emotional memory and amygdala circuitry

James-Lange Theory

Emotions are our brain’s interpretation of physiological changes in the body

Cannon-Bard Theory

Emotional experiences and physiological responses occur independently

schacter-singer theory (two-factor)

our experience of our own emotions depends on physiological arousal and cognitive interpretation

cognitive interpretation

the environment and other people inform our interpretation of the emotions we are feeling

physiological arousal

the body’s immediate response to a stimulus

results of twoo-factor theory of emotion experiment

participants in the adrenaline groups behaved more emotionally than the placebo, but the interpretation influenced how participants felt and acted; people informed about the adrenaline showed reduced emotional responses compared to the uninformed 

(physiological arousal + environmental cues = emotional/behavioral response)

amygdala

our internal threat detector that triggers fight or flight response. activates to real dangers and the thought of memory or danger

subregions of the amygdala

lateral amygdala, basolateral amygdala, central nucleus of the amygdala

lateral amygdala (LA)

receives sensory input from the thalamus

Basolateral amygdala (BLA)

integrates information from LA and hippocampus

Central nucleus of the amygdala (CeA)

receives info from BLA and sends signals to other brain areas to initiate a behavioral response

Kluver-Bucy Syndrome

a rare condition caused by damage to the medial temporal lobe that can result in compulsive eating, hyperoality/putting things in mouth, hypersexuality, visual agnosia, and docility

amygdala damage in non-human primates

rhesus monkeys results in decreased fear and aggression

amygdala damage in humans

results in a blunting or dampening of emotions

Patient S.M.

partial amygdala damage that resulted in difficulty characterizing the emotion of fear, inability to appreciate emotional expression, and impaired pain response

Urbach-Wiethe disease

an autosomal recessive condition impacting chromosome 1 that result in skin lesions and scars, hoarse voice, speech difficulty, and, in S.M., a calcification in the MTL including the amygdala

Patient H.M.

had parts of the amygdala removed, which results in a very high pain tolerance and difficulty recognizing physiological cues like hunger and fatigue.

Alex Honnold

a famous “free solo” climber who trained regions of his prefrontal cortex to inhibit fear responses initiated by the amygdala through mental visualization

Post-traumatic stress disorder (PTSD)

develops after a person has experienced, witnessed, or repeatedly been exposed to a traumatic event

brain areas involved in PTSD

amygdala, prefrontal cortex, and hippocampus

amygdala is activated by traumatic events and turns off after the event ceases

PFC mediates the extinction of conditioned fear; symptions may occur when PFC is not inhibiting conditioned fear responses

the hippocampus encodes memory of cues and emotion

systemic desensitization

widely used behavioral therapy for phobias where one creates a hierarchy of feared things, learns relaxation techniques, and practices techniques with increasingly intense fears

exposure therapy

gradually becomes exposed to the feared situation or object over time, which increases the feeling of control

results of exposure therapy

exposure therapy increased connectivity between the prefrontal cortex and the basolateral amygdala and hippocampus in people with PTSD

main types of anxiety disorders

panic disorder, agoraphobia, social anxiety, specific phobias, generalized anxiety disorder

fear

has an obvious cause and subsides when the cause is gone, an emotional response to current dangers; the amygdala (CeA) initiates a response to sudden aversive events or threats

anxiety

general feeling of dread or apprehension that has less clear causes than fear and can be more pervasive and long-lasting; Bed Nucleus of the Stria terminalis (BNST) integrates input from amygdala and hippocampus

GABA

The major inhibitory neurotransmitter in the brain that most successful medications for anxiety increase or mimic; as increasing activity may suppress over-reactive brain regions

hippocampus and emotion

stores and remembers information, helps us navigate and recognize places, does not function as well when the threat system is active

Hypothalamic pituitary adrenal axis (HPA axis)

consists of three endocrine glands that mediate our response to stress and cause the release of cortisol, a key stress hormone. intense/ongoing stress can cause it to malfunction and can lead to mental health problems

neurobiology of stress and impacts on memory

1. amygdala detects a threat and activates the paraventricular nucleus of the hypothalamus

2. the hypothalamus releases corticotropic releasing factor (CRF) to the pituitary gland

3. the pituitary gland releases adrenocorticotropic releasing hormone (ACTH) to the adrenal gland

4. the adrenal gland releases glucocorticoids (cortisol)

glucocorticoids

feed back on the hippocampus and can reduce brain-derived neurotrophic factor (BDNF) in high doses; further activate the amygdala and enhance HPA activity