Biological Basis of Behavior

Biological Basis of Behavior

Part 1 of 5 — Neurons & the Action Potential

Neuron Structure & Signal Flow

$\text{Dendrites} \to \text{Cell body (soma)} \to \text{Axon hillock} \to \text{Axon} \to \text{Axon terminals}$

• Dendrites receive input; the axon hillock sums inputs and initiates the action potential if threshold (~ −55 mV) is reached.
• Myelin (oligodendrocytes in CNS, Schwann cells in PNS) speeds conduction via saltatory conduction (jumping node to node).

Resting Membrane Potential (~ −70 mV)

Set by the $Na^{+}/K^{+}$-ATPase (pumps 3 $Na^{+}$ out, 2 $K^{+}$ in) plus $K^{+}$ leak channels. The membrane is most permeable to $K^{+}$ at rest, so $V_m$ sits near the $K^{+}$ equilibrium potential.

The Action Potential — Phases

All-or-None & the Refractory Period

• All-or-none: above threshold, every AP has the same amplitude; intensity is coded by FREQUENCY, not size.
• Absolute refractory period: $Na^{+}$ channels inactivated → no new AP possible (ensures one-way propagation).
• Relative refractory period: a stronger-than-normal stimulus can fire (during hyperpolarization).

Neurons & Action Potentials 🎯

Worked Examples — Action Potentials

Question: A local anesthetic (e.g., lidocaine) blocks voltage-gated $Na^{+}$ channels in a sensory neuron. Predict the effect on action potentials and on pain sensation.

Solution:

1. Voltage-gated $Na^{+}$ channels drive the depolarizing (rising) phase. Blocking them prevents the membrane from reaching the AP upstroke. ✓
2. No action potentials can propagate → the sensory signal (pain) never reaches the CNS → numbness. ✓

MCAT note: This is exactly how local anesthetics work — they silence the axon by blocking $Na^{+}$ entry.

Question: Extracellular $K^{+}$ is raised experimentally. Qualitatively, what happens to the resting membrane potential and excitability?

Solution:

1. Raising external $K^{+}$ reduces the $K^{+}$ concentration gradient, so $K^{+}$ efflux at rest decreases.
2. The membrane DEPOLARIZES (moves toward less negative). ✓
3. Initially the neuron is closer to threshold (hyperexcitable), but sustained depolarization inactivates $Na^{+}$ channels → eventual loss of excitability (depolarization block). ✓

Connection: This is why severe hyperkalemia is dangerous to cardiac and neural tissue.

Question: Why does an action potential propagate down the axon in only one direction rather than back toward the soma?

Solution:

1. Behind the advancing AP, $Na^{+}$ channels are INACTIVATED (absolute refractory period). ✓
2. They cannot reopen until the membrane repolarizes, so the region just traversed cannot be re-excited.
3. Only the unexcited region ahead can fire → unidirectional propagation toward the terminals. ✓

Key idea: The refractory period enforces one-way, non-decremental signaling.

Key Takeaways — Part 1

• Signal flow: dendrites → soma → axon hillock (threshold ~ −55 mV) → axon → terminals.
• Resting potential ~ −70 mV set by $Na^{+}/K^{+}$-ATPase (3 $Na^{+}$ out / 2 $K^{+}$ in) and $K^{+}$ leak.
• AP: $Na^{+}$ IN (depolarize) → $K^{+}$ OUT (repolarize) → hyperpolarize; all-or-none; intensity coded by FREQUENCY.
• Refractory period ensures one-way conduction; myelin enables fast saltatory conduction (lost in MS).

Biological Basis of Behavior

Part 2 of 5 — Synapses & Neurotransmitters

Synaptic Transmission Steps

$\text{AP at terminal} \to \text{voltage-gated } Ca^{2+} \text{ IN} \to \text{vesicle fusion} \to \text{NT release} \to \text{receptor binding} \to \text{postsynaptic potential}$

• $Ca^{2+}$ influx is the trigger for vesicle exocytosis.
• Signal terminated by reuptake (transporters), enzymatic degradation, or diffusion.

EPSPs vs. IPSPs

Summation: temporal (rapid succession from one input) + spatial (many inputs at once) determine whether the axon hillock reaches threshold.

High-Yield Neurotransmitters

Agonists vs. Antagonists

• Agonist: mimics/enhances the neurotransmitter's effect.
• Antagonist: blocks the receptor or the neurotransmitter's action.
• Drugs can act by altering synthesis, release, reuptake, or degradation.

Synapses & Neurotransmitters 🎯

Worked Examples — Synaptic Pharmacology

Question: A drug inhibits acetylcholinesterase, the enzyme that degrades ACh in the synaptic cleft. Predict the effect at the neuromuscular junction and a clinical use.

Solution:

1. Blocking degradation → ACh accumulates and persists in the cleft → prolonged/enhanced cholinergic signaling. ✓
2. At the neuromuscular junction this strengthens muscle activation; clinically, AChE inhibitors treat myasthenia gravis (where ACh receptors are reduced) and are used in Alzheimer's. ✓

MCAT note: Blocking the degrading enzyme is functionally an indirect AGONIST — more neurotransmitter stays around.

Question: (a) A drug binds dopamine receptors and activates them. (b) A drug binds dopamine receptors but produces no effect and blocks dopamine. (c) A drug blocks dopamine reuptake. Classify the net effect of each.

Solution:

• (a) Activates the receptor → agonist. ✓
• (b) Occupies the receptor and blocks signaling → antagonist. ✓
• (c) Reuptake blockade leaves more dopamine in the cleft → net agonist-like (indirect agonist). ✓

Connection: Antipsychotics are dopamine antagonists (reduce mesolimbic dopamine); stimulants like cocaine are reuptake inhibitors (indirect agonists).

Question: A neuron simultaneously receives three EPSPs (+5 mV each) and one IPSP (−8 mV) while at −70 mV with threshold −55 mV. Does it fire?

Solution:

1. Net change = 3(+5) + (−8) = +15 − 8 = +7 mV.
2. New $V_m$ = −70 + 7 = −63 mV, which is still below threshold (−55 mV). ✓
3. The neuron does NOT fire. ✓

Key idea: The axon hillock integrates (spatially and temporally) all EPSPs and IPSPs; only if the net depolarization reaches threshold is an AP generated.

Key Takeaways — Part 2

• AP → $Ca^{2+}$ influx → vesicle fusion → NT release; cleared by reuptake, enzymes, or diffusion.
• EPSP ($Na^{+}$ in, depolarize) vs. IPSP ($Cl^{-}$ in / $K^{+}$ out, hyperpolarize); summed at the axon hillock.
• Know the NTs: ACh (muscle/memory; Alzheimer's), dopamine (reward/movement; Parkinson's, schizophrenia), serotonin (mood; SSRIs), GABA (main inhibitory; benzos), glutamate (main excitatory; LTP).
• Agonist mimics/enhances; antagonist blocks; reuptake/enzyme inhibitors act as indirect agonists.

Biological Basis of Behavior

Part 3 of 5 — Brain Regions & Their Functions

Organizing the Brain: Hindbrain, Midbrain, Forebrain

Cortical Lobes

Key Subcortical & Limbic Structures

Language: Broca vs. Wernicke

• Broca's aphasia (frontal): non-fluent, effortful speech; comprehension intact ("broken" speech).
• Wernicke's aphasia (temporal): fluent but meaningless speech; impaired comprehension.

Methods to Study the Brain

• EEG (electrical activity, great time resolution), fMRI/PET (blood flow/metabolism, spatial), lesion studies, CT/MRI (structure).

Brain Regions 🎯

Worked Examples — Brain Localization

Question: A patient develops dramatic personality changes, poor planning, and impulsivity but normal sensation and movement. Which brain region is most implicated?

Solution:

1. Personality, planning, and impulse control are EXECUTIVE functions of the frontal lobe (prefrontal cortex). ✓
2. Intact sensation/movement argues against parietal or primary motor damage.

Historical tie-in: The Phineas Gage case (frontal damage → personality change) is the classic illustration tested on the MCAT.

Question: A study needs to map WHICH brain regions activate during a memory task with good spatial detail and no radiation. Which imaging method fits, and why not EEG or PET?

Solution:

1. Good SPATIAL resolution, no radiation → fMRI (tracks blood-oxygen-level-dependent signal). ✓
2. EEG has poor spatial resolution; PET requires a radioactive tracer. ✓

Key trade-off: EEG = temporal precision; fMRI = spatial precision. Choose by which dimension the question emphasizes.

Question: Damage to the lateral hypothalamus vs. the ventromedial hypothalamus produces opposite eating behaviors. Predict each.

Solution:

1. Lateral hypothalamus = the "hunger center"; damage → reduced eating (aphagia). ✓
2. Ventromedial hypothalamus = the "satiety center"; damage → overeating (hyperphagia, obesity). ✓

Connection: The hypothalamus governs homeostatic drives (hunger, thirst, temperature) and links the nervous system to the endocrine system via the pituitary.

Key Takeaways — Part 3

• Hindbrain = vital reflexes/coordination; midbrain = arousal/reflexes; forebrain = cognition/emotion/homeostasis.
• Frontal (executive, motor, Broca's), parietal (somatosensory), temporal (hearing, Wernicke's), occipital (vision).
• Hypothalamus = homeostasis + pituitary; amygdala = fear; hippocampus = new explicit memory; thalamus = sensory relay.
• Broca's aphasia = non-fluent/comprehension intact; Wernicke's = fluent but meaningless/comprehension impaired. EEG = timing, fMRI = location.

Biological Basis of Behavior

Part 4 of 5 — Endocrine System & Behavior + Stress (HPA Axis)

Hormones modulate behavior more slowly and diffusely than neurotransmitters, but with longer-lasting effects.

Nervous vs. Endocrine Signaling

Behaviorally Relevant Hormones

The HPA Axis (Slow Stress Response)

$\text{Hypothalamus (CRH)} \to \text{Anterior pituitary (ACTH)} \to \text{Adrenal cortex (cortisol)}$

• Cortisol mobilizes glucose, suppresses immune function, and provides negative feedback on the hypothalamus and pituitary to shut the axis off.
• Chronic stress → sustained cortisol → impaired immunity, hippocampal damage/memory problems, and metabolic effects (allostatic load).

The SAM Axis (Fast Stress Response)

$\text{Sympathetic nervous system} \to \text{Adrenal medulla} \to \text{epinephrine/norepinephrine}$

Immediate fight-or-flight: ↑ heart rate, ↑ blood pressure, ↑ blood glucose, pupil dilation.

General Adaptation Syndrome (Selye)

$\text{Alarm} \to \text{Resistance} \to \text{Exhaustion}$

Prolonged stress depletes resources, increasing disease vulnerability.

Endocrine & Stress 🎯

Worked Examples — Endocrine & Stress

Question: A patient takes high-dose synthetic glucocorticoids for months. What happens to their endogenous CRH, ACTH, and adrenal output, and why is abrupt withdrawal dangerous?

Solution:

1. Exogenous glucocorticoids mimic cortisol → strong NEGATIVE feedback on hypothalamus (CRH↓) and pituitary (ACTH↓). ✓
2. Low ACTH → the adrenal cortex atrophies (less stimulation). ✓
3. Abrupt withdrawal removes the drug before the suppressed axis recovers → adrenal insufficiency (too little cortisol) → crisis. Hence steroids are TAPERED. ✓

MCAT key: Negative feedback means giving the end product downregulates the whole upstream axis.

Question: A person is startled by a near car accident. Describe the sequence of responses over seconds versus minutes.

Solution:

1. Within SECONDS: the SAM axis fires — sympathetic activation → adrenal medulla → epinephrine → racing heart, dilated pupils, raised blood glucose. ✓
2. Over MINUTES: the HPA axis ramps up — CRH → ACTH → cortisol → sustained glucose mobilization and immune suppression. ✓

Connection: Two complementary axes: SAM for the immediate jolt, HPA for the sustained response.

Question: A study finds chronically stressed caregivers have more infections and slower wound healing than controls. Propose the hormonal mechanism.

Solution:

1. Chronic stress → sustained HPA activation → persistently elevated cortisol. ✓
2. Cortisol SUPPRESSES immune function (reduces inflammation and lymphocyte activity), so chronic elevation impairs immune defense and wound healing. ✓
3. This cumulative physiological wear is called "allostatic load"; at its extreme it parallels the exhaustion stage of Selye's General Adaptation Syndrome. ✓

Why it matters: This links the biological stress axis to real health outcomes — a favorite Psych/Soc integration.

Key Takeaways — Part 4

• Endocrine signaling = slow, broad, prolonged vs. fast/targeted neurotransmission.
• HPA axis (slow): CRH → ACTH → cortisol; cortisol mobilizes glucose, suppresses immunity, and gives negative feedback.
• SAM axis (fast): sympathetic → adrenal medulla → epinephrine → immediate fight-or-flight.
• Chronic stress/high cortisol → impaired immunity + hippocampal damage; Selye's GAS = alarm → resistance → exhaustion.

Biological Basis of Behavior

Part 5 of 5 — Nervous System Organization, Genetics & Review

Divisions of the Nervous System

$\text{Nervous system} \to \begin{cases} \textbf{CNS} & \text{brain + spinal cord} \\ \textbf{PNS} & \text{somatic + autonomic} \end{cases}$

Sympathetic and parasympathetic are largely ANTAGONISTIC, maintaining homeostasis.

Reflex Arc

$\text{Receptor} \to \text{sensory (afferent) neuron} \to \text{spinal cord (± interneuron)} \to \text{motor (efferent) neuron} \to \text{effector}$

A monosynaptic reflex (e.g., knee-jerk) bypasses the brain for speed.

Behavioral Genetics & Methods

$\text{Phenotype} = \text{Genotype} \times \text{Environment (gene–environment interaction)}$

Nature vs. Nurture & Plasticity

• Most behaviors are POLYGENIC and shaped by gene–environment interaction.
• Neuroplasticity: the brain reorganizes (synaptic strengthening/pruning) with experience; greatest in development but lifelong (e.g., learning, recovery from injury).

Evolutionary Perspective

• Behaviors that enhanced survival/reproduction were selected (e.g., fear of heights, kin altruism). Useful for "ultimate cause" explanations of behavior.

NS Organization & Genetics 🎯

Worked Examples — Organization & Genetics

Question: You touch a hot stove and jerk your hand away before feeling pain. Order the components and explain why withdrawal precedes the conscious pain.

Solution:

1. Receptor (nociceptor) → sensory (afferent) neuron → spinal cord interneuron → motor (efferent) neuron → muscle (effector) → withdrawal. ✓
2. This spinal reflex arc acts locally and quickly; the pain signal continues UP to the brain separately, arriving slightly later → you move before you consciously feel pain. ✓

Key idea: Protective reflexes are processed at the spinal level for speed.

Question: A study reports that a trait has heritability of 0.6 in a population. What does this mean, and what does it NOT mean?

Solution:

1. It MEANS ~60% of the VARIANCE in the trait ACROSS the population is attributable to genetic differences. ✓
2. It does NOT mean any individual's trait is "60% genetic," nor that environment is unimportant, nor that the trait is fixed/unchangeable. ✓
3. Heritability is population- and environment-specific; change the environment and the estimate can change. ✓

MCAT trap: Heritability describes population variance, not the make-up of one person's trait.

Question: A gene variant raises depression risk ONLY in individuals who also experience severe early-life stress; neither factor alone has much effect. Name this phenomenon and its implication.

Solution:

1. The genotype's effect depends on the environment (and vice versa) → gene–environment interaction. ✓
2. Implication: behavior arises from the JOINT action of genes and environment, not either alone — undermining strict "nature vs. nurture" framings. ✓

Connection: This is the modern, interactionist view the MCAT favors over single-cause explanations.

Key Takeaways — Part 5 (and Suite Review)

• CNS (brain + cord) vs. PNS (somatic = voluntary; autonomic = sympathetic fight-or-flight vs. parasympathetic rest-and-digest).
• Reflex arc: receptor → afferent → spinal cord → efferent → effector; monosynaptic reflexes bypass the brain for speed.
• Behavioral genetics: twin/adoption studies separate genes from environment; heritability = proportion of population VARIANCE from genes (not individual %).
• Behavior = genes × environment (interaction) plus neuroplasticity and evolutionary selection.