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Amygdala
Enhances the startle reflex; responds to fear; controls autonomic fear responses; damage reduces fear recognition and prevents PTSD.
Bed nucleus of the stria terminalis
Controls long-term, generalized emotional arousal (long-lasting anxiety).
Prefrontal cortex
Involved in learned behavior, decision-making, and regulating stress responses.
Panic disorder neurotransmitters
Linked to decreased GABA and increased orexin.
Benzodiazepines
Anti-anxiety drugs that bind to GABAA receptors and increase the effects of GABA.
Behavioral Activation System (BAS)
Left hemisphere activity; approach behaviors; linked with happiness and anger.
Behavioral Inhibition System (BIS)
Right hemisphere activity; increases attention/arousal; inhibits actions; linked with fear and disgust.
General Adaptation Syndrome
The three-stage stress response: Alarm → Resistance → Exhaustion.
Alarm stage
Sympathetic nervous system activation; release of epinephrine and cortisol.
Resistance stage
Sympathetic response declines; adrenal cortex releases cortisol to prolong alertness.
Exhaustion stage
Energy resources depleted; weakened immunity.
HPA axis
Stress response route: Hypothalamus → Pituitary (ACTH) → Adrenal cortex (cortisol).
Cortisol
Stress hormone that mobilizes energy.
Chronic stress effects
Weakens immune system and damages the hippocampus.
Classical conditioning
Learning by pairing two stimuli so one predicts the other.
Conditioned stimulus (CS)
Stimulus that produces a response only after pairing with the US.
Unconditioned stimulus (US)
Stimulus that automatically triggers a response.
Conditioned response (CR)
Learned response to the conditioned stimulus.
Amygdala and fear conditioning
Receives sensory input and creates learned fear associations.
Operant conditioning
Behavior followed by reinforcement or punishment.
Reinforcement
Increases likelihood of a behavior.
Punishment
Decreases likelihood of a behavior.
Declarative memory
Explicit memory for facts and events.
Procedural memory
Memory for skills and habits (implicit).
Hippocampus
Critical for forming new declarative memories and spatial memory.
Basal ganglia
Involved in habit learning and gradual, probabilistic learning.
H.M. amnesia type
Severe anterograde amnesia (cannot form new long-term memories).
H.M. abilities intact
Working memory and procedural memory.
Korsakoff's syndrome
Memory disorder caused by thiamine (B1) deficiency; common in alcoholism.
Confabulation
Filling memory gaps with guesses.
Stress and memory
Emotional memories consolidate quickly; chronic stress harms the hippocampus.
LTP (Long-Term Potentiation)
Strengthening of synapses after repeated stimulation.
LTP specificity
Only active synapses are strengthened.
LTP cooperativity
Multiple simultaneous inputs produce stronger LTP.
LTP associativity
Weak input strengthened when paired with strong input.
AMPA receptor
Activated by glutamate and causes depolarization.
NMDA receptor
Opens after magnesium is displaced; allows calcium to enter.
Calcium in LTP
Triggers synaptic strengthening such as added AMPA receptors and dendritic growth.
Sensitization
Increased response to a mild stimulus after exposure to a strong one.
Aplysia
Animal model used to study sensitization.
Serotonin in sensitization
Blocks potassium channels → prolongs transmitter release.
Nucleus accumbens
Central brain region for reward and reinforcement.
Dopamine and addiction
Nearly all addictive drugs increase dopamine in the nucleus accumbens.
Tolerance
Decreased effect of a drug over time.
Withdrawal
Body's reaction when a drug is absent.
Agonist
Drug that mimics or increases neurotransmitter activity.
Antagonist
Drug that blocks neurotransmitter activity.
Major depression key symptom
Absence of happiness.
Bipolar disorder
Alternating episodes of depression and mania/hypomania.
Positive symptoms of schizophrenia
Hallucinations and delusions.
Negative symptoms of schizophrenia
Weak emotion, speech, and socialization.
Panic disorder cause
Low GABA and high orexin.
PTSD symptoms
Distressing recollections, nightmares, strong reactions to stimuli.
Dopamine hypothesis
Excess dopamine (especially D2) causes schizophrenia.
Glutamate hypothesis
Low glutamate activity contributes to schizophrenia.
BDNF
Low levels linked to depression and reduced hippocampal function.
Tricyclic antidepressants
Block reuptake of serotonin, dopamine, and norepinephrine.
SSRIs
Block reuptake of serotonin only.
Antipsychotics (typical)
Block dopamine D2 receptors; treat positive symptoms of schizophrenia.
Atypical antipsychotics
Block serotonin 5-HT2 receptors more than dopamine.
MAOIs
Prevent breakdown of monoamines (dopamine, norepinephrine, serotonin).