PSY 210 Final Exam (Matthew)

Learning

acquiring new information or skills

Memory

storing and retrieving that information later.

Classical conditioning

stimulus-stimulus learning (what predicts what).

Operant conditioning

behavior-consequence learning (what happens when I do this).

Flow of info through memory

Sensory memory, short-term/working memory, long-term memory (via encoding).

Short-term memory

brief storage of information.

Working memory

short-term storage plus manipulation of info.

Working memory capacity

5-9 items, varies with attention

Chunking

grouping items to increase memory capacity

Primacy effect

better memory for items at the start of a sequence

Recency effect

better memory for items at the end of sequences

Types of long-term memory

declarative, non-declarative

Declarative memory

facts/events (semantic vs episodic).

Non-declarative memory

skills, habits, conditioning, priming.

Hippocampus (role in memory)

Critical for forming new declarative and spatial memories.

HM showed that . . .

Hippocampus is needed for new episodic and semantic memories, and spatial memory; not required for old memories or procedural skills.

Trisynaptic circuit

The three-step excitatory pathway inside the hippocampus that supports memory formation

Trisynaptic circuit (steps in order)

DG, CA3, CA1

Hippocampus' role in spatial memory

Place cells in the hippocampus map memories of physical spaces.

Engram

The physical/biological trace of a memory in the brain.

PFC role in memory

Supports working memory, planning, and retrieval strategies.

Striatum role in memory

Procedural/habit learning and habit formation.

Amygdala (role)

fear

Anterior cingulate cortex

part of medial frontal cortex responsible for attention, error monitoring, emotion regulation in memory.

Hebbian synapse

"Cells that fire together wire together"—synapse strengthened by repeated co-activation.

Long-term potentiation (LTP)

Long-lasting strengthening of synapses following high stimulation.

Steps of LTP + key mechanisms

Glutamate binds AMPA/NMDA, NMDA opens after depolarization, Ca²⁺ influx, Ca²⁺ activates kinases, more AMPA receptors inserted.

Post-synaptic effect of LTP

more AMPA receptors, larger spine.

Pre-synaptic effect of LTP

increased glutamate release probability.

Korsakoff's syndrome

Severe anterograde/retrograde amnesia from thiamine deficiency (often alcoholism); damage to thalamus & mammillary bodies.

Alzheimer's disease

Progressive memory loss; associated with β-amyloid plaques, tau tangles, cell death, especially in hippocampus.

Role of ANS in emotion

changes (HR, BP, sweating) accompany and help shape emotional experience.

James-Lange theory

Emotion = brain's interpretation of bodily responses.

Cannon-Bard theory

Emotion and bodily responses occur simultaneously, independently.

Schachter-Singer theory (Two-factor)

Emotion = physiological arousal + cognitive interpretation.

Basic emotion theory

a few preset categories of emotions are innate in all humans

Core emotions (basic emotion theory)

happiness, sadness, anger, fear, disgust, surprise.

Evidence for basic emotion theory

specific brain regions activated for specific emotions (amygdala/fear, insula/disgust, etc.)

Theory of constructed emotion

Emotions built by brain from context, signals, past experiences, no fixed circuits

Evidence for constructed emotion theory

the same brain region can be active across many emotions, context changes labeling of arousal.

Basolateral (amygdala subregion)

learning emotional significance.

Central nucleus (amygdala subregion)

autonomic & behavioral responses.

Medial (amygdala subregion)

social/olfactory emotional info.

Damage to amygdala causes . . .

reduced fear, impaired fear learning, poor threat detection.

Amygdala connections

hippocampus (emotion + memory), hypothalamus (autonomic), PFC (regulation)

Key features of anxiety disorders

excessive fear, worry, avoidance, physical symptoms.

GAD (generalized anxiety disorder)

chronic worry, tension.

Panic disorder

sudden panic attacks.

Phobia

intense fear of specific object/situation.

PTSD

trauma-related intrusion, avoidance, arousal.

OCD

intrusive thoughts + compulsions.

General neurobiology of anxiety

Hyperactive amygdala, hypoactive PFC, altered serotonin, GABA, and HPA axis regulation.

Acoustic startle (animal research)

measures fear reactivity.

Open field (animal research)

measuresanxiety (avoid center).

Elevated plus maze (animal research)

avoid open arms = anxiety.

Light-dark box (animal research)

avoid light = measures anxiety.

Benzodiazepines

enhance GABA affects, reduce anxiety.

SSRIs

increase serotonin over time, reduce anxiety

Tricyclics

Prevent reuptake of serotonin and norepenephirine, reduce anxiety

MAOIs

blockbreakdown of NTs like serotonin, dopamine, and norepinephrine, reduce anxiety

Psychedelics

psilocybin, MDMA (experimental) may decrease anxiety via emotional processing + neuroplasticity, potentially reduce anxiety

Stress & general adaptation syndrome

Alarm, resistance, exhaustion.

HPA axis is

the brain's major stress response system

HPA axis path

Hypothalamus (CRH), Pituitary (ACTH), Adrenal cortex (cortisol).

Acute stress . . .

boosts immunity

chronic stress . . .

suppresses immunity.

Journal Club

MDMA-assisted therapy produced greater PTSD symptom reduction vs. placebo+therapy.

CAPS-5 (measures)

PTSD severity.

SDS (measures)

disability/functional impairment.

BDI-II (measures)

depression symptoms.

Core categories of SUD symptoms

Impaired control, social impairment, risky use, tolerance, withdrawal.

General SUD mechanism

Drugs hijack reward learning systems, dopamine bursts, craving, habit circuitry.

Mesolimbic pathway

VTA, nucleus accumbens, PFC; central reward circuit using dopamine.

Craving

Intense desire driven by dopamine prediction errors and cues.

Cycle of SUD

Use, intoxication, withdrawal, craving, relapse.

Stimulants (synaptic mechanism)

increase dopamine (block reuptake or cause release).

Opioids(synaptic mechanism)

activate mu-opioid receptors, inhibit GABA, disinhibition of dopamine neurons.

Alcohol (synaptic mechanism)

enhances GABA, inhibits NMDA, increases dopamine.

Cannabinoids (synaptic mechanism)

CB1 receptor activation suppress neurotransmitter release.

Hallucinogens (synaptic mechanism)

5-HT2A agonists, altered sensory processing.

Opioid addiction treatments

methadone, buprenorphine (agonists), naltrexone (antagonist).

Alcohol addiction treatments

naltrexone, acamprosate, disulfiram.

Major depressive disorder core symptoms

Sadness, anhedonia, changes in sleep/appetite, fatigue, worthlessness, impaired concentration.

Bipolar disorder

mood disorder involving cycles of mania and depression

Bipolar I

full mania

Bipolar II

hypomania + depression.

Lithium mechanisms

Reduces excess dopamine, increases GABA, modulates second-messenger systems

Antidepressant categories

SSRIs, SNRIs, TCAs, MAOIs

TRD

Treatment resistant depression

ECT (TRD)

induces controlled seizures; very effective.

TMS (TRD)

magnetic stimulation of cortex; modulates activity.

Ketamine/esketamine (TRD)

Glutamate antagonists, rapid plasticity.

Psilocybin (TRD)

5-HT2A agonist, emotional flexibility + plasticity.

Monoamine hypothesis

Depression caused by reduced serotonin, norepinephrine, dopamine.

Other explanations for depression

Inflammation, HPA axis dysfunction, network connectivity problems, reduced plasticity.

BDNF

Brain Derived Neurotropic Factor, growth-supporting protein that helps neurons grow, survive, and form stronger connections

Neuroplasticity & BDNF

Low BDNF = reduced synaptic plasticity; antidepressants increase BDNF over time.

Diagnostic criteria schizophrenia

delusions, hallucinations, disorganized speech/behavior, negative symptoms.

Positive symptoms

things present that aren;t in normal population, like hallucinations or delusions

Negative symptoms

things missing in schizophrenia patients that are present in regular population,