PSYC 527 Neuro Test 1

What is Tinbergen’s mechanistic question?

How does this behavior physiologically/neurologically occur?

What is Tinbergen’s ontogenetic question?

How does this behavior develop across the lifespan?

What is Tinbergen’s functional question?

What is the adaptive value or purpose of this behavior?

What is Tinbergen’s evolutionary question?

How did the behavior evolve across species?

What is face validity with animal models?

Does the model have surface similarity to the human condition?

What is predictive validity with animal models?

Does the model respond to treatments the same way humans do?

What is construct validity with animal models?

Does the model accurately capture the theoretical mechanisms underlying the human condition?

Eliminativism

Mental states/folk psychology should be eliminated and replaced with neuroscience. There is no mind beyond the physical (strictest philosophical answer)

Reductive physicalism

Mental phenomena are reduced to physical brain processes

Functionalism

Mental states are defined by their function, not their physical makeup

Substance Dualism

Mind and body are separate substances.

Epiphenomenalism

Mental states are by-products of physical processes with no casual power.

Emergentism

Mental states emerge from physical states but are not reducible to them. The whole is greater than the sum of the parts.

Sympathetic nervous system

Fight/Flight, increases heart rate, blood pressure, inhibits digestion, dialates pupils,

Parasympathetic nervous system (PNS)

rest and digest, slows heart rate, increases digestion

Layer 1 Cerebral Cortex

Dendritic Layer, few cell bodies

Layers 2/3 Cerebral Cortex

Cortical-Cortical Communication

Layer 4 Cerebral Cortex

Input cortex layer, receives sensory input, dense with axons

Layer 5 Cerebral Cortex

output to the cerebral cortex, large pyramidal neurons, and motor control. Bigger somas support axons and action potentials

Layer 6 Cerebral Cortex

Outputs to the thalamus

dlPFC (Dorsolateral Prefrontal Cortex)

working memory, planning, and conscious attention.

vlPFC (Ventrolateral Prefrontal Cortex

response inhibition, inhibitory control

dmPFC (Dorsomedial Prefrontal Cortex)

attention, error detection, monitoring emotional stimuli

vmPFC (Ventromedial Prefrontal Cortex)

value-based decision making, moral reasoning, emotion-based decisions.

lOFC (Lateral Orbitofrontal Cortex)

learning guided by reinforcement/punishment.

mOFC (medial orbitofrontal cortex)

decision making guided by reinforcement/punishment

Rostral PFC (Rostral Prefrontal Cortex)

higher-order social cognition, multitasking

Hippocampus

memory consolidation, spatial navigation

Amygdala

emotional processing, especially fear/threat

Cingulate cortex

emotional regulation, pain, attention

Mammillary bodies

memory, part of Papez circuit

Parts of the limbic system

Hippocampus, amygdala, cingulate cortex, mammillary bodies

Nucleus accumbens

Part of ventral striatum, central in reward, motivation, reinforcement learning, dopamine pathways.

Parts of Basal Ganglia

globus pallidus, caudate nucleus, putamen.

Basal Ganglia Direct Pathway

stimulates movement (putamen → GPi (globus pallidus internus) → thalamus → motor cortex

Basal Ganglia Indirect Pathway

inhibits movement (putamen → GPe (globus pallidus externus)→ subthalamic nucleus → GPi → thalamus → motor cortex).

Hypothalamus

Primary behavioral functions: fighting, feeding, fleeing, mating. Regulates autonomic nervous system and pituitary gland.

Major stress hormone cascade

CRF → ACTH → cortisol (stress)

Major reproductive hormone cascade

GnRH → LH/FSH → sex hormones

Major metabolic hormone cascade

TRH → TSH → thyroid hormones

Main stress hormones

CRF, ACTH, cortisol

Main reproductive hormones

GnRH, LH, FSH, estrogen, testosterone, progesterone

Oxytocin

bonding, lactation, uterine contractions, social affiliation

Vasopressin

water retention, blood pressure regulation, social bonding, and exits through the posterior pituitary gland.

Tectum

Dorsal midbrain structure containing superior colliculus (visual reflexes) and inferior colliculus (auditory reflexes)

Pons

Contains reticular formation; regulates sleep, arousal, motor control pathways

Astrocytes

Support neurons, maintain BBB, regulate neurotransmitters and give metabolic support

Oligodendrocytes

form the myelin in the central nervous system

Microglia

Immune defense in CNS, remove debris and shuttles other things.

Blood brain barrier

Protective barrier formed by endothelial tight junctions and astrocytes; regulates passage of substances. 3 ways to enter: lipid soluble, active transport, very small molecule.

Resting membrane potential

Approximately –65 mV. Maintained by Na+/K+ pump (actively transports 3 Na+ and 2 K+ in per APT) and leaky K+ channels (allows passive movement of K+ out of cell, crucial for resting potential)

Action potential steps

Threshold reached → Na+ channels open (depolarization, Na+ influx).
Na+ channels inactivate, K+ channels open (repolarization, K+ efflux).
Hyperpolarization due to continued K+ efflux. Return to resting state via Na+/K+ pump

Outward rectifying

K+ channels, open during depolarization, allow K+ efflux (repolarization), which slows down the action potential by increasing the refractory period and delaying repolarization

Inward Rectifying

stabilize resting potential, allow K+ influx at negative potentials,   speed up refractory period, faster repolarization

Steps of Synaptic Transmission

1. NT synthesis & transport to the terminal.
   2. Action potential reaches presynaptic terminal.
   3. Voltage-gated Ca2+ channels open → Ca2+ influx.
   4. Vesicles fuse with the membrane → NT release.
   5. NT binds postsynaptic receptors (ionotropic or metabotropic).
   6. Postsynaptic potential generated (EPSP/IPSP).
   7. NT cleared via reuptake (transporters) or degradation (enzymes).

Ionotropic and metabotropic postsynaptic receptors

Ionotropic – ligand-gated ion channels, fast response (e.g., AMPA, GABA-A).
Metabotropic – G-protein coupled, slower but modulatory (e.g., mGluR, GABA-B).

Agonist

A substance that binds to a receptor and activates it, mimicking the natural neurotransmitter

Antagonist

A substance that binds to a receptor but blocks or dampens its activation

Inverse Agonist

Binds to receptor and produces the opposite effect of an agonist. Ex: clozapine)

Partial Agonist

Binds to receptor and activates it, but produces a weaker response than a full agonist.

Competitive antagonist

Competes with agonist at the same binding site; effect depends on relative concentration.

Noncompetitive antagonist

Binds to a different site and reduces receptor function regardless of agonist concentration

Positive allosteric modulator

Binds at a site distinct from the agonist and increases receptor activity (e.g., benzodiazepines on GABA-A). Increases efficacy

Negative allosteric modulator

Binds at an allosteric site and decreases receptor activity. Decreases efficacy

Acetylcholine

First NT discovered.

• Brain regions / pathways: Basal forebrain → cortex & hippocampus (learning, memory). Pons (REM sleep), Neuromuscular junction & autonomic nervous system

• Behavioral functions: Learning, memory, REM sleep, muscle contraction

• Receptors: Muscarinic (M1–M5): excitatory or inhibitory (metabotropic), Nicotinic: ionotropic, excitatory (Na+ influx). Think about ACh as the knuckles, 1,3,5 are excitatory, 2-4 are inhibitory

• Drug examples: Nicotine (agonist, nicotinic), Atropine (antagonist, muscarinic)

Dopamine

Brain regions/pathways: Nigrostriatal system: substantia nigra → striatum (motor control), Mesolimbic system: VTA → limbic system (reward, motivation), Mesocortical system: VTA → cortex (cognition, planning, problem solving)

Behavioral functions: Motor control, reward & reinforcement, motivation, executive functioning

Receptors:

D1 family (D1, D5): excitatory (Na+ channels, phasic firing)

D2 family (D2, D3, D4): inhibitory (K+ channels, tonic firing)

Drug examples: Chlorpromazine (D2 antagonist, antipsychotic)

Norepinephrine

• Brain regions / pathways: Locus coeruleus → widespread forebrain targets (arousal, attention, vigilance), Sympathetic nervous system

• Behavioral functions: Arousal, vigilance, stress response, appetite regulation (increases hunger)

• Receptors:

  • Alpha-1 (excitatory) → agonist: phenylephrine (decongestant)

  • Alpha-2 (inhibitory, autoreceptors) → agonist: clonidine (antihypertensive, reduces feeding)

  • Beta (excitatory) → antagonist: propranolol (reduces anxiety, treats social phobia)

• Drug examples: Clonidine (α2 agonist), Propranolol (β antagonist)

Serotonin

Brain regions/pathways: Cell bodies in raphe nuclei (brainstem) → limbic system & cortex, 98% in gut, ~2% in brain

Behavioral functions: Mood regulation, sleep & arousal, appetite, pain modulation

Receptors: 5-HT1 (inhibitory, autoreceptors), 5-HT2 (excitatory), 5-HT3 (ionotropic, inhibitory), 5-HT4–7 (metabotropic, mixed roles)

Drug examples: Buspirone (5-HT1A partial agonist, anxiolytic/antidepressant)

Glutamate

Brain regions / pathways: Widespread in cortex & hippocampus (primary excitatory NT)

Behavioral functions: Excitation, learning, memory, synaptic plasticity

Receptors: NMDA: Ca²+ channel (learning/memory, LTP), AMPA: Na+ channel, Kainate: Na+ channel, Metabotropic glutamate receptors (mGluRs)

Drug examples: Ketamine (NMDA antagonist, anesthetic/antidepressant), PCP

GABA

Brain regions/pathways: Widespread in cortex, hippocampus, cerebellum (main inhibitory NT)

Behavioral functions: Inhibition, prevents seizures, regulates anxiety, sleep, and motor control

Receptors: GABA-A: ionotropic, Cl- channel, GABA-B: metabotropic, K+ channel

Drug examples:

Diazepam (Valium, benzodiazepine, GABA-A agonist)

Barbiturates (stronger GABA-A agonists)