Biological Basis of Behavior - Complete Interactive Lesson
Part 1: Neurons & Action Potentials
Biological Basis of Behavior
Part 1 of 5 — Neurons & the Action Potential
Neuron Structure & Signal Flow
Dendrites→Cell body (soma)→Axon hillock→Axon→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 Vm sits near the K⁺ equilibrium potential.
The Action Potential — Phases
Phase
Channel event
Voltage change
Resting
Leak channels
~ −70 mV
Depolarization
Voltage-gated Na⁺ IN
rises toward +30 mV
Repolarization
Na⁺ inactivate, K⁺ OUT
falls
Hyperpolarization
K⁺ channels slow to close
undershoots below −70 mV
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
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<summary><b>Example 1: Predict the effect of a Na⁺-channel blocker</b></summary>
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:
Voltage-gated Na⁺ channels drive the depolarizing (rising) phase. Blocking them prevents the membrane from reaching the AP upstroke. ✓
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.
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<summary><b>Example 2: Reason about a changed K⁺ gradient</b></summary>
Question: Extracellular K⁺ is raised experimentally. Qualitatively, what happens to the resting membrane potential and excitability?
Solution:
Raising external K⁺ reduces the K⁺ concentration gradient, so K⁺ efflux at rest decreases.
The membrane DEPOLARIZES (moves toward less negative). ✓
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.
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<summary><b>Example 3: Explain why APs travel one direction</b></summary>
Question: Why does an action potential propagate down the axon in only one direction rather than back toward the soma?
Solution:
Behind the advancing AP, Na⁺ channels are INACTIVATED (absolute refractory period). ✓
They cannot reopen until the membrane repolarizes, so the region just traversed cannot be re-excited.
Only the unexcited region ahead can fire → unidirectional propagation toward the terminals. ✓
Key idea: The refractory period enforces one-way, non-decremental signaling.
Executive function, planning, motor cortex, Broca's area (speech production), personality
Parietal
Somatosensory cortex, spatial processing
Temporal
Hearing, Wernicke's area (language comprehension), memory (hippocampus nearby)
Part 4: Endocrine & Stress (HPA Axis)
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
Feature
Nervous
Endocrine
Messenger
Neurotransmitter
Hormone
Speed
Fast (ms)
Slow (sec–hr)
Duration
Brief
Prolonged
Specificity
Targeted synapse
Broad (any cell with receptor)
Behaviorally Relevant Hormones
Hormone
Source
Behavioral role
Cortisol
Adrenal cortex
Stress response, metabolism, memory effects
Epinephrine/norepinephrine
Adrenal medulla
Fight-or-flight, arousal
Part 5: NS Organization & Behavioral Genetics
Biological Basis of Behavior
Part 5 of 5 — Nervous System Organization, Genetics & Review
Divisions of the Nervous System
Nervous system→{CNSPNS
NT release
→
receptor binding→
postsynaptic potential
Ca²⁺ influx is the trigger for vesicle exocytosis.
Signal terminated by reuptake (transporters), enzymatic degradation, or diffusion.
EPSPs vs. IPSPs
Potential
Ion movement
Effect
EPSP (excitatory)
Na⁺ in (depolarize)
Toward threshold
IPSP (inhibitory)
Cl⁻ in / K⁺ out (hyperpolarize)
Away from threshold
Summation: temporal (rapid succession from one input) + spatial (many inputs at once) determine whether the axon hillock reaches threshold.
High-Yield Neurotransmitters
Neurotransmitter
Major roles
Clinical link
Acetylcholine (ACh)
Muscle contraction, memory, PNS
↓ in Alzheimer's; myasthenia gravis
Dopamine
Reward, movement, motivation
↓ Parkinson's; ↑ schizophrenia (mesolimbic)
Serotonin (5-HT)
Mood, sleep, appetite
↓ depression (SSRIs raise it)
Norepinephrine
Alertness, arousal, fight-or-flight
Mood, anxiety
GABA
Main INHIBITORY (CNS)
Anxiolytics (benzodiazepines)
Glutamate
Main EXCITATORY (CNS), LTP
Excitotoxicity
Endorphins
Natural pain relief
Opioid receptors
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
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<summary><b>Example 1: Predict the effect of an acetylcholinesterase inhibitor</b></summary>
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:
Blocking degradation → ACh accumulates and persists in the cleft → prolonged/enhanced cholinergic signaling. ✓
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.
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<summary><b>Example 2: Classify drugs as agonists or antagonists</b></summary>
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).
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<summary><b>Example 3: Integrate EPSPs and IPSPs at the axon hillock</b></summary>
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:
Net change = 3(+5) + (−8) = +15 − 8 = +7 mV.
New Vm = −70 + 7 = −63 mV, which is still below threshold (−55 mV). ✓
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.
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Key Takeaways — Part 2
AP → Ca²⁺ 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.
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
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<summary><b>Example 1: Localize a deficit from a lesion description</b></summary>
Question: A patient develops dramatic personality changes, poor planning, and impulsivity but normal sensation and movement. Which brain region is most implicated?
Solution:
Personality, planning, and impulse control are EXECUTIVE functions of the frontal lobe (prefrontal cortex). ✓
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.
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<summary><b>Example 2: Match the method to the research question</b></summary>
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:
Good SPATIAL resolution, no radiation → fMRI (tracks blood-oxygen-level-dependent signal). ✓
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.
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<summary><b>Example 3: Predict the effect of hypothalamic damage</b></summary>
Question: Damage to the lateral hypothalamus vs. the ventromedial hypothalamus produces opposite eating behaviors. Predict each.
Connection: The hypothalamus governs homeostatic drives (hunger, thirst, temperature) and links the nervous system to the endocrine system via the pituitary.
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<summary><b>Example 1: Apply negative feedback to a lab result</b></summary>
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:
Exogenous glucocorticoids mimic cortisol → strong NEGATIVE feedback on hypothalamus (CRH↓) and pituitary (ACTH↓). ✓
Low ACTH → the adrenal cortex atrophies (less stimulation). ✓
Abrupt withdrawal removes the drug before the suppressed axis recovers → adrenal insufficiency (no cortisol) → crisis. Hence steroids are TAPERED. ✓
MCAT key: Negative feedback means giving the end product downregulates the whole upstream axis.
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<summary><b>Example 2: Distinguish the fast and slow stress responses</b></summary>
Question: A person is startled by a near car accident. Describe the sequence of responses over seconds versus minutes.
Solution:
Within SECONDS: the SAM axis fires — sympathetic activation → adrenal medulla → epinephrine → racing heart, dilated pupils, raised blood glucose. ✓
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.
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<summary><b>Example 3: Interpret a stress-and-illness study (allostatic load)</b></summary>
Question: A study finds chronically stressed caregivers have more infections and slower wound healing than controls. Propose the hormonal mechanism.
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
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<summary><b>Example 1: Trace a reflex arc</b></summary>
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.
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.
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<summary><b>Example 2: Interpret a heritability estimate correctly</b></summary>
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:
It MEANS ~60% of the VARIANCE in the trait ACROSS the population is attributable to genetic differences. ✓
It does NOT mean any individual's trait is "60% genetic," nor that environment is unimportant, nor that the trait is fixed/unchangeable. ✓
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:
The genotype's effect depends on the environment (and vice versa) → gene–environment interaction. ✓
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.
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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.