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Frontal lobes
o Responsible for executive and higher order functioning (e.g. decision making,
moral reasoning, complex problem solving)
o ‘Executive brain’ that makes possible conscious thought, planning, memory,
deliberate action, directed attention, and abstract reasoning
o Orbitofrontal cortex = thinking part of emotional brain. Plays a key role in affect
regulation, which has been seen as both the purpose for, and the outcome of,
relationships with secure attachment.
 Modulates the amygdala’s rapid responses and contextualizes the threat
and determines its degree
 OFC damage or deficit is associated with difficulty in managing one’s
emotions, gauging one’s impact on others, and responding appropriately to
their social signals and states of mind
Amygdala
o Central to processing emotional stimuli and memories (Mendez & Shapira, 2011)
and assessment of threatening information
o Involved in the enhancement of long-term memory of emotionally arousing
events, unconscious emotional fearful learning and emotional processing of
fearful targets (Sartorius et al., 2008)
o Primary part of the brain responsible for fight or flight
 Anxiety and panic occur when amygdala senses environmental stressors
that stimulate fight or flight response
 Amygdala may be responsible for emotional reactions of PTSD
 People with Bipolar Disorder show greater amygdala activity
Hippocampus
o Critical in the formation, organization, and storage of new memories, and
connects these memories to emotions
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Part of the parasympathetic nervous system -- enables us to settle down
Memories that register with the help of the hippocampus are explicit,
linguistically retrievable, and contextualized according to time, place, and person
Acute relational trauma can shut down the hippocampus temporarily or inhibit its
development → unmodulated reactivity of the over vigilant amygdala (Wallin,
2007)
Neurotransmitters:
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Dopamine
o Feel good, love, reward-motivated behavior, helps regulate emotional responses
o Associated disorders:
 Low → Parkinsons, ADHD, Depression
 High → Schizophrenia
o Excitatory & Inhibitory
o Movement & flow of information to front of brain; Mediate desire and motivation
o Linked to reward systems
 Rewards tend to increase Dopamine (eg. social media likes)
 Impacts anticipation & drive
o Schizophrenia <> High Dopamine
 Anti-psychotics block Dopamine
 Drugs that release dopamine cause Schizophrenia
o ADHD <> Low Dopamine
o Linked to substance abuse
Serotonin
o Well-being and happiness
o Associated with mood disorders
o Inhibitory
o Feel good
o Physiological processes: Mood, appetite, sleep, and pain
o Depression <> Low Serotonin
o OCD
Epinephrine (Adrenaline)
o Vigilant alertness, increased heart rate, underlines the fight or flight response
o Mostly excitatory (during times of stress)
o Raises blood pressure
o May trigger anxiety
GABA
o Regulates communication btwn brain cells
o Inhibits activity of neurons
o Helps control fear and anxiety
o Associated Disorders
 Low → Anxiety
o Inhibitory (primary one)
o Benzodiazepine system – bind to same receptors as GABA
o Reduces anxiety
Oxytocin
o The love hormone
o Produced during hugging, orgasm, child-birth
o Influences social behavior and emotion – reduces stress and anxiety
o Can be helpful for anxiety, depression (esp. postpartum), autism
Homeostasis: body responds to environment in way that makes internal workings of body stable.
Maintain right pH, temperature…
Threats of dangers = stressors
HPA axis
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Control’s body’s response to stress
Amygdala senses threat and activates HPA axis
Hypothalamus synthesizes CRH which stimulates the pituitary gland to secrete ACTH
ACTH stimulates adrenal glands to produce cortisol (stress hormone) and epinephrine
(adrenaline) – primes body for instant action
Fight or Flight Response
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Sympathetic Nervous System – get out of danger mode – adrenaline causes physiological
changes
o Increased heart rate
o Increased respiratory rate (breathing faster to get more oxygen in blood and expel
more Co2)
o Increased peripheral vasoconstriction (arms and legs tighten to push more blood
to core area)
o Digestion, immune function, ovulation shut down (butterflies)
After the Threat
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Negative feedback loop: The hypothalamus recognizes higher level of cortisol and sends
messages to suppress CRH and ACTH production
Parasympathetic Nervous System activates the “rest and digest” response and returns the
body to homeostasis after the flight-or-fight response by activating the release of the
neurotransmitter acetylcholine
o Vasodilation (opening of blood vessels), decreases heart rate, increases digestion
Chronic Stress
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Repeated exposure causes individual to habituate with repeated HPA axis activation and
decreases ability to regulate HPA axis activation
HPA becomes too responsive and doesn’t turn off
Continuously increases the cortisol secretion which desensitizes the glucocorticoid
receptors in hypothalamus (negative feedback loop) resulting in hyperactivity of the HPA
axis (Jeon & Kim, 2018).
o increases activity level and number of neural connections in amygdala
o In excess cause atrophy of the hippocampus (learning, memory, stress control),
resulting in impaired memory, decrease in ability to learn, and impaired ability to
respond appropriately to stress.
Brain shrinks in size (loss in synaptic connections between neurons)
Frontal cortex (concentration, judgment, decision making) shrinks
Early Life Stress/Trauma
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Exposure to mild or moderate stressors early in life has been shown to enhance HPA
regulation and promote a lifelong resilience to stress versus early-life exposure to
extreme or prolonged stress can induce a hyper-reactive HPA Axis and may contribute to
lifelong vulnerability to stress
Nurturing mother gives to baby determines how well baby deals with stress – neglect
leads baby to develop more cortisol receptors (dampens stress response) and become
more sensitive to stress (DeBellis 2001).
o More cortisol = hyperactive HPA axis, increased activity of amygdala, atrophy of
hippocampus (decrease in memory, learning, stress control)
If HPA Axis is impacted early in life (e.g. childhood trauma or maltreatment), a lot of
cortisol is released over a long period of time, damaging the circuit and making you less
sensitive, the system (negative feedback loop) no longer works as an effective signaling
device because its desentized (e.g. no longer can identify cues for danger in
environment).
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Exposure to trauma → cascade of biological changes and stress responses, which are
associated w/PTSD, mental illnesses, and substance use disorders. This in turn increases
a person's vulnerability to encountering subsequent traumas/violence as an adult.
Transgenerational trauma can also occur, with traumatic experiences as well as resilience
patterns being developed and inherited from subsequent generations (e.g. children of
Holocaust survivors, Braga 2012).
Trauma (Rasmussen and Bliss)
 Overactive limbic system and hypoactive frontal lobe interferes cognitive processing, lead to
trauma reenactment;
 Activated SNS (activated by amygdala; increase energy output to respond to threat)
responsible for fight-or-flight response, lead to hypervigilance; PNS (regulate stress by
inhibiting SNS) related to freeze response, lead to dissociation;
 Elevated cortisol and norepinephrine interferes hippocampus functioning, inhibiting
cognitive evaluation and memory storage, lead to blanking in memory;
 HPA axis: Hypothalamus release CRH, stimulates pituitary gland release ACTH, then
adrenal gland releases cortisol, sensitizing the nervous system to threats; CRH stimulates the
release of beta-endorphin, which reduces physical and emotional pain related to trauma and
leads to avoidance and numbing; increase cortisol level relates to improved emotionally
relevant memories, contribute to overgeneralization of negative experience to situations that
others might judge as nonthreatening.
 Interfered hemispheric integration. Left: conscious logic, linearity and language; Right:
process unconscious social and emotional information. So, either raw emotion without
cognitive mediation or raw logic without the benefit of emotional awareness.
 Holsboer & Ising (2010)
o Real or perceived stress, both psychological and psychosocial, are associated with
structural changes of the prefrontal cortex, amygdala, septum, hypothalamus, and the
hippocampus, a region of the brain that is sensitive to stress
o Structural changes
o HPA Axis:
 The biological stress response is generally adaptive but researchers have
hypothesized that in PTSD it becomes maladaptive and leads to long-term
negative consequences
 Chronicity of stress leads to changes in HPA Axis
o Hippocampus:
 PTSD is linked with decreased volume in the hippocampus (learning,
memory, stress response)
o Studies
o (Carter, 2009): The external cause of PTSD is the experience of trauma. In the
brain itself, various abnormalities in areas involved in memory, the stress
response and the processing of emotions have been identified. The amygdala
(involved in memory and emotion processing) is overactivated (it is hyperresponsive and has a smaller volume among PTSD patients) in response to
memories of traumatic events whereas the PFC is under-responsive to fearful
stimuli, which may result in its failure to inhibit the amygdala and thereby inhibit
traumatic memories.
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Impact of trauma on the brain:
o Increased secretion of cortisol
Decreased size of hippocampus (negative impact on memory)
o Increased amygdala function
o Decreased medial prefrontal cortex function (learning, judgement)
o Increase in epinephrine
o Name neurotransmitters that can be dysregulated by trauma, and give examples.
o Increased dopamine (modulated HPA axis responses),
o increased norepinephrine (hyperarousal, heightened startle response,
increased encoding of fear memories),
o decreased serotonin (hypervigilance, heightened startle response,
impulsivity), increased glutamate (derealization and dissociation).
o If the stressor doesn’t go away, high levels of cortisol can be problematic
o Alterations in the way you perceive the world and express emotions
o Suppress reproductive functioning (menstrual cycle stops, infertility)
o Suppress growth hormone release
o Increases insulin resistance → weight gain
o Inhibits bone remodeling → puts them at risk for osteoporosis
Effects of Stress
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Most Glucocorticoid receptors in hippocampus (learning, memory) and frontal cortex
(impulse control, judgment, planning, reasoning)
o Atrophy (Death) in neurons of these areas – leads to emotional and behavioral
responses
o Depression – anterior cingulate stops making and responding to serotonin
(perceive more stressors)
o Anger – fight part of fight or flight – can lead to vascular disease (heart attack)
o Anxiety – amygdala (fear center) flight part of fight or flight – perceive more
things as fearful which increases anxiety
o Addiction – drugs as coping mechanism. Impairment of frontal cortex (impaired
reasoning and judgment) increases likelihood of being consumed by inappropriate
coping mechanisms
Coping with Stress
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Perceived control - lack of control is perceived threat – low SES, minority population
Optimism – humor
Social support – not alone in feelings, better eating, exercise, sleeping patterns
Exercise – decrease chance of cardiovascular disease, increase blood to brain heart and
body, increase neurogenesis (growth of new neurons), planning for daily exercise,
increase size of hippocampus
Meditation – lower heart rate and blood pressure, increase size of hippocampus
Faith – (really more social support)
Cognitive Flexibility – know what you can change and what you can’t a.k.a therapy.
Mirror Neurons System
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Lacoboni et al. Mirror neurons echoes not only actions but also intentions; may play a
significant role in our ability to infer another's state of mind based on their actions or
description of events.
Corradini and Antonietti (2013) noted that areas of the brain that are normally activated
by one’s own emotion are also activated when one looks at the others feeling the same
emotion or sensation, supporting the role of the mirror neuron in cognitively understood
empathy.
Wallin (2007) neural substrate for empathy, affect attunement, mentalizing and
intersubjectivity
Studies of mirror neurons: (Monkeys -- Rizolatti, 1996)(Humans -- Lacaboni, 2005).
OFC damage or deficit is associated with difficulty in managing one’s emotions, gauging
one’s impact on others, and responding appropriately to their social signals and states of
mind
Prolonged childhood stress can also led to deficits in oxytocin and GABA
o Oxytocin is considered the “love hormone” because it allows individuals
to trust others and form securely attached relationships (De Boer, et al
2012)
o GABA is a NT that inhibits excitation and anxiety
 The stress Ms. X experienced may have altered her body’s ability to produce an
adequate amount of oxytocin given that she did not receive enough love from her
caregivers.
o Deficiencies in oxytocin may account for inability to trust others or form
securely attached relationships
 Further, Ms. X may also have deficiencies in GABA
o Those with anxiety disorders tend to have deficiencies in GABA, making
it difficult to calm down.
o Because she constantly needed to be alert in the environment she lived
growing up, her brain may have altered and decreased its production of
GABA
 Depressant medications such as Xanax and Klonopin are GABA agonists,
meaning that they work to increase the amount of GABA in the brain
  There is evidence that Ms. X experiences GABA deficits given that she is
treating her symptoms with other depressants such as alcohol and uses them to
relax
What biological systems are implicated in regulating social relations
Childhood exposure to severe stress, especially if chronic, can alter individuals’ brain and neurochemical
development as well as individuals’ future responses to stressful situations. What are the most likely
biological mechanisms (systems/ anatomy/interactions) by which these long-term effects are mediated?
What biological changes could we expect to see as a result of his experiences of trauma and stress
reactivity, and how would these physiological markers be expressed through his behavior in his
relationships in and out of the consultation room?
1) Describe the biological aspects of high levels of stress, how the effect varies when
stresses are repeated chronically, and the long-term effects on both brain and behavior,
including the future ability to identify and manage stressful environments.