they cannot see
4. can describe past events
5. can make original requests
Using language in a creative manner and describing events not just in the present
III-2f
The first mechanism is hormonal before experience between the mother and infant can
create a bond. Oxytocin is one such hormone that kicks in during the first few days of
life. After that, the hormonal effect dissipates and bonding becomes experiencedependent.
III-9f
In the alarm phase of stress response, cortisol gets produced. Small to moderate
amounts of it actually stimulate memory, activating the amygdala and hippocampus.
This enhances memory consolidation and storage. But prolonged stress damages the
hippocampus and impairs memory.
III-9d
1. hippocampus size-- as people age, their hippocampus shrinks; but hippocampus
size does not predict memory loss
2. rate of shrinkage-- this is correlated with memory performance; higher rate of
shrinkage results in greater memory impairment.
3. less than average activity less in the hippocampus is related to memory performance
(supported by data).
11/20/07The visual system is wired such that the information from the right visual field in both
eyes goes to the right hemisphere and left visual field to the left hemisphere.
Split-brain patient-- Generally, these were patients who had severe epileptic seizures
that crossed the midline of the brain, and so the corpus callosum was severed in these
patients, along with the anterior commissure, to try and prevent the most seizures from
crossing over.
In split brain patients, the two hands sometime operate independently; some complex
tasks that involved both hands or perhaps visual and auditory processing
simultaneously could cause problems, but in general these patients are high-functioning
and it's hard to know in most situations that they have a deficit.
When information is presented to the left hemisphere, which is the area where language
processing happens, they can name objects they see but they difficulty drawing them.
Objects to the right hemisphere show the opposite pattern.
Left hemisphere is dominant for speech in more than 95% of right handers and in 80%
of left handers; it is also better at language comprehension, although the right
hemisphere has SOME language comprehension. The right hemisphere is better at
visuopatial processing, and that includes drawing information.
The left hemisphere is more likely to process detailed information about visual stimuli
and the right hemisphere overall patterns.
The left hemisphere has a larger planum temporale, which is a structure found in the
temporal lobes and associated with language process. It's larger in the left hemisphere
for 65% of people.
Young children resemble split-brain patients in some ways, because the commissures
in their brains are not fully developed yet.
For example, and infant with one arm restrained will not reach across his/her body to
grab an object.
If you give toddlers two fabrics, one placed in each hand, and ask them to determine
whether the fabrics are the same or different, they will have a hard time with the task,
showing high error rates.
Some people are born without a corpus collosum and they do much better than splitbrain patients in a number of tasks involving auditory and visual processing, the use of
both hands simultaneously, or language processing by the right hemisphere.
The two hemispheres are less specialized, so that more language processing occurs in
the right hemisphere and more visual/spatial processing in the left. Moreover, these
individuals still have an intact anterior commissure and a hippocampal commissure,
which allows the two hemispheres to communicate to some degree.
In right handers, left hemisphere is dominant for speech. In lefties, you can have lefthemisphere dominance, right-hemisphere dominance, or a mixture of left and right.
Language Processing
(in animals and children)
Kanzi/Malika are a type of bonobo called a bonobo. They use language in creative
ways, they refer to events in their past and to objects that are not in their field of vision,
and they refer to objects not just when they want or need them.
Why are they so much more advanced in language production than other animals that
have been taught languages?
1. Bonobos may have more language ability than chimps.
2. Kanzi/Malika started young.
3. They may have learned from observing their mother.
Alex the grey parrot- Give give spoken answers to spoken questions involving color,
number, shape, and other characteristics of objects.
Children- In the first five years, they go from a vocabulary of zero to several thousand
words, but perhaps more significantly, they learn to use the grammatical rules of their
language.
The study of language acquisition had been dominated by behaviorists, who claimed
that language was just a learned behavior, until Noam Chomsky introduced his ideas
about nativism, which are based on the premise that children are born with a language
acquisition device. In other words, language acquisition is hardwired so that children
have an innate understanding of grammar, syntax, and other language-related rules.
There is also the idea of a critical period in language acquisition: language is most
easily acquired prior to a certain age. This point is somewhat controversial because
there is evidence for and against a critical period.
For: Children are much more likely than adults to learn a second language.
Against: No sharp cutoff in terms of learning a second language. Two-year-olds are
better than 4-y.o.'s, who are better than 6-y.o's.
Language Deficits
Broca's and Wernicke's aphasia-- Broca's aphasia affects language production
whereas Wernicke's affects language comprehension. The story is more complicated:
In Broca's aphasia, the patient has trouble with pronouns, prepositions, conjunctions,
and articles. Patients with Wernicke's aphasia show anomia, or the inability to utter or
remember certain kinds of words, mostly nouns and verbs.
Dyslexia-- people who are born dyslexic have certain anomalies in brain structure:
1. Their planum temporale is more likely to be bilaterally symmetrical as opposed to
being larger on the left side.
2. In some cases, they have more development of language-related centers in the right
hemisphere compared to the left hemisphere.
3. Fewer connections of lnanguage-related brain areas.
Theories that account for dyslexia:
1. Impairment in visual processing- This theory is not well-supported.
2. Impairment in auditory processing-- There is evidence of less-than-normal response
to certain speech sounds.
3. Problems connecting visual and auditory information.
4. Differences in attention-- Dyslexics don't shift their attention from one target to the
next in the same way that "normal" individuals do, and when they focus their visual
attention directly on a word, they are more likelty to process a word or letter that is 5-10
degrees to the right of their focal point.
ATTENTION
Does the brain exert more effort to attend to a salient (ie. relevant) stimulus or to tune
out a distractor stimulus? Research has shown that the brain is more active when
attending to a salient stimulus compared to a non-salient stimulus, but that brain areas
are not necessarily more active in tuning out some types of irrelevant stimuli over
others.
See example in Fig 14.18 on p. 443
Deficits in attention
Spatial neglect-- Tendency to ignore the left side of visual space and of the body,
directing attention to the right.
If a patient with neglect is asked to cross out all of the H's that make up a larger letter
"E", they will only cross out the ones on the right. However, if asked, they will correctly
identify the letter as an E, suggesting that their deficit is NOT one of visual processing.
How to deal with these deficits:
1. You can teach patients with neglect to look left, but the benefit will be short-term.
2. You can have them cross their arms and that tends to improve their awareness of
their left side and specifically of their left arm.
3. You can have them turn to the left when looking or hearing something on their left
side.
Attention deficit hyperactivity disorder (ADHD) is a disorder that is characterized by
hyperactivity, impulsiveness, temper flairs, difficulty being organized, and problems both
inhibiting and disinhibiting attention.
People with ADHD show specific patterns of performance on certain tasks:
1. Choice delay task-- Do you want the smaller reward now or the bigger one later?
The vast majority of people ADHD go for immediate gratification.
2. Stop signal task-- You see a signal and are asked to press a button unless you get
the "stop" signal ("Don't press the button"). People with ADHD are less likely to be able
to stop the button press in response to the stop signal.
3. Attentional blink-- You see a string of letters and you have to respond to a letter that
is a different color than the rest. Then, you have to report whether or not a particular
letter such as an R appeared after that colored letter. "Normal" people tend to miss the
R if it appears 100-700 ms after the colored letter. For people with ADHD, this
"attentional blink" lasts much longer--well over a second.
Brain Differences:
People with ADHD have:
1. Smaller brain volume (95% of normal)
2. Smaller right prefrontal cortex
3. Smaller cerebellum
The main drug treatment for ADHD has been the use of stimulants, such as Ritalin
(methylphenidate) and Aderrall (amphetamine).
11/13/07Learning & Memory
Classical conditioning- Pair a conditioned stimulus (CS) with an unconditioned stimulus
(UCS) to produce a conditioned response (CR)
Operant conditioning- A reinforcer changes the probability of a certain behavior.
Is there a specific brain area or brain change associated with learning?
Karl Lashley-- Search for the "engram," which is the physical representation of learning.
Lashley's research generated two principles:
1. Equipotentiality-- All parts of the cortex are equally involved in learning, and any part
could substitute for another.
2. Mass action-- The cortex works as a whole and the more cortex is involved in a task,
the better.
Two faulty assumptions:
1. The cortex is the best or only brain area to study if we understand learning.
2. All kinds of memory and learning are the same physiologically.
Possible sites of engram:
1. The cerebellum has a structure called the lateral interpositus nucleus (LIP); in
classical conditioning, cells in the LIP show greater activation for the conditioned
stimulus once conditioning has happened.
2. The prefrontal cortex, which maintains a high level of activity during certain kinds of
learning task, such as the delayed response task, which requires the individual to
respond to a stimulus that was presented sometime in the recent past.
Since the advent of cognitive neuropsychology (the study of cognitive deficits caused by
damage to specific brain areas):
Patient HM-- Because of severe epilepsy, HM had parts of his medial temporal cortex
removed, including the hippocampus.
Anterograde vs. retrograde amnesia-- Retrograde amnesia is when your memory less
is for events occurring prior to your brain damage; anterograde is memory loss for
events after your injury (i.e., the inability to lay down new memory traces).
HM shows severe anterograde amnesia.
Short-term memory (STM) vs. long-term memory (LTM)-- STM has a capacity of 7 plusor-minus 2; LTM has a possibly infinite but unknown capacity. Duration: STM lasts
about 30 seconds at the most; LTM lasts a lifetime. Forgetting: once something is
forgotten from STM, it's lost; but information forgotten from LTM can be recovered.
Baddeley & Hitch-- STM is overly simplistic, because--among other things--it focuses on
auditory processing (STM has an acoustic code). New concept: working memory,
which includes:
a) a phonological loop-- stores auditory info
b) visuospatial sketchpad-- stores visual info
c) central executive-- directs attention to a specific stimulus and determines which items
of information will be stored in working memory.
HM has intact STM or working memory but damaged LTM.
Procedural vs. declarative knowledge-- Procedural knowledge is "knowing how"
(knowledge of how to carry out specific tasks); declarative knowledge is "knowing that"
(knowledge of facts)
HM has intact procedural knowledge but impaired declarative knowledge.
Episodic vs. semantic memory-- Episodic memory is memory for specific events in your
life; semantic memory is knowledge of basic facts that are "disembodied" (you do not
necessarily remember the context in which you learned those facts).
HM has a little bit of semantic memory but no real episodic memory. He can't form new
memories of events in his life, but he can learn an occasional fact.
What is the relationship between the hippocampus and memory?
1. Hippocampus size: There is not a good correlation between hippocampus size and
memory loss in older adults, but there is a correlation between the extent of memory
loss and the rate of shrinkage of the hippocampus.
2. Hippocampus activity- Evidence of increased activity in the hippocampus during
memory tasks, and there is an especially strong correlation between verbal memory and
hippocampus activity.
What kind of memory is associated with the hippocampus?
1. Declarative memory, especially episodic memory. Damage to the hippocampus
tends to impair performance on certain kinds of memory tasks, such as delayed
matching-to-sample tasks (Example: "Concentration" game show).
2. Spatial memory. Rats with damage to their hippocampus have problems on a radial
maze task, in which they have to locate the arm of maze that has a food reward at the
end of it. Impaired rats will keep going down the arms where they already found food,
suggesting that they don't remember where they've been. They also struggle with the
Morris maze task, in which they have to navigate through water to locate a platform.
3. Configural learning-- Learning that specific stimuli (e.g., shaped objects) are
associated with specific outcomes. Example: you get a reward if you choose the circle
over the square.
Types of memory damage:
1. Korsakoff's syndrome-- Caused by brain damage due to thiamine (a type of B1
vitamin) deficiency for very long periods of time, usually related to alcoholism. Severe
alcoholics will use alcohol as their primary energy source, and will suffer nutritional
deficiencies as a consequence. Symptoms of Korsakoff's: retrograde and anterograde
amnesia, confusion, apathy, and extensive confabulation (make up stuff), usually about
the events in their lives.
2. Alzheimer's-- Better procedural than declarative memory, and they show deficits in
both implicit and explicit memory. Progressive, leading gradually to more sever memory
loss and confusion, as well as delusions, restlessness, sleeplessness, loss of appetite,
hallucinations.
Is Alzheimer's disease genetic?
Evidence for: Link between Alzheimer's disease and chromosome 21. People with
Down's syndrome almost always get Alzheimer's if they live long enough, and a specific
gene on chromosome 21 has been linked to early-onset Alzheimer's.
Evidence against: Half of all Alzheimer's patients have no family history (i.e., no known
relatives with the disease). Environmental factors such as diet have been linked to
some extent to Alzheimer's. Smoking and drinking coffee reduce your likelihood of
having the disease.
Mechanism of Alzheimer's onset involves the metabolism of amyloid proteins in the
brain. A normal amyloid protein has 40 amino acids, and in Alzheimer's, a form of the
protein is produced that has 42 amino acids. These proteins produce a type of deposit
called plaques that are the result of the degeneration of axons and dendrites. A
separate protein called a tau protein produces tangles, which are the result of damage
to cell bodies.
Current methods of treatment:
1 Drugs that stimulate acetylcholine receptors or that prolong acetylcholine release
delay the onset of memory deficits.
2. Drugs that stimulate cannabinoid receptors can slow the progression of the disease.
3. Drugs that block amyloid production (antioxidants).
4. Immunization-- Introduce amyloid 42 into young people's bodies, they will produce
antibodies to destroy it (because it's seen as a foreign protein).
11/6/07CH.11: Reproductive Behavior
Menstrual Cycle
1. After the end of a menstrual cycle, the anterior pituitary releases follicle-stimulating
hormone (FSH), which promotes the growth and release of a follicle in the ovary. The
follicle contains the egg, as well as nutrients and hormone systems. It produces
estradiol (form of estrogen).
2. Toward the middle of the cycle, the follicle produces more FSH receptors (which
trigger more hormone release), which causes an increase in the release of estradiol.
3. The increased release of estradiol causes an increase in the release of luteinizing
hormone (LH) from the anterior pituitary, which triggers the release of the egg from the
follicle.
4. The remnant of the follicle releases progesterone, which prepares the uterus for
implantation of the fertilized egg and which inhibits the release of more LH.
5. Toward the end of the cycle, levels of LH, FSH, estradiol, and progesterone all
decline. If the egg is not fertilized, the lining of the uterus is cast off and the cycle
begins again.
Towards the end of pregnancy, the female secretes large amounts of estradiol,
prolactin, and oxytocin. Prolactin is necessary for milk production, but all three are
important for stimulating maternal behavior.
Men have vasopressin, which helps with bonding with both one's mate and offspring.
Emotion
What is it?
It is some combination of cognition, behavior and feeling state. Behavior includes
psychophysiology.
James-Lange- Autonomic arousal and skeletal muscle movements come first; the
interpretation follows.
According to William James, we experience fear when we observe ourselves running
from the bear.
Facial efference- Output of facial muscles affects our mood.
Schachter & Singer- The body cannot differentiate arousal based on any two emotions.
Only by interpreting situational cues do we define and label that undifferentiated arousal
as a specific emotion.
Is arousal necessary for emotion?
No. Patients with pure autonomic failure, who have no changes in heart rate, bp,
perspiration during psychological stress, still report the same emotions as anyone else.
Is arousal sufficient for emotion?
No. You can autonomic arousal without emotion. For example, let's do jumping jacks!
Some folks claim that emotions evolved out of physiological responses. The classic
example is DISGUST:
Disgust activates the insula, which is the primary taste area in the cortex, and the
olfactory bulb, which processes smell. In fact, both of those areas are close to the
amygdala, which is one of the primary emotion centers in the brain.
Fear-- escape from danger
Anger-- to defend oneself from an attacker
Disgust-- to protect us from something toxic
Prefrontal cortex (specifically the orbitofrontal cortex)- Related to emotional decision
making in which we weigh risks and rewards.
Iowa Gambling Task-- The player chooses cards from $50 and $100 decks and the
objective is to collect as much money as possible. The decks have occasional penalties
associated with specific cards. It turns out that the $100 decks have greater penalties
and result in overall losses, whereas the $50 decks result in overall gains.
Patients with damage to the OFC cannot delay short-term gratification long enough to
receive the long-term gains, and so they keep playing the $100 decks.
Aggressive Behavior
Is it genetic or environmental?
There is evidence for both:
Genetic-- Monozygotic twins resemble each other much more in terms of violent
behavior than do dizygotic twins or non-twins. Those resemblences are more likely to
be true in childhood and adolescence, however. Also, adopted children more closely
resemble their biological vs. their adoptive parents in terms of criminal record and other
signs of aggression.
Environment-- The resemblence between twins goes down with age. Also, prenatal
environmental plays a role in aggressive behavior. Women who smoke during
pregnancy are more likely to have male offspring who engage in violent behavior.
In the genetic corner is testosterone levels. Testosterone levels are significantly higher
in men imprisoned for violent crimes compared to control subjects, but these effects are
small.
Serotonin turnover-- the rate with which serotonin is released and resynthesized in the
brain. There is evidence that low turnover is correlated with aggressive behavior:
1. Suicide rates are highest in the spring, when serotonin turnover is lowest.
2. Serotonin levels in the brain predict a number of violent behaviors, including juvenile
delinquency, suicide attempts, and convictions for violent crimes.
3. People fed diets low in tryptophan show a tendency to aggressive behavior, as do
people who have low levels of tryptophan hydroxylase, an enzyme that is important for
the synthesis of serotonin from tryptophan.
Amygdala-- Enhances the startle response. The amygdala gets input from pain fibers,
vision and hearing. And its output goes to the hypothalamus, which controls autonomic
response. It also has axons that project to the prefrontal cortex, which controls
approach/avoidance behavior (risk/reward assessment).
Kluver-Bucy syndrome-- The monkeys with amygdala damage become placid and
tame. They are not afraid of stimuli that would normally induce fear, such as fire and
snakes and large animals. They also don't react normally to other monkeys' threat
gestures.
In humans, facial expressions of other people are important emotional cues. We
recognize angry expressions faster if they are directed at us and fearful expressions
faster if they are directed to our side.
The amygdala shows a greater response to fearful expressions directed towards us and
to angry expressions directed toward our side. Why? Those stimuli are more
ambiguous and require more ffort to process. So, the amygdala is trying to interpret
emotional stimuli.
People with amygdala damage report normal emot5ions but have a hard time
processing subtle emotional cues, and they are more likely to pay attention to irrelevant
cues in an emotion-inducing situation than normal individuals.
Benzodiazepines (including valium) interact with the amygdala. They bind to GABA
recpetors in the amygdala, hypothalamus, midbrain, and some cortical areas. GABA is
an inhibitory neurotransmitter. By binding to the receptor, BDZs cause GABA to bind
more tightly to the receptors. Because GABA is inhbitory, the net effect is to turn off
fear-related responses.
STRESS
Hans Selye-- general adaptation syndrome; the body responds to stressors in three
stages:
1. alarm-- increases sympathetic arousal
2. resistance-- the body repairs damage created in teh alarm phase, and the adrenals
secrete corticosteroids such as cortisol, which functions to increase blood sugar levels.
3. exhaustion-- the nervous system and immune system no longer have the energy to
function properly.
HPA axis (hypothalamus, pituitary and adrenal)
1. hypothalamus releases corticotrophin releasing factor (CRF)
2. this triggers the anterior pituitary to release ACTH (adrenocorticotropic hormone)
3. this triggers the adrenals to release cortisol
The adrenals also secrete epinephrine and norepinephrine, which stimulate sympathetic
arousal
The effects of stress on the immune system are as follows:
1. During the resitance phase, there is an increase in immune activity.
2. During the exhaustion phase, energy gets directed towards glucose metabolism and
away from protein synthesis, including the synthesis of immuno-proteins.
10/30/07Sex hormonesOrganizing effects-- At a sensitive/critical period, hormones determine whether or not
the brain body will develop male or female characteristics.
Activating effects-- At specific points in the life cycle, when a hormone temporarily
activates a certain response.
The default setting for humans is female. Unless testosterone is released at a critical
period, the individual will have the secondary sexual characteristics of a female.
Sex and gender-- Sex is simply your genetic makeup (XX or XY), but gender is far
more complex because it's due to a combination of factors, including cognition. Gender
has to do with how individuals perceive themselves.
Sexual variationsHermaphrodites-- a small percentage of newborns have a combination of male and
female genitalia or genitals that are somewhere in-between.
Pseudohermaphrodites are more common (1 in 2000 individuals)-- There is enough
ambiguity at birth to make a proper identification of sex difficult.
Androgen insensitive males-- Androgen refers to male hormones, including
testosterone. Genetically male but has the secondary sexual characteristics of a
female, more or less. Generally, these individuals have broader shoulders and
narrower hips than the prototypical female, and no body hair whatsoever.
A tribe in the Dominican Republic that is fairly isolated geographically and so is
susceptible to intermarriage. A genetic anomaly has occurred in that population, a
group of individuals who are called "huevo-doces." These people have a deficiency in
an enzyme that converts testosterone to dihydrotestosterone, which is what signals the
production of secondary sexual characteristics.
At puberty, other enzyme systems kick in. When that happens, these individuals go
from being girls to men.
congenital adrenal hyperplasia (CAH)-- overdevelopment of the adrenal glands from
birth. This causes larger-than-normal levels of testosterone in the body. Genetically,
the individual is female, but the effect is one of masculinizing the external genitals.
10/23/07-
Announcements:
1. Midterm 2 next Tuesday
CH.10: Internal Regulation
Homeostasis-- Self-regulation. There is a set point, which is the point at which a
variable needs to be held (e.g. an ideal temperature) and the body regulates the
variable to hit that set point.
Thermostat-- When the temperature drops below the set point, the heat turns on, and
when it goes above it, the AC turns on.
Body Temperature
Animals' body temp is determined by certain factors: a) ambient temperature; b)
physiological mechanisms--sweating, panting, licking, shivering, decreasing blood flow
to the skin surface and extremities, fluffing fur; behavioral mechanisms-- finding a warm
or cool place; clothing; activity; huddling/cuddling.
Why 37C (98.6)?
Much above that temperature, the proteins in our bodies denature.
Much below that temperature, muscle fibers don't operate at their peak.
Brain areas associated with temperature regulation are the preoptic area and anterior
hypothalamus (POA/HA).
Fever- Why do we get a fever?
Benefits: It keeps bacteria from growing at the higher temperatures because the
bacterial proteins denature.
Risk- A fever above 39C can be harmful, and above 41 can be deadly.
ThirstVasopressin- secreted by the posterior pituitary and raised bp by constricting blood
vessels; this conserves water; and increases pressure for a given blood volume. It is
also known as antidiuretic hormone (ADH) because it allows the kidneys to reabsorb
water from urine, which in turn makes the urine more concentrated.
Two kinds of thirst:
1. Osmotic thirst-- this comes from eating salty foods, which causes sodium ions to build
up in the blood and the extracellular fluid. The sodium buildup causes water to move
from the inside of the cell to the extracellular fluid. Neurons in two brain structures
called the OLT subfornical orgal, which line the third ventrical, detect water loss and
signal to the hypothalamus that there is a need for more hydration.
2. Hypovolemic ("low volume") thirst- this comes from a loss of fluids, which can occur
through sweating, bleeding, vomiting, diarrhea.
There are two mechanisms in the body for detecting loss of blood volume
1. Receptors in the veins signal the kidneys to release renin, which is a precursor to
angiotensin II (this hormone is similar to vasopressin in function; among other things, it
constricts blood vessels and increases blood flow).
2. Subfornical organ detects lower blood volume.
Sodium-specific thirst: When you have osmotic thirst, you can quench that thirst by
drinking pure water, but when you have hypovolemic thirst, you need to add
electrolytes. Sodium-specific thirst occurs when you dilute sodium and other ions in
your blood stream.
When sodium reserves are low, the adrenal glands secrete aldosterone, which causes
the kidneys, salivary glands, and sweat glands to retain salt.
HUNGER
The factors that determine food selection:
1. Types of enzymes available in the digestive system.
Lactase--an enzyme that helps in the digestion of lactose in dairy products
2. Imitation-- learn from those around us
3. Taste-- We tend to select sweet foods, avoid bitter foods, and eat salty and sour
foods in moderation.
4. Learning-- We learn to reinforcement the consequences of eating certain foods.
The factors that affect hunger:
1. Oral factors--if we don't taste, chew, and swallow our food, we tend to find it
unsatisfying.
2. Stomach/intestines-- distension of the stomach sends messages to the brain about
the stretching of the stomach (vagus nerve) and about the contents of the stomach
(splanchnic nerve). Between the stomach and small intestine is the duodenum, which
releases the hormone CCK. This hormone acts to limit meal size by closing the
sphincter between the stomach and duodenum. CCK also signals fullness to the
hypothalamus.
3. Blood glucose levels- trigger the secretion of insulin by the pancreas. Insulin allows
glucose to enter the cells. Insulin levels increase after a meal, and this increase tends
to sginal fullness.
Brain areas associated with hunger:
Lateral hpothalamus-- controls insulin secretion and facilitates feeding behavior. An
animal with damage to that area refuses food and water.
VMH- Damage to this area leads to overating and weight gain because the individual or
animal will eat normal-sized meals but more frequently. VMH has something with
fullness but regulates the frequency rather than the size of the meal.
PVN-- Inhibits the lateral hypothalamus and thus limits eating and drinking. Damage to
this area result in much larger than normal meals.
Arcuate nucleus-- there are two sets of neurons in this nucleus; one signals fullness and
the other signals hunger. The output of this structure connects to the PVN.
Genetic evidence for obesity:
Twin and adoption studies
REVIEW SESSION
II-7e. Indicate which cortical structures process auditory information
Primary auditory cortex-- superior temporal lobes
Secondary auditory cortex-- surrounds the primary auditory cortex
II-7d. Explain the volley principle
No single auditory receptor can fire at a rate compatible with the highest frequency
sounds. So, instead of one receptor firing 10,00 times, you could have 10,000
receptors firing at one time, and the effect would be the same. A volley is a
synchronized firing of receptors (or cannons).
II-9f Explain why there seems to be so much specialization among olfactory receptors.
There are thousands of smells, and unlike tastes, which reduce to combinations of five
basic flavors, there are no known basic or fundamental smells that serve as the
"building blocks" for other smells.
II-9c Explain how you would prove the existence of the five kinds of taste receptors
Cross-adaptation- If you puts drops of a certain flavor, like sweet, on the right
receptors, eventually you get adaptation, which means that the receptors become
fatigued. But then if you introduce a different flavor, the receptors will be able to taste it
"fresh," indicating that there is NO cross-adaptation.
II-9j Compare the VNO of adult humans with that of other mammals.
The vomeronasal organ (VNO) is associated with the detection of pheromones. In
humans, it is relatively small compared to other mammals.
II-18d
Discuss the role of leptin in regulating eating behavior.
Leptin is a peptide that is produced by the body's fat cells. It signals the brain in a more
long-term ways whether to eat more or less. It's more of a mechanism that indicates
whether or not there are famine conditions. When leptin levels are high, animals eat
less and become more active.
Ghrelin is a peptide that is associated with fullness. Eating causes a decrease in
ghrelin levels. In people with certain types of obesity, ghrelin levels are much higher in
the bloodstream than they are in normal individuals.
Sodium hunger = sodium-specific thirst
*supertaster- someone with a highly developed sense of taste
II-13a Give examples of endogenous circannual and circadian rhythms
Circannual-- migratory pattern
Circadian-- sleep and wakefulness
II-4a
Offer two possible explanations for the phenomenon of blindsight:
1. Weiskrantz-- Even though area V1 is damaged, other brain areas that process
visual information are intact.
2. Gazzaniga-- There are tiny islands of healthy tissue intact in and around V1.
II-3a Give a brief overview o the mammalian visual system
The optic nerves, which are the set of axons coming off the receptors in the retina, meet
at the optic chiasm, where half go to the left hemisphere and the other half to the right
hemisphere. Most of the axons go to the lateral geniculate nucleus (LGN) in the
thalamus, which sends its output to the visual cortex, starting with area V1. From V1,
there are two pathways leading to other visual areas in the cortex:
a) Ventral stream-- visual pathway that leads to areas in the temporal cortex that are
specialized for identifying and recognizing objects, including object shape (V4).
b) Dorsal stream-- Visual pathway that leads to the parietal cortex, with a "side route"
that leads to the medial temporal (MT) and medial superior temporal (MST) cortex. This
pathway detects "where" and "how", including motion detection. It lets the individual
determine how to find and grasp objects.
II-6d Discuss the visual impairments of people born with cataracts in either one eye or
both eyes.
Both eyes- The person will have near-normal vision after cataract surgery, but will have
mild prosopagnosia and may have problems with subtle visual discrimination tasks.
Cataracts in left eye-- Moderate prosopagnosia after cataract surgery
Hunger:
10/16/07CH.9: Wakefulness & Sleep
Biological Clock
Circadian rhythms-- daily patterns of sleep and wakefulness
Circannual rhythms-- yearly patterns such as those migratory animals
Suprachiasmatic nucleus (SCN) in hypothalamus- Neurons in the SCN fire at specific
times of day; this area controls activity in the pineal gland, which release the hormone,
melatonin, that increases sleepiness. The free-running rhythm of the SCN is more than
24 hours.
There are cues, called "zeitgebers" (time-giver), are used by the SCN to set its rhythms.
One zeitgeber is light; others are temperature, meals, exercise.
Disruptions of the biological clock:
1. jet lag-- Disruption of the circadian rhythm due to changing time zones; it's harder
going EAST than WEST, because you have to go to bed earlier than you're used to.
2. Shift work-- When you're sleeping in the morning or afternoon, when your body
temperature and metabolism are peaking, you will not sleep soundly or for more than a
brief duration.
Stages of Sleep
NREM stages:
Stage 1-- Body relaxes, muscle tone diminishes, heart rate slows, breathing becomes
deeper; brain wave activity becomes slower, more irregular; increase alpha activity
compared to waking
beta 14-30Hz
alpha 8-13 Hz
theta 4-7 Hz
delta 0.5-4 Hz
Stage 2- Brain wave activity that is characterized by sleep spindles (which are bursts of
relatively fast, 12-14 Hz activity), and K complexes (which are bursts of high-amplitude
activity).
Stage 3-- An increase in slow wave activity (i.e., theta and delta), with 20% delta.
Stage 4-- Primarily theta and delta activity; defined by having at least 50% delta activity.
REM Sleep: Paradoxical sleep
REM seems like deep sleep in some ways and very light sleep in other ways.
Increased activity: Brain-wave activity is relatively high (closest of any sleep stage to
waking), increase in eye moevements, increases in heart rate, bp, and respiration rate
(although irregular), increased genital arousal.
Decreased activity: Nearly complete loss of muscle tone (the skeletal muscles become
relaxed to the point of paralysis).
80-90% of REM awakenings produce a dream report. These dreams are characterized
by a PLOT (narrative storyline) and mental imagery (usually visual).
REM sleep deprivation-- Mental fatigue; REM rebound-- When you're allowed to have
REM sleep, you have more than the normal amount to compensate for what you lost.
Brain areas associated with sleep and wakefulness:
1. The SCN in the hypothalamus
2. Reticular formation-- axons from this area extend into the hypothalamus, thalamus,
and basal forebrain; regulates arousal levels.
3. Locus coeruleus-- found in the pons; it's inactive most of the time but has bursts of
activity that increase wakefulness and that strengthen the storage of recent memories;
The LC is silent during sleep.
4. Basal forebrain-- This area is located just in front of and above the hypothalamus;
axons from the BF extend into the thalamus and cortex; it releases acetylcholine, which
is an excitatory neurotransmitter and that thends to increas arousal; but it also releases
GABA, which is inhibitory and essential for sleep.
Parts of the BF stimulate sleepiness, and other parts stimulate arousal.
Adenosine (amino acid) inhibits the BF cells responsible for arousal; caffeine blocks
adenosine receptors.
Physiology of REM Sleep
PGO Wave-- Pons-->Lateral Geniculate Nucleus-->Occipital Cortex
Every eye movement in REM is accompanied by a PGO spike.
Activity in the pons triggers the onset of REM sleep.
Sleep Disorders
Insomnia- Sleep onset and sleep maintenance.
Sleep apnea- Inability to breathe during sleep; often associated with individuals who
are obese.
Narcolepsy-- Considered a "parasomnia" which is a condition in which sleeping intrudes
on waking life. There are four characteristics of narcolepsy:
1. Gradual or sudden attacks of sleepiness during the day.
2. Occasional cataplexy-- Muscle weakness while awake.
3. Sleep paralysis-- The inability to move while falling asleep or waking up.
4. Hypnogogic hallucinations-- Dreamlike experiences that cannot be distinguished
from waking reality.
Periodic limb disorder- Involuntary muscle movements during NREM; most common in
older adults who have possibly had a microstroke or other brain trauma.
REM behavior disorder- Movement during REM
Night terrors- Waking up from NREM with intense anxiety; most common in children
NREM "sleep mentation" is different from dreams; when people are awakened from
Stage 3 or 4 sleep, they report vague, abstract experiences, but nothing that resembles
a REM dream in terms of plot or imagery.
Why do we sleep?
1. Conserve energy- Why can't we conserve energy by just lying still for several hours?
Why do we have to undergo the changes in consciousness associated with sleep?
2. Restorative function-- Sleep increases the repair and synthesis of proteins in the
brain; synapses get reorganized during sleep.
3. Strengthening of memories- When people learn information during the day, certain
brain areas are activated, and those same areas get re-activated that night during
sleep. The extent to which the individual learns the information is directly correlated
with the amount of activation during sleep.
None of these theories accounts for REM sleep.
Why do we have to undergo this strange paradoxical stage of sleep?
1. Maurice (1998)-- REM shakes the eyeballs so that the corneas can get the oxygen
they need.
2. Activation-synthesis (Hobson & McCarley)-- Random activation in the pons and other
brain areas, and the mind tries to make sense of that activation. For example,
activation of the vestibular system, which provides information about orientation in 3D,
may give the impression of flying. Firing of the motor cortex might result in a chase
dream.
One criticism is that this theory has put too much emphasis on the pons, and there is
evidence of dreaming in people who have "pontine" damage.
There is no established correlation between activity in specific areas and the content of
dreams.
Lucid dreaming research indicates that dreams are not solely the result of random brain
activity.
3. Clinico-anatomical theory-- Dreaming is thinking that occurs in the absence of
information from the sensory organs or from the primary motor cortex.
10/9/07Prosopagnosia-- Damage to the boundary between the occipital and temporal cortex.
"Cognitive Neuropsychology" by Elizabeth Warrington
CH.8: Movement
Three types of muscles:
Striated-- skeletal muscles that control movement of the body relative to the
environment
Smooth-- muscles of the internal organs
Cardiac-- muscles of the heart, usually considered smooth muscle fiber but have certain
properties in common with striated muscle
Striated muscles are antagonistic-- Paired muscles that move a part of the body in
opposing directions (flexors vs. extensors, adductors vs. abductors)
Proprioceptors-- Receptors that detect the position or movement of a body part.
One kind of proprioceptor is a muscle spindle, which attached to a muscle and when the
spindle is stretched, it sends a message to a motor neuron, which causes the muscle to
contract
A second distinction among muscles is fast-twitch vs. slow-twitch:
Fast-twitch muscles produce fast contractions but fatigue easily; they are need for
intense, strenuous activity of short duration (anaerobic); slow-twitch produce less
vigorous contractions without fatiguing easily.
There are three types of reflexes that occur in newborns but not in adults:
Grasp reflex- You put an object in an infant's hand and it will grasp tightly.
Babinski- You stroke the sole of the foot and the big toe will extend while the other toes
fan out.
Rooting- You touch the infant's cheek and the head will tirn and the infant will begin
sucking movements.
The parts of the brain associated with the control of movement:
Many cortical areas associated with movement are in the frontal lobes:
1. The motor cortex-- This area does not have any direct connections of the muscles of
the body; its axons connect to the brainstem and spinal cord. It is more important for
comple movements (talking, writing, hand gestures) than for basic movements
(coughing, sneezing, gagging, laughing).
2. Premotor cortex-- This area is most active in preparation for a movement; it receive
information about the location of a target in space towards which a movement is
directed.
3. Supplementary motor cortex-- This area is responsible for planning and organizing a
rapid sequence of events, such as pushing, pulling, or turning an object.
4. Prefrontal cortex-- This area responds to sensory stimuli (noises, lights) that lead to
a movement and calculate the probable outcomes of the movement.
5. Posterior parietal cortex-- This area keeps track of the position of the body relative to
space.
Figure 8.8
The cerebellum is involved in coordination and "ballistic movements" (movements that
are performed all at once, in a "single shot")
People with damage to the cerebellum have trouble with movements requiring accurate
aim and timing: tapping a rhythm, clapping hands, pointing at a moving object,
speaking, writing, typing, or playing a musical instrument; most athletic activities.
The ways to test for cerebellar damage include:
1. Asking the subject to move his/her eyes from one fixation point to another.
Normal, healthy individuals do it in a single saccade, with perhaps a small correction at
the end. Someone with cerebellar damage does it in a series of smaller saccades.
2. Finger-to-nose test
Normal, healthy individuals do it in three steps: a) finger moves balistically to a point in
front of the nose; b) finger remains steady at a point close to the nose for a fraction of a
second; c) the finger moves to the nose in a slower movement that doesn't depend on
the cerebellum.
Someone with cerebellar damage either stops too soon or goes too far.
Motor pathways-- There are two main pathways coming off the motor cortex:
1. Dorsolateral tract-- This tract (set of axon fibers) controls contralateral movements in
hands, toes, fingers.
2. Ventromedial tract-- Controls movements involving both sides of the body, such as
neck shoulders, trunk.
Consciousness and movement
Do we consciously control our movements?
People report their decision to move a body part occurs 200 ms before the actual
movement. But the brain activity associated with the movement (i.e, a readiness
potential) starts 500 ms before the movement.
Basal Ganglia in movement
Globus pallidus releases GABA, which is an inhibitory neurotransmitter, and thus
inhibits movment. Input from the putamen (and also the caudate nucleus) essentially
tells the globus pallidus which movments to inhibit. Damage to the globus pallidus
results in involuntary, jerky movements.
(See Fig 8.17)
Parkinson's-- Causes: Early onset (before age 50 is believed to be genetic); late onset
(after 50) also be due to environmental factors (exposure to herbicides, pesticides).
The mechanism of Parkinson's involves damage to the substantia nigra.
Lifestyle note: People who smoke cigarettes or drink coffee are less likely to develop
Parkinson's.
Symptoms: rigidity, muscle tremors, slow movements, and difficulty initiating physical
and mental activity.
Treatment: L-dopa, which is a precursor of dopamine that can cross the blood-brain
barrier.
Stimulation of the substantia nigra and the globus pallidus has resulted in at least
temporation cessation of symptoms.
Antioxidants are used to slow down the destruction of dopaminergic neurons.
Neurotrophins are used to decrease the rate of apoptosis.
Huntington's disease-- Damage to caudate nucleus, putamen, globus pallidus, and
cerebral cortex.
Symptoms: arm jerks, facial twitches, tremors, writhing, depression, memory
impairment, anxiety, hallucinations, delusions, alcoholism and drug abuse, sexual
disorders.
Cause: Genetic; an autosomal (not on a sex chrosome) dominant gene.
Onset of the disease occurs between the ages of 30 and 50.
Presymptomatic test-- Looks for the gene on Chromosome 4.
This gene produces a mutant form of a protein called Huntingtin, that prevents the
release of neurotrophins and also interferes with mitochondria in neurons.
If the globus pallidus, which inhibits certain movements, is damaged, the result is
uncontrolled and possibly violent movement.
There is no treatment for Huntington's.
10/2/07
Announcements:
1. Exam scores are posted online.
2. To contact the grader (respectfully): katrina@email.arizona.edu
3. Answer Keys are posted in the glass case in the third-floor hallway of the Psyc Bldg.
4. Grade Cutoffs are as follow:
A
B
25-30
20-24
C
D
15-19
10-14
5. Gandhi's Birthday
THE VISUAL SYSTEM (Part 2)
Types of cells in the visual cortex:
1. Simple cells- Feature detectors that detect edges and contours
2. Complex cells- Detect changes in orientation
3. Hypercomplex cells- Detect movement within the visual field (primarily located in V1)
Bottom-up processing-- The sensory apparatus (e.g., eyes) provide the information from which
your perceptual representations are formed.
Top-down-- Your "set", which includes your expectations, will dtetermine what you see.
There are visual pathways leading from areas V1 and V2 in the occipital cortex:
1. Ventral stream (downward)-- visual pathway leads to areas in the temporal cortex that are
specialized for indentifying and recognizing objects, including detecting color, brightness, and
shape.
2. Dorsal stream (up or back)-- visual pathway leading to the parietal cortex and to two areas in
the temporal cortex (Medial Temporal Cortex--MT--and Medial Superior Temporal Cortex-MST); this pathway provides information about movement, including "where" and "how"
information ("how" means that it lets the motor system find objects and determine how to grasp
them)
(Figure 6.19 shows the two pathways)
MT (V5)- Processes information related to the movement of an object within the visual field
MST- Processes information related to the movement of the field relative to the observer
(detects rotation or expansion/contraction of the visual field).
Disorders of visual processingVisual agnosia-- inability to recognize objects, usually linked to damage in the occipital lobes
Prosopagnosia- inability to recognize faces, usually linked to damage in the temporal lobes
Developmental issuesCritical or sensitive period in development-- If visual information is impaired in some way during
this period, it can have lasting effects on the individual.
Suppose that you close off an eye in a kitten. The cortex becomes unresponsive to information
from that eye.
Suppose you close off both eyes. For the first few weeks, the cortex remains responsive to both
eyes, but then it begins to have trouble with acuity, orientation
People who are born with cataracts:
1. in both eyes--after the cataract surgery, they tend to have near-normal vision, but they can
have mild prosopagnosia.
2. in left eye- after the cataract surgery, serious prosopagnosia continues
Patient MM suffered cornea damage at age 3.5. When the damage was corrected surgically, he
could detect simple shapes, as well as direction and orientation, but had problems seeing
details, and those problems were never corrected fully.
HEARING
Auditory system detects patterns of compression and decompression of air molecules (sound
waves).
All waves have a frequency (number of cyles per second, measured in Hz) and an amplitude
(height of the wave). For sound waves, frequency corresponds to the perception of pitch and
amplitude to the perception of sound intensity (loudness).
Parts of the ear
Pinna- The outer ear structure, which includes the flesh and cartilage attached to the head.
Middle ear-Tympanic membrane (eardrum)-- Thin membrane that vibrates at the same frequency as the
sound waves that strike it.
The eardrum is connected to three bones in the middle ear called ossicles (hammer, anvil,
stirrup), that convert the vibration of the eardrum to a motion that strikes the oval window of the
cochlea.\
The oval window pushes against the fluid inside the cochlea, and as the fluid moves past hair
cells (auditory receptors) that are found on the basilar membrane of the cochlea, these cells
generate an electrical impulse or action potential.
How do hair cells detect differences in frequency? There are two theories:
1. Frequency theory-- The fluid in the cochlea vibrates at a frequency that synchronized to the
sound waves, and causes the hair cells to fire at that frequency.
Problem: The human auditory system can detect frequencies as high as 4000Hz, whereas a
hair cell can fire at a rate closer to 1Hz.
2. Place theory-- Hair cells at different points in the basilar membrane are attuned to different
frequencies and fire at those frequencies.
Volley principle-- That hair cells fire in groups, or volleys. In other words, to get 4000 Hz, you
could have 4000 hair cells firing simultaneously.
The auditory nerve, which is the set of axons from hair cells in the cochlea, goes through the
thalamus, and to the primary auditory cortex (A1), which is in the superior temporal cortex, and
also to the secondary auditory cortex, which surrounds A1.
There are two types of deafness:
1. Conductive deafness-- Due to damage of the middle ear and the inability of the middle ear to
transmit sound waves to the cochlea.
2. Nerve deafness- Damage to the cochlea, to the hair cells specifically, or to the auditory
nerve.
Sound localization-- We use both ears to determine where a sound is coming from, and we do
so based on three types of cues:
a. Differences in intensity between the two ears.
b. Differences in the time arrival of sound to the two ears.
c. Phase differences between the two ears-- The sound reaches the ears at two different
points in its compression cycle
TOUCH
Three types of touch receptors
1. Simple bare neuron endings-- tend to be pain receptors
2. An elaborated ending (Ruffini endings and Meissner's corpuscles)- Ruffini are specialized to
detect heat, whereas the Meissner's corpuscles detect light touch.
3. Pacinian corpuscles-- Bare ending surrounded by non-neuronal cells that modify its function.
Detect large-scale joint movements.
These receptors cover the skin surface of the body and connect to the central nervous system
at various points in the spinal cord.
How does pain work
Pain receptors release Substance P, which is a neurotransmitter that transmits pain signals in
the body.
There are a number of ways to alleviate pain:
1. Opiate drugs, and endorphins specifically in the body, bind to opiate receptors on neurons
that release Substance P, and in doing so, inhibit that release.
2. Gate theory- Non-pain stimuli can minimize the intensity of pain signals because neurons in
the spinal cord that receive pain signals also receive other types of touch signals.
This explains why massage can be effective in minimizing pain.
3. Capsaicin, found in peppers, releases Substance P faster than neurons can resynthesize it,
leaving cells essentially "drained" so that they cannot transmit pain signals. But high doses of
capsaicin can damage pain receptors.
CHEMICAL SENSES (Taste and Smell)
The chemical senses are unique because they have to respond to a wide range of stimuli.
Taste receptors die off every two weeks, and olfactory receptors every month.
Theories about how these receptors work:
1. Labeled-line theory-- Each receptor corresponds to a limited range of stimuli and sends a
direct line to the brain.
2. Across-fiber pattern-- Each receptor responds to a wide range of stimuli and contributes a
piece of the whole puzzle in terms of the perception of each.
There are five kinds of taste receptors, found primarily on the edge of tongue. They detect:
sweet, sour, bitter, salty, and "umami" (glutamate taste; MSG)
Saltiness-- These receptors detect sodium ions and permit those ions to cross the sodium
channels, leading to depolarization of the membrane and action potentials.
Sourness-- When acids bind to receptors, they close off the potassium channels, keeping
potassium trapped in the neuron and depolarizing the membrane, causing an action potential.
Sweetness, bitterness, and "umami" receptors are all metabotropic. They stimulate the
production of a G-protein in the neuron, which produces a second messenger that will
eventually trigger an action potential.
Information from the front 2/3 of the tongue is carried to the brain along a nerve bundle called
the chorda tympani, a branch of the 7th cranial neve; taste info from the back of the tongue and
the throat is carried along branches of the 9th & 10th cranial nerve.
Taste receptors project to a part of the medulla called the nucleus of the tractus solitarius (NTS),
which then leads to the following areas:
Pons- That's a relay for cranial nerves
Lateral hypothalamus-- Regulates appetite
Amygdala-- Emotion
Ventral posterior thalamus-- Relay for all senses (except olfaction)
Somatosensory cortex-- Detects texture
Insula-- Primary taste area of the brain
OLFACTION
Olfactory information does not break down into categories like taste.
Olfactory receptors are highly specialized and there are many different types.
Signal moves from the nose to the olfactory bulb to olfactory areas of the cortex and then to
areas controlling feeding (hypothalamus) and reproduction.
Vomeronasal organ (VNO)--set of receptors located near the olfactory receptors but in a
separate area of the nose. In adult humans, it is tiny and appears "vestigial."
Yet, there is evidence of pheromone detection in humans. Two examples given in your book:
1. Women who spend time together find that their menstrual cyles become more synchronized.
2. Women who are in a steady sexual relationship tend to have more regular menstrual
periods.
There are gender differences in smell detection: Women detect odors more readily and their
brains respond more strongly to odors; they also pay more attention to smells, and care more
about the smell of a potential partner.
Olfactory receptors are exposed to many toxins and pollutants; that is why they only survive a
month.
9/25/07The Visual System:
The Eye-- light (electromagnetic energy) enters through the pupil, which is an opening in the iris.
It is focused by the cornea and the lens, and then is projected onto the retina, which has the
following types of cells:
1.
2.
3.
4.
Receptor cells--transduce light into an electrochemical signal
Horizontal cells--inhibit other cells in the eye
Bipolar cells-- intermediary cell that sends the signal to the ganglion cells
Ganglion cells- the cells that transmit the signal out of the eye through the optic nerve.
The axons of the ganglion cells make up the optic nerve that carries electrochemical signals out
of the eye and to the thalamus.
Two types of receptors:
1. Rods--abundant in the peripheral area of the retina and respond to faint light but not as well
to bright light.
2. Cones-- abundant in the fovea, which is the central part of the retina, they are more useful in
bright light and in color vision, less useful in night vision.
How do receptors carry color information?
Young-Helmholtz (trichromatic) theory-- three kinds of cones in the eye, each being sensitive to
a specific part of the color spectrum (short wavelength= blue receptors; medium
wavelength=green; and long=red). The ratio of activity among the three types of cones
determines what colors we see.
Doesn't account for afterimages.
Opponent-process theory - We perceive color in terms of three paired opposites: red-green,
yellow-blue, and white-black. This explains why there are afterimages. In the absence of
activation of blue receptor, we see yellow.
Neither theory accounts for color constancy, which is when we can still identify a color correctly
under different types of light.
Retinex theory-- "retinex" = retina + cortex. This theory says the cortex compares information
from various parts of the retina to determine brightness and color.
Color blindness-- Some people with color blindness lack one or two types of cones. Some have
all three, but one kind is abnormal. But the most common form of color blindness is one in
which the red and green cones have the same photopigment.
The optic nerve-- Axons from ganglion cells in the retina. The point at which the axons exit the
eye produces a blind spot in the retina. The optic nerve from the two eyes meet at a point
called the optic chiasm. Half of the axons from each eye cross over to the opposite side of the
brain.
After crossing the optic chiasm, these axons travel to the lateral geniculate nucleus (LGN) of the
thalamus, which in turns sends the axons to other pars of the thalamus and to the visual areas
of the occipital cortex. There are two main areas in the occipital cortex: V1 and V2. From the
occipital cortex, the signal travels to other parts of the cortex, including the inferior temporal
cortex and the parietal cortex, and some of the signal returns to the thalamus in a feedback
loop.
Types of ganglion cells:
1. Parvocellular neurons ("parvo" means small)- small receptive field, adapted to color and
visual detail; their axons travel primarily to the LGN.
2. magnocellular neurons ("magno" means large)- larger receptive field, not color sensitive, and
connect to the LGN and to other nuclei in the thalamus.
3. koniocellular neurons- also have a small receptive field, connected to the LGN, other nuclei
in the thalamus, and the superior colliculus
Before the signal leaves the eye, information about edges and contours is refined. This
happens through a process called lateral inhibition.
The horizontal cells inhibit all the bipolar cells doubly, except those at the edge of the activation
area of receptors, which only get inhibited on one side. As a result, the bipolar cells on the
edge appear brighter. So, lateral inhibition serves to enhance the edges of what you're seeing.
Area V1 in the occipital cortex is responsible for processing a great deal of information
concerning shape and contour. It is also important for the subjective experience of being aware
of visual stimuli. If V1 is damaged, we get cortical blindness, which is called "blindsight."
Blindsight patients can distinguish some visual features with better-than-chance accuracy.
How is it possible for someone with damage to V1 to distinguish visual stimuli?
There are two theories:
1. Weiskrantz-- Even though V1 is damaged, other brain areas associated with visual
processing are still intact, and they provide enough information to perform certain types of tasks.
2. Gazzaniga- "Islands" of healthy tissue remain in an otherwise damaged V1, and even a few
cells are enough to be able to do certain rudimentary visual processing tasks.
In the visual cortex, there are three different types of cells that process visual information:
1. Simple cells-- in V1 (primary visual cortex), their receptive fields are attuned to edges and
rectangular areas.
2. Complex cells- found in V1 and V2 and they respond to angle or orientation
3. End-stopped (hypercomplex cell)- detect movement of an object within the visual field.
9/18Announcements:
1. Midterm 1 is next week. We will cover CH.6 first and then start the exam by 6:45pm. Please
make sure to be in class no later than 6:45.
2. Review session today--After we cover CH.5
3. CH.6 is NOT on the first midterm. Just CH. 1-5.
Brain Development and Plasticity
Stem cells-- Undifferentiated cells that have the potential of developing into just about any kind
of cell.
Development of neurons in five stages:
1. Proliferation-- New cells are formed.
2. Migration- Neurons move to their eventual destination in the brain
The migration of neurons and of axons within neurons happens through chemical attractants.
An axon will follow one attractant for a certain distance until it becomes insensitive to it, and
then it follows another attractant.
3. Differentiation- The neurons form axons and dendrites and then develop the specific
structure and shape relevant to their eventual function.
4. Myelination- Glial cells help produce the myelin sheath that insulates the axon.
5. Synaptogenesis-- Formation of dendritic branches and new synapses.
After prenatal development, the only two kinds of neurons that have been observed to
regenerate in mammals are olfactory receptors and hippocampal cells (in rats, but not YET in
humans).
Although neurons may not regenerate, they can form new dendritic branches.
Neural Darwinism-- The nervous system produces far larger numbers of neurons than it will
keep, as well as a larger number of synapses. Through a selection process, they get weeded
out. Some neurons are destroyed and others are kept.
apoptosis-- A self-destruction program that is built into every neuron. The default setting on
that program is cell death.
The only thing that keeps neurons from self-destructing at some point in development is the
release of specific proteins called neurotrophins that promote the growth and maintenance of
neurons and synapses. The specific type of neurotrophin that prevents apoptosis is called
nerve growth factor.
Other neurotrophins trigger the branching process of both axons and dendrites in adults (not
just in children).
In late adolescents, there is substantial loss of brain cells in parts of te prefrontal cortex. At the
same time, adolescents show increase brain activity in these areas and improved cognitive
ability. The loss of less successful neurons and synapses makes the brain more efficient.
Fetal alcohol syndrome- The symptoms of FAS include mental retardation, hyperactivity,
behavior problems such as impulse control, diffficulty with attention, heart problems, motor
deficits, and facial abnormalities.
The mechanism by which FAS occurs has to do with the reaction of ethanol in the developing
fetus' brain, causing an inhibition of the release of glutamate (excitatory neurotransmitter) and
an activation of GABA (inhibitory).
Interesting deviations from normal brain development
In blind people, PET and fMRI data have shown that while reading Braille, the visual cortex is
activated. So, areas of the occcipital that would normally be dedicated to vision get reassigned
to a certain form of touch reception.
Similarly, what we do can affect brain development. For example, professional musicians have
a 30% larger right temporal cortex than non-musicians.
Focal hand dystonia- "musicians cramp"; touch response in the brain associated with one finger
overlaps the touch response associated with adjacent fingers, leading to clumsiness and
involuntary hand movements.
Recovery from stroke and head injury
The brain can be damaged by the following: tumors, infections, exposure to radiation or toxins,
degenerative diseases, closeh head injury, stroke
Closed head injury-- impact that does not puncture the brain
Stroke-- a temporary change in blood flow to the brain that causes damage
There are two types of strokes:
1. Ischemia-- Obstruction of an artery, usually by a blood clot.
2. Hemorrhage-- The result of a ruptured artery
Ischemia is like a drought whereas hemorrhage is like a flood. In ischemia, neurons are
deprived of blood and therefore of oxygen and nutrients. In hemorrhage, they are essentially
drowned in a flood of nutrients that throws them out of balance, overwhelming the sodiumpotassium pump.
Both result in edema, which is an accumulation of fluid.
The most effective ways of treating stroke are:
1. Cooling the brain-- Slow down brain activity
2. Tissue plasminogen activator (tPA) breaks up blood clots in brain arteries.
3. Cannabinoids-- Lower the amount of glutamate released in the brain (glutamate inhibitors).
What happens after the brain is damaged by stroke or other means?
1. Diaschesis-- Decreased activity in areas connected to the neurons that were killed by the
stroke.
Area around the stroke that is called the penumbra. Neurons in this area may not be killed but
are damaged or affected in some way.
2. Regrowth of axons-- This occurs primarily in the peripheral nervous system, and at a rate of
about 1 millimeter per day. In the CNS, axons regenerate 1-2 mm at most, totally.
3. Sprouting-- New branches form, called collateral sprouts, that attach to vacant synapses.
4. Denervation supersensitivity-- The loss of certain neurons makes the remaining neurons (of
the same kind) more sensitive to specific neurotransmiitters.
An interesting effect of amputation
Reorganization of sensory information in the brain and also "phantom limb"
REVIEW
I-1e Distinguish between Chalmers' easy problem and hard problem
Easy problem-- The observation and description of certain aspects of consciousness, such as
the relationship between sleep and waking. There is an excellent understanding, for instance,
of the relationhsip between the psychophysiology of sleep and the experiential aspects of sleep.
Hard problem-- Understanding how the brain gives rise to consciousness.
I-2c Explain why it is difficult to distinguish between heredity and prenatal influences.
The genetics we share with our parents are going to dictate the kind of environment they create
for us.
Obesity runs in families for at least two reasons: One is shared genetics and the other is a
shared environment that is the result, at least in part, of those genetic tendencies.
I-5a Explain why an axon must regenerate an impulse instead of just conducting it
Axons conduct impulses for long distances and so those signals would weaken as a result of
resistance and other factors if it weren't regenerated.
I-5e Describe the molecular basis of the ACTION POTENTIAL
1. Voltage increases, resulting in depolarization (due to the flow of positive ions from adjacent
areas).
2. When the voltage crosses a threshold, voltage-activated sodium channels open up
3. Sodicum rushes into the cell, driven by both concentration and electrical gradients. This
raises the voltage to +30mV.
4. Voltage-activated potassium channels open and potassium flows out, drawn out of the cell
by concentration gradients and no longer held back by an electrical gradient.
5. Sodium-potassium pump takes out the excess sodium and brings in potassium.
I-4d
Identify the cells of the brain that can and cannot divide
Cannots: neurons (with two notable exceptions)
Cans: glial cells
I-6b Explain how saltatory conduction works.
Action potentials are only generated at nodes (spaces between sections of myelin sheath). In
the sections of the axon that are myelinated, positive ions move rapidly along the inside of the
membrane, conducting the signal without regenerating the action potential.
I-6c Indicate when impulses are transmitted without action potentials.
Local neurons have graded potentials in which the depolarization of the membranes is based on
the intensity of the stimulus.
I-9e
Describe the relationship of D2 and D4 receptors with personality.
These are two different types of dopamine receptors.
One form of D2 receptors are more likely to develop in severe alcoholism. D2 receptors are
correlated specifically with alcoholism.
D4 receptors are correlated to "novelty-seeking" personality types, who are characterized by
high impulsivity, a short temper, and exploratory behavior.
I-15e
Explain how gray and white matter relate to intelligence
Does brain size correlate with intelligence? Not very well, but the amount of gray matter in the
brain correlates to a greater extent.
I-3b
Name at least two plausible ways for altruistic genes to spread in a population
1. reciprocal altruism-- it's adaptive for animals to help those who will help them in return
2. kin selection- help relatives and therefore benefit your gene pool
I-10f
Summarize the findings of Pert & Snyder (1973)
These researchers were the first to propose the existence of endorphin receptors.
I-8c
Describe the process by which neurotransmitters are released
1. The action potential reaches the end of the axon.
2. At the axon terminal, the depolarization causes calcium gates to open.
3. The flooding of calcium into the axon terminal causes exocytosis, in which the
neurotransmitter is released from the axon terminal in bursts.
I-1b
Discuss the four biological explanations of birdsong
1. physiological explantation- the brain area that is linked to birdsong is larger in breeding
males than in females and grows under the influence of testosterone
2. ontogenetic-- young males learn songs from adult males; development of birdsong requires
both the genes that prepare that male to learn to sing and the opportunity to hear the song at a
sensitive period
3. evolutionary- Birds that have similar songs have evolved from a single ancestor
4. functional-- The function of birdsong is to attract females and to warn away other males.
9/11/07Caffeine- Antagonist for adenosine. It binds to adenosine receptors without activating them.
Normally, adenosine acts as an inhibitor for monoamines. When adenosine receptors ar
blocked, the result is an increase in the activity of serotonin, dopamine, epinephrine, and
norepinephrine.
Alcohol- Alcohol sensitizes glutamate receptors; it binds to them in a way that causes them to
respond more effectively to glutamate. This is true in moderate doses, and glutamate is an
excitatory neurotransmitter. So, in moderate doses, alcohol actually can stimulate receptors in
the cortex, hippocampus, and nucleus accumbens. But in larger doses, alcohol overwhelms the
glutamate receptors to the point that they become unresponsive. At the same time, alcohol in
large doses will activate GABA recerptors. GABA is an inhibitory neurotransmitter that inhibits,
among other things, glucose metabolism.
CH.4: Anatomy of the Nervous System
Anatomical terms for direction
Coronal (crown)- separates front and back
Sagittal (side)- separates left and right
Horizontal- separates top and bottom
Dorsal- back
Ventral-front
Posterior- back
Anterior- front
Medial- towards the middle
Ipsilateral- On the same side
Contralateral- On the opposite side
Components of the Nervous System
(See diagram)
The Brain
I. Hindbrain
A. Medulla-- Breathing, heart rate, salivation, coughing, vomiting, sneezing. It's the point of
connection for most of the cranial nerves (12 cranial nerves), which monitor sensations and
control muscle movements in the head.
B. Pons-- This is the point wehre motor neurons cross over. It contains the reticular formation
(reticulated = having grooves). The descending fibers of the reticular formation control motor
areas of the spinal cord and the ascending fibers are associated with arousal and attention.
C. Raphe system-- Associated with attention
D. Cerebellum-- Controls movement, coordination, timing, sensory attention.
II. Midbrain
A. Tectum
B. Superior colliculus/inferior colliculus-- Sensory information
C. Tegmentum/substantia nigra- Part of the brain's dopamine system. Dopaminergic neurons
originate ONLY in these two areas (i.e. these are the only places where cell bodies reside).
III. Forebrain
A. Limbic system
1. olfactory bulb-- sense of smell
2. hypothalamus-- basic drives (hunger, thirst, sexuality, sleep)
3. hippocampus- memory (Lynn Nadel)
4. amygdala- emotions (fear)
B. Basal ganglia
Caudate nucleus, putamen, globus pallidus, nucleus accumbens-- Memory, emotion,
movement, attention, reward/addiction
C. Nucleus basalis-- Arousal/wakefulness, attention, emotion
D. Thalamus-- Sensory relay
E. Cerebral cortex- 4 lobes (in each hemispheres)
Occipital cortex- Back of head; visual processing
Parietal cortex- Top of head; touch, somatosensory cortex (sensory nerves from the body),
spatial information, numerical information
Temporal Cortex- Sides of the head; auditory information, spoken language, some visual
information, including face recognition, memory, emotion, and motivation
Frontal Cortex- Front of head; primary motor cortex, planning, problem-solving, willpower,
attention
Methods of studying neuroanatomy
Types of brain scans:
1. CT scans-- X ray slices of the brain
2. MRI--nuclei of atoms in the brain react with magnetic fields; high spatial resolution images
3. PET- positron emission tomography, injection of a radioisotope that produces gamma
radiation, functional imagery (does not give good resolution of structures in the brain but it does
allow the researcher to look at functional changes occurring over time)
4. fMRI- looks at changes in the magnetic properties of hemoglobin when it's oxygenated and
deoxygenated, measuring changes in oxygen consumption; offers good spatial and temporal
resolution.
Research methods to study brain damage:
1. Lesions-- Damage a specific brain area (total removal = ablation)
2. Gene-knockout- Blocks a gene that produces certain neurotransmitters or receptors
3. Transcranial magnetic stimulation-- Can temporarily inactivate neurons in a region close to
the magnetic stimulation
Does size matter?
Brain size & intelligence
In humans, there is only a low to moderate correlation between IQ and brain size (.3).
Across species, brain-to-body ratios are predictive of intelligence.
9/4/07The Synapse
Research on Reflex ArcsReflex- automatic muscle response
Reflex arc- circuit that goes from the sensory neuron to the muscle, via an interneuron and a
motor neuron, bypassing the brain.
Three characteristics of reflex arcs that suggested the existence of synapses.
A synapse is a specialized gap between neurons where electrochemical signals are transmitted.
1. The rate of conduction of impulses in a reflex arc (15 m/s) is much slower than the rate of
conduction along an axon (40 m/s).
2. Impulses in a reflex arc do not follow the all-or-nothing law but are cumulative.
a) Temporal summation- Two stimuli occuring close to each other in time produce a greater
reflex response than either one by itself.
b) Spatial summation- Two stimuli occurring close to each other in space produce a greater
reflex response than either one by itself.
3. Reflex arc can excite certain muscles and inhibit other muscles.
Excitatory postsynaptic potential (EPSP)- The electrochemical signal transmitted from one
neuron (presynaptic neuron) across the synapse to a second neuron (postsynaptic neuron)
produces a depolarization of the membrane of the second neuron, just like an action potential.
In other words, the signal causes more activation of the postsynaptic neuron compared to
baseline.
Inhibitory postsynaptic potential (IPSP)- The electrochemical signal causes a hyperpolarization
of the postsynaptic neuron, causing it to be less activated than it would at baseline.
All neurons have a spontaneous firing rate. They are going to generate action potentials at a
certain rate regardless of any stimulation from other neurons. EPSPs cause the neuron to fire
at a faster rate compared to that baseline, and IPSPs cause the neuron to fire at a slower rate.
What happens at the synapse?
1. The presynaptic neuron produces neurotransmitters. Small molecules are produced in the
axon terminal (presynaptic terminal) and larger molecules (e.g., peptides) are produced in the
cell body.
2. The neuron transports larger molecules to the axon terminal. This transportation occurs in a
spherelike storage "container" called a vesicle.
3. Action potentials travel along the axon until they reach the terminal. There, they trigger the
release of the neurotransmitter into the synaptic cleft, which is the gap between the presynaptic
and postsynaptic neuron.
This release happens by a mechanism that involves calcium channels in the presynaptic
terminals. As the channels open and calcium binds to sites on the vesicle, the reaction causes
the membrane of the vesicle to open up so that the neurotransmitter is released.
4. The neurotransmitter travels across the synapse and attaches to receptor sites on the
postsynaptic neuron. In binding to the receptor, the neurotransmitter can have an excitatory or
inhbitory effect.
5. After the neurotransmitter reacts with the receptor, it gets released into the synapse.
6. Once the neurotransmitter is released by the postsynaptic receptor, it reenters the synaptic
cleft, where it can either be broken down by enzymes or recycled by the presynaptic neuron.
7. The postsynaptic neuron may release some type of neurotransmitter that signals to the
presynaptic neuron to slow down or stop the production of further neurotransmitter.
Types of neurotransmitters
Amino acids-- buildings blocks of proteins; they contain an amine (-NH2) and a carboxylic acid
(-COOH); examples include glutamate, GABA.
Modified amino acids- Acetylcholine; the Hydrogens on the amine are replaced by methyl
groups (CH3).
Monoamines- Molecules that contain a single amine group.
a) Catecholamines- dopamine, epinephrine, norepinephrine
b) Indoleamines-serotonin
Peptides- Chains of amino acids; endorphins, substance P
Purines- Building blocks for DNA; ATP, adenosine
Gases- Nitric oxide (NO)
How does a neurotransmitter exert its effect on the postsynaptic neuron?
1. Ionotropic effect-- The binding of the neurotransmitter to the receptor causes ion channels
(e.g., sodium, chloride, calcium) to open in the membrane of the postsynaptic neuron.
Simple, fast, and short-lasting mechanism. Excitatory ionotropic effects (e.g., glutamate) or
inhibitory ionotropic effects (e.g, GABA).
2. Metabotropic effect-- The binding of the neurotransmitter to the receptor sets off a chain
reaction that involves a "second messenger," which is another neurotransmitter that gets
released by the postsynaptic neuron and that delivers the signal to other parts of the same
neuron.
This is a slower, longer-lasting mechanism.
Hormones vs Neurotransmitters-- The same molecules can serve as both, but hormones are
more widely broadcast throughout the body, whereas neurotransmitter tend to localized
specifically within certain structures in the nervous system.
The hypothalamus and the pituitary gland are important and closely linked structures in the
brain that play a central role in the production and release of hormones in the body.
The pituitary can be divided into two parts:
1. The anterior pituitary secretes hormones that trigger the release of other hormones in the
body:
ACTH-activates the adrenals
TSH- activates the thyroid
FSH and LH- activate the gonads (gonadotropins)
GH - growth hormone
prolactine- activates the mammary glands
2. The posterior pituitary gland is closely linked to the hypothalamus, where two important
hormones are produced: oxytocin (regulates sexual and parenting behaviors), and vasopressin
(regulates water balance in the body). The posterior pituitary delivers these hormones into the
bloodstream.
Process #6 that takes place synapse is really two processes: Inactivation of the
neurotransmitter and Reuptake.
Inactivation is the breakdown of the neurotransmitter by enzymes
Monoamine oxidase (MAO) breaks down monoamines such as dopamine and serotonin.
Reuptake involves transporter proteins in the presynaptic terminal that bind to the
neurotransmitters and bring them back into the terminal.
Dopamine transporters (DAT) - proteins that specifically bind to dopamine and are involved in
the reuptake
Drugs and the Synapse
The body seeks homeostasis. Anything that causes an imbalance in a neurotransmitter system
results in some set of counterbalancing processes.
StimulantsAmphetamines cause increases in the release of dopamine, whereas cocaine blocks the
reuptake of dopamine by the presynaptic neuron.
Methylphenidate (Ritalin) acts in a manner similar to cocaine, by blocking the reuptake of
dopamine. Why isn't it more addictive? The answer has to do with the method of ingestion.
Taking Ritalin in oral form produces a slow release of the drug into one's system, and the drug
stays in the system longer.
OpiatesDerivatives of poppy. Opium, heroin, and methadone. Of the three, heroin is most addictive
because of its speed of action.
Opiates bind to a receptor in the brain for endorphins (endogenous morphine). So, opiates are
mimicking a naturally occurring neurotransmitter and binding to a receptor site that is specific to
that neurotransmitter, i.e. endorphins.
Psychoactive drugs mimic some type of neurotransmitter in the body.
Cocaine mimics dopamine.
Psychedelic drugs (LSD, psilocybin) mimic serotonin.
Opiates mimic endorphins.
Marijuana mimics endogenous cannabinoids such as anandamide.
The drug can act as an agonist that either causes an increase in production of the
neurotransmitter or that mimics the neurotransmitter at either a receptor site or a transporter
site, or the drug can act as an antagonist, interfering with a neurotransmitter.
Nicotine- Acts on receptors in the nucleus accumbens that release dopamine. They actually
have receptor called "nicotinic receptors" that are really acetylcholine receptors. Acetylcholine
is an excitatory neurotransmitter. When acetylcholine or nicotine bind to the nicotinic receptors,
they excite the dopamine receptors in the brain, causing more dopamine to be released in the
nucleus accumbens.
Marijuana mimics endogenous cannabinoids and binds to cannabinoid receptors in the
hippocampus, cerebellum, basal ganglia, and cerebral cortex.
Hallucinogenic drugs like psilocybin and LSD mimic serotonin, which is involved in mood
regulation but also in perceptual processes.
Drugs have an affinity and efficacy. Affinity has to do with how easily it binds to a receptor and
efficacy has to do with how tightly it binds or how long it stays bound to the receptor.
8/28/07Announcements:
1. Lecture notes are posted online: http://vas.web.arizona.edu, click on "Psyc 302 Notes."
2. Book release party, Thurs, Sept 20, 4:30pm, UA Bookstore
Basic cell structures:
membrane- separates the inside of the cell from its surroundings
nucleus- contains the chromosomes
mitochondria-- metabolic activities
ribosomes- protein synthesis (ribosomes tend to be found on the endoplasmic reticulum, which
is a set of tubes that transport proteins throughout the cell)
Basic neuronal structuresDendrites- receive electrochemical signals
Cell body- contains the nucleus, mitochondria, ribosomes
Axon- neuron only has one; sends electrochemical signals
Parts of the axon
1. myelin sheath-- electrical insulation layer on the axons that improves the speed and efficiency
of electrical conduction.
(Lorenzo's Oil)
2. nodes of Ranvier (nodes)-- gaps in the myelin that exist to allow "saltatory conduction."
3. presynaptic terminal-- the tip of the axon where chemical messengers, called
neurotransmitters, are released into the synapse or gap between cells.
Glial cells-- Unlike neurons, glial cells can regenerate. They do the "dirty work" of the nervous
system, providing structural support, removing waste, and facilitating certain processes.
Types of glial cells
1. astrocytes-- involved in the reuptake and re-release of neurotransmitters (help recycle
neurotransmitters); also remove waste materials produced by dead neurons, and they help
control the amount of blood flow to certain brain areas.
2. microglia- remove waste materials, viruses, fungi, and other microbes, acting as a quasiimmune system for the brain.
3. oligodendrocytes-- important in building the myelin sheath in the brain and spinal cord (i.e.,
central nervous system)
4. Schwann cells- build myelin sheath in the peripheral nervous system
5. Radial glia- type of astrocyte that guide the migration of neurons and the growth of their
axons and dendrites during embryonic development.
Blood-brain barrier-- The walls of capillaries in the brain that are made up of endothelial cells
that arranged so tightly that they leave virtually no gap for chemical substances to get through.
This keeps toxins out of the brain.
Some substances need to get through. How does that happen?
1. Passive transport-- Small molecules like oxygen and carbon dioxide can get through the
gaps in the blood-brain barrier. There are also specialized channels in the membrane that will
draw in certain molecules such as certain vitamins like A and D that are fat soluble.
2. Active transport- Proteins in the membrane that expend energy to pump substances from
the blood into the brain, such as glucose, amino acids, other vitamins, and hormones.
Types of neurons:
1. motor, sensory and interneurons
motor neuron-connects to a muscle or gland; if it connects to a muscle, it controls muscle
contraction
sensory neuron- part of a sense organ that receives some type of stimulation, such as
electromagnetic energy in the eye or mechanical vibration in the ear, and converts it into a
nerve impulse.
interneurons-- neurons that are only connected to other neurons; they are contained within a
specific structure such as the cortex of the brain.
2. efferent vs. afferent
efferent- carries a signal away from a structure
afferent- carries a signal to the structure
NERVE IMPULSES
Resting potential-- When the neuron is at rest, it has a potential of -70 mV.
Forces involved in resting potential:
1. Selective permeability-- You need a membrane that keeps certain substances out of the
neuron. There are sodium channels in the membrane of a neuron that are closed at rest.
Those sodium channels are voltage activated; at -70mV, they remain closed. As the voltage
approaches zero (depolarization), the channels open.
2. Electrical gradient-- Difference in charge across the membrane will attract positive charge to
the source of negative charge. Having a negative potential in the cell causes sodium ions to be
attracted inward.
3. Concentration gradient-- A difference in concentration will draw sodium ions (or anything
else for that matter) from an area of higher concentration to an area of lower concentration.
Sodium ions are 10 times more concentrates outside the neuron than inside it at rest.
Potassium ions, on the other hand, are slightly more concentrated inside the neuron.
4. Sodium-potassium pump- Pump is a set of proteins embedded in the membrane that can
pump in sodium and pump out potassium. This is an active transport process that takes energy.
ACTION POTENTIAL
1. Slight depolarization of the cell-- The voltage increase, moving towards zero. Positive ions,
primarily sodium, move along the inside of the membrane towards a particular spot. That
makes the spot more positive, or less negative.
2. When the voltage reaches a certain threshold, the sodium channels open because they are
voltage activated.
3. This causes sodium ions to rush into the cell until potential rises to +30mV.
4. Potassium ions are going to flow out, drawn out of the neuron by concentration and electrical
gradients.
5. The sodium-potassium pump takes out the excess sodium and brings in additional
potassium to restore the initial balance. At rest, the concentration of sodium is much higher
outside the cell, the concentration of potassium is slightly higher inside the cell, and the inside is
slightly negative compared to the outside.
local anesthetics-- Block the sodium channels and keep action potentials from happening.
Refractory period- Time period in which the neuron resists the production of further action
potential. Regardless of the stimulation, no action potential can occur at this time.
Propagation of the Action PotentialSodium ions that enter the cell during an action potential migrate along the inside of the
membrane, causing depolarization of adjacent areas.
Inside of an axon, the action potential moves from node to node through the process of saltatory
conduction. The potential zips along the stretches that are insulated by myelin until the positive
ions reach the next node, where there are sodium channels that can open.
Local neurons that have very short axons don't need to generate an action potential; instead,
they have what is called a graded potential.
Action potentials operate by the all-or-nothing principle. You need a strong enough
depolarization to open the sodium channels. Otherwise, nothing happens.
8/21/07CH.1: Major Issues in Biopsychology
I. Causal Relationships: Explaining why certain behaviors happen from a biopsychological
standpoint.
There are at least four types of explanations in biopsychology:
1. Physiological- Relates a behavior to activity in the brain or other organs
Music perception example: Physiological approach would look at the brain areas that are
associated with music perception.
2. Ontogenetic- Describes the development of a structure or behavior.
Music perception example: Music perception first appears at ages 4-6 months.
3. Evolutionary perspective- Reconstructs the evolutionary history of a structure or function.
Music perception example: Comparative study of music perception in primates and humans.
4. Functional explanation- Answering the question of why a structure or behavior evolved as it
did.
Music perception example: Why does music perception exist? What adaptive benefits are
there in being able to perceive and appreciate and play music?
II. Mind-Body Problem
Biopsychologists have to decide how they view the relationship between physiological and
psychological processes.
Three philosophical positions:
a) Materialism- Everything that exists is ultimately material or physical in nature. Even if
psychological processes have an independent existence as a unique entity, they are
hypothesized to be caused by physiological processes.
Monism- There is only one kind of "stuff" in the universe; In the West, most monists are
materialists.
b) Mentalism- Everything that exists is ultimately mental. Even physical events that surround us
are filtered through our own consciousness.
(Recommended reading: Mindscience, interviews with the Dalai Lama about neuroscience)
c) Identity position (double-aspect theory)- Mental and physical "stuff" are just two aspects of
the same thing.
The position that is considered untenable by just about everyone is strict dualism. Descartes
said that mental and physical processes occur at distinct levels of reality that do not interact
except at one point in the universe: the pineal gland.
solipsism-- the assumption that I alone exist or I alone am conscious
III. Heredity and environment
Two main ways to study heredity:
a) twin studies--we compare identical and fraternal twins, and also twins and non-twin siblings
b) adoption studies - compare the traits of adopted children with their adoptive and biological
parents
How do genetics affect behavior?
a) Directly--Our genetic makeup predisposes us to behave in certain ways (e.g., criminal
behavior, IQ, mental illness)
b) Indirectly-- Our genetic makeup causes us to shape our environment in ways that affect our
behavior, at least by magnifying certain tendencies.
Why is it difficult to sort out heredity and environmental influences (e.g. prenatal influences)-We don't know if children's behavior is due to their genetic makeup or the environment in which
they were conceived and raised (which is also, indirectly, related to their genetic makeup).
Phenyketonuria (PKU)--Genetic inability to metabolize phenylalanine, an amino acid. This
amino acid builds up in the body and can poison a child, impairing development, leaving a child
mentally retarded and irritable. Environmental conditions can have a moderating effect on this
disorder. If PKU is detected early enough, the child can be put on a special, low-phenylalanine
diet that will minimize brain damage. This diet avoids meat, eggs, certain grains, aspartame
(NutriSweet) and dairy.
Diathesis-stress model of mental illness- A diathesis is a predisposition towards certain mental
health issues such as depression. But it is usually an environmental stressor that leads to the
display of symptoms.
IV. Evolution
Four misconceptions about evolution:
1. The use of disuse of some structure or behavior causes an evolutionary increase or
decrease in that feature.
Lamarck--assumed incorrectly that acquired characteristics could be inherited.
2. Humans have stopped evolving.
3. Evolution means improvement: All it REALLY means is improved fitness, which has to do
with procreation and the development of the next generation.
4. Evolution acts to benefit the individual or the species. Neither of these is true: Evolution
benefits the genes.
Darwin's theory of natural selection was influenced by the economic theories of his era, which
were based on the strength of competition. And so his theory emphasizes competition over
cooperation.
How does evolutionary theory account for altruistic behavior?
a) reciprocal altruism--animals help those who them in return
b) kin selection-- animals act in ways that benefit their relatives, even if those relatives are not
necessarily progeny.