Biological Bases of Behavior

Neurons and Neurotransmitters

Neurons are the fundamental signaling units of the nervous system, specialized for rapid electrochemical communication. A typical neuron has four functional regions: dendrites (receive signals), soma (cell body, integrates inputs), axon (conducts action potentials), and axon terminals (release neurotransmitters). The resting membrane potential is approximately -70 mV, maintained by the Na+/K+-ATPase pump which moves 3 Na+ out for every 2 K+ in. When a stimulus depolarizes the membrane to the threshold potential (around -55 mV), voltage-gated Na+ channels open, triggering an action potential — a self-propagating wave of depolarization that travels down the axon without decrement. The rising phase is driven by Na+ influx; repolarization by K+ efflux; and the undershoot (hyperpolarization) by delayed K+ channel closure. The absolute refractory period (Na+ channels inactivated) ensures unidirectional propagation and limits firing rate. At the presynaptic terminal, the action potential opens voltage-gated Ca2+ channels; Ca2+ influx triggers synaptic vesicles to fuse with the membrane and release neurotransmitter into the synaptic cleft via exocytosis. Neurotransmitters bind to postsynaptic receptors, producing either excitatory postsynaptic potentials (EPSPs, typically via Na+ influx) or inhibitory postsynaptic potentials (IPSPs, typically via Cl- influx or K+ efflux). Key neurotransmitters for the MCAT: acetylcholine (ACh, muscle contraction, autonomic function, learning; myasthenia gravis involves ACh receptor destruction), dopamine (reward, motor control; Parkinson’s = low dopamine in substantia nigra, schizophrenia linked to excess dopamine), serotonin (mood, sleep, appetite; SSRIs block reuptake), norepinephrine (alertness, sympathetic activation), GABA (primary inhibitory; benzodiazepines enhance GABA), glutamate (primary excitatory; NMDA receptors critical for learning), and endorphins (endogenous opioids, pain relief). Neurotransmitter clearance occurs via enzymatic degradation (acetylcholinesterase breaks down ACh), reuptake (SSRIs block serotonin reuptake), or diffusion. Summation of EPSPs and IPSPs at the axon hillock determines whether the postsynaptic neuron fires: spatial summation (multiple synapses simultaneously) and temporal summation (rapid firing at one synapse).

Nervous-System Organization

The nervous system is organized hierarchically into the central nervous system (CNS: brain and spinal cord) and the peripheral nervous system (PNS: all nerves outside the CNS). The PNS is further divided into the somatic nervous system (voluntary control of skeletal muscle) and the autonomic nervous system (involuntary control of internal organs). The autonomic nervous system has two branches that typically act in opposition: the sympathetic nervous system (fight-or-flight) and the parasympathetic nervous system (rest-and-digest). Sympathetic activation: pupils dilate, heart rate and contractility increase, bronchi dilate, digestion and bladder contraction are inhibited, glucose is released from the liver, and epinephrine/norepinephrine are released from the adrenal medulla. Preganglionic sympathetic neurons are short and release ACh; postganglionic neurons are long and release norepinephrine (except sweat glands, which use ACh). Parasympathetic activation: pupils constrict, heart rate slows, bronchi constrict, digestion and bladder contraction are stimulated. Preganglionic parasympathetic neurons are long and release ACh; postganglionic neurons are short and also release ACh. The enteric nervous system, a mesh-like network of neurons lining the GI tract, is sometimes considered a third autonomic division — it can function independently but is modulated by sympathetic and parasympathetic input. The CNS is protected by meninges (dura mater, arachnoid mater, pia mater) and cerebrospinal fluid (CSF), which cushions the brain and removes metabolic waste. The blood-brain barrier, formed by tight junctions between capillary endothelial cells, restricts passage of many substances from the bloodstream into the brain — a critical consideration for drug delivery. Spinal cord organization: sensory (afferent) neurons enter through the dorsal root (dorsal root ganglion contains cell bodies); motor (efferent) neurons exit through the ventral root. The dorsal column-medial lemniscus pathway carries fine touch and proprioception; the spinothalamic tract carries pain and temperature. The corticospinal tract carries voluntary motor commands. All three pathways decussate (cross the midline) at different levels — knowing which side of the body is affected relative to a lesion location is a classic MCAT reasoning task.

Brain Structures

The brain is organized into three major divisions: hindbrain, midbrain, and forebrain. The hindbrain includes the medulla oblongata (vital autonomic functions: breathing, heart rate, blood pressure), pons (relay between cortex and cerebellum; sleep regulation), and cerebellum (motor coordination, balance, procedural memory). The midbrain contains the substantia nigra (dopamine-producing neurons; degeneration causes Parkinson’s disease) and the superior and inferior colliculi (visual and auditory reflexes). The reticular formation runs through the brainstem and regulates arousal and alertness. The forebrain includes the thalamus (sensory relay station — all sensory information except olfaction passes through), hypothalamus (homeostasis: hunger, thirst, temperature, circadian rhythms; controls pituitary gland), limbic system, and cerebral cortex. The limbic system comprises: hippocampus (consolidation of episodic memories; HM case study — bilateral removal caused anterograde amnesia), amygdala (fear processing and emotional memory), and cingulate cortex. The cerebral cortex is divided into four lobes: frontal lobe (prefrontal cortex = executive function, reasoning, impulse control; primary motor cortex in precentral gyrus; Broca’s area = speech production, typically left hemisphere), parietal lobe (somatosensory cortex in postcentral gyrus; spatial processing), temporal lobe (auditory cortex; Wernicke’s area = language comprehension; memory via hippocampus embedded within), and occipital lobe (primary visual cortex). Hemispheric lateralization: left hemisphere dominant for language in most people (Broca’s, Wernicke’s); right hemisphere dominant for spatial reasoning and attention. The corpus callosum connects the hemispheres; split-brain patients (severed corpus callosum) reveal lateralized functions — an object in the left visual field (processed by right hemisphere) cannot be named because language centers are in the left hemisphere. Subcortical structures include the basal ganglia (motor control, habit learning; caudate, putamen, globus pallidus) and the nucleus accumbens (reward, addiction). Key methods for studying brain function: fMRI (blood-oxygen-level-dependent signal, good spatial resolution but poor temporal), EEG (electrical activity at scalp, excellent temporal resolution but poor spatial), PET (radioactive tracer uptake, measures metabolism), and lesion studies (infer function from deficits after damage).

Endocrine System

The endocrine system communicates via hormones secreted into the bloodstream, producing slower but longer-lasting effects than neural signaling. The hypothalamus-pituitary axis is the master control system. The hypothalamus synthesizes releasing and inhibiting hormones that travel through the hypothalamic-pituitary portal system to the anterior pituitary, which then releases tropic hormones that stimulate target endocrine glands. Anterior pituitary hormones: GH (growth), TSH (stimulates thyroid to release T3/T4, which regulate metabolism), ACTH (stimulates adrenal cortex to release cortisol), FSH and LH (stimulate gonads to produce sex hormones and gametes), and prolactin (milk production). The posterior pituitary stores and releases hormones synthesized by the hypothalamus: oxytocin (uterine contractions, milk ejection, social bonding) and ADH/vasopressin (water retention by kidneys, vasoconstriction). The adrenal glands have two functional regions: the adrenal medulla (modified sympathetic ganglion, releases epinephrine and norepinephrine for acute stress response) and the adrenal cortex (releases cortisol for sustained stress, aldosterone for Na+ retention/K+ excretion, and androgens). Chronic stress follows a pathway: hypothalamus releases CRH -> anterior pituitary releases ACTH -> adrenal cortex releases cortisol -> cortisol provides negative feedback to hypothalamus and pituitary. Cortisol increases blood glucose, suppresses immune function, and aids metabolism. The thyroid produces T3 (triiodothyronine) and T4 (thyroxine), which increase basal metabolic rate; hypothyroidism causes fatigue, weight gain, cold intolerance. The pancreas has both endocrine (islets of Langerhans: alpha cells secrete glucagon, beta cells secrete insulin) and exocrine (digestive enzymes) functions. Insulin lowers blood glucose by promoting glucose uptake into cells and glycogen synthesis; glucagon raises blood glucose by stimulating glycogenolysis and gluconeogenesis. Diabetes mellitus: Type 1 = autoimmune destruction of beta cells (no insulin); Type 2 = insulin resistance. Gonads: testes produce testosterone; ovaries produce estrogen and progesterone. The MCAT frequently tests feedback inhibition in endocrine axes — knowing which hormone feeds back negatively helps predict the consequences of gland removal, hormone supplementation, or receptor defects.

Genetics and Behavior

Genetics influences behavior through complex pathways involving gene expression, protein synthesis, and nervous system development. The genome is the complete set of DNA; the genotype is an individual’s specific genetic makeup; the phenotype is the observable trait resulting from genotype-environment interaction. Heritability (h^2) estimates what proportion of phenotypic variance in a population is attributable to genetic variance — it ranges from 0 to 1, is population-specific, and does not indicate how ‘genetically determined’ an individual’s trait is. Twin studies compare monozygotic (MZ, identical) and dizygotic (DZ, fraternal) twins; higher concordance in MZ than DZ twins suggests genetic influence. Adoption studies compare adopted children to biological and adoptive parents to disentangle genetic and environmental contributions. Monogenic inheritance involves a single gene: Huntington’s disease (autosomal dominant, CAG repeat expansion on chromosome 4, causes neurodegeneration with behavioral symptoms including depression, irritability, and psychosis), phenylketonuria or PKU (autosomal recessive, inability to metabolize phenylalanine leads to intellectual disability if untreated), and Fragile X syndrome (X-linked, CGG repeat expansion, leading inherited cause of intellectual disability with behavioral features including social anxiety, hyperactivity). Most behavioral traits are polygenic (many genes each contributing small effects) and multifactorial (genes + environment). The diathesis-stress model proposes that genetic predisposition (diathesis) combined with environmental stressors produces psychological disorders. Epigenetics involves heritable changes in gene expression that do not alter the DNA sequence: DNA methylation (typically silences genes), histone modification (acetylation opens chromatin for transcription, deacetylation closes it). Early life stress, nutrition, and toxins can produce epigenetic changes that alter stress reactivity and disease risk. Evolutionary psychology examines behavior through the lens of natural selection: behaviors that increased reproductive success were selected for. Key concepts: inclusive fitness (an organism’s genetic success derives from both its own reproduction and aiding relatives who share genes), kin selection (altruistic behavior toward relatives explained by shared genes — you help those who carry copies of your genes), and reciprocal altruism (altruism between non-relatives with expectation of future reciprocation). The MCAT tests whether you can distinguish evolutionary explanations (why a behavior exists in a species) from proximate explanations (what mechanism produces it in an individual).

Neuroplasticity

Neuroplasticity is the brain’s ability to reorganize its structure, function, and connections in response to experience, learning, and injury. Long-term potentiation (LTP) is the cellular mechanism underlying learning and memory. At glutamatergic synapses, repeated high-frequency stimulation leads to sustained strengthening of synaptic transmission. When glutamate binds to both AMPA and NMDA receptors on the postsynaptic neuron, the NMDA receptor’s Mg2+ block is relieved by depolarization, allowing Ca2+ influx. Elevated intracellular Ca2+ triggers a signaling cascade that phosphorylates AMPA receptors (increasing their conductance) and inserts additional AMPA receptors into the postsynaptic membrane, making the synapse more responsive to future stimulation. This is Hebb’s rule in action: ‘neurons that fire together, wire together.’ Long-term depression (LTD), the converse, weakens synapses via low-frequency stimulation, producing smaller Ca2+ signals that activate phosphatases — important for memory refinement and forgetting. Synaptic pruning is the elimination of excess synapses during development (peaks in adolescence), guided by use-dependent competition — frequently used connections are strengthened and retained; unused connections are eliminated. Experience-dependent plasticity alters cortical maps: in violinists, the cortical representation of the left hand (used for fingering) is enlarged; in London taxi drivers, the posterior hippocampus (spatial navigation) shows increased gray matter volume. After brain injury, several plastic mechanisms can support recovery: axonal sprouting (undamaged neurons grow new branches to reinnervate denervated targets), denervation supersensitivity (postsynaptic neurons upregulate receptors when presynaptic input is lost), and cortical remapping (adjacent cortical areas take over functions of damaged regions). Constraint-induced movement therapy for stroke patients illustrates clinical application — forcing use of the impaired limb drives beneficial cortical reorganization. Sensitive/critical periods are developmental windows when specific experiences are required for normal brain development: ocular dominance columns in visual cortex require normal binocular input during early childhood; language acquisition shows a sensitive period ending around puberty; attachment formation in infancy depends on caregiver responsiveness. The MCAT often pairs neuroplasticity with learning, memory, or recovery from brain injury passages.

How it works

Behavior emerges from hierarchical biological systems. At the molecular and cellular level, neurons fire action potentials (all-or-none electrical signals) and communicate via neurotransmitter release at synapses. Summed excitatory and inhibitory inputs determine whether a neuron fires, and the pattern of firing encodes information. At the circuit level, specific brain regions perform specialized functions — the amygdala processes fear, the hippocampus consolidates memory, and the prefrontal cortex handles executive control — but they function as interconnected networks. The autonomic nervous system provides the physiological backdrop for behavior: sympathetic activation primes the body for action; parasympathetic activation enables recovery. The endocrine system adds a slower, sustained dimension — cortisol shapes the stress response over hours; sex hormones organize and activate reproductive behaviors over development. Genetics provides the blueprint, but environment and experience continuously shape expression through epigenetics and neuroplasticity. To answer an MCAT question, identify which level (molecular, circuit, system, genetic) the scenario implicates, trace the causal pathway from biological mechanism to behavior, and check for common confounds like mistaking excitatory for inhibitory neurotransmitters or confusing sympathetic and parasympathetic effects.

How it works

Behavior emerges from hierarchical biological systems. At the molecular and cellular level, neurons fire action potentials (all-or-none electrical signals) and communicate via neurotransmitter release at synapses. Summed excitatory and inhibitory inputs determine whether a neuron fires, and the pattern of firing encodes information. At the circuit level, specific brain regions perform specialized functions — the amygdala processes fear, the hippocampus consolidates memory, and the prefrontal cortex handles executive control — but they function as interconnected networks. The autonomic nervous system provides the physiological backdrop for behavior: sympathetic activation primes the body for action; parasympathetic activation enables recovery. The endocrine system adds a slower, sustained dimension — cortisol shapes the stress response over hours; sex hormones organize and activate reproductive behaviors over development. Genetics provides the blueprint, but environment and experience continuously shape expression through epigenetics and neuroplasticity. To answer an MCAT question, identify which level (molecular, circuit, system, genetic) the scenario implicates, trace the causal pathway from biological mechanism to behavior, and check for common confounds like mistaking excitatory for inhibitory neurotransmitters or confusing sympathetic and parasympathetic effects.

Comparisons

• P/S (Sensation PS-002): Sensory receptor neurons transduce physical stimuli (light, sound, pressure) into graded potentials that can trigger action potentials; different receptor types respond to different stimulus modalities.
• P/S (Learning PS-003): Classical conditioning involves strengthening of synapses between CS and US pathways; operant conditioning is mediated by dopamine signaling in reward circuits; long-term potentiation is the cellular basis of all learning.
• P/S (Memory PS-004): Hippocampal LTP underlies episodic memory consolidation; amygdala modulation of hippocampal encoding explains why emotional events are better remembered; sleep-dependent memory consolidation involves replay of neural activity patterns.
• P/S (Consciousness PS-006): Psychoactive drugs act on neurotransmitter systems — stimulants increase dopamine and norepinephrine; depressants enhance GABA; hallucinogens act on serotonin; opioids mimic endorphins.
• P/S (Emotion PS-007): The amygdala is the central processor of fear; autonomic nervous system (sympathetic) mediates the physiological arousal component of emotion (James-Lange theory); stress activates both SAM (sympathetic-adrenal-medullary) and HPA (hypothalamic-pituitary-adrenal) axes.
• B/B (Nervous System BIO-017): Overlap with MCAT Biology nervous system coverage — action potential mechanism, synaptic transmission, CNS/PNS organization; PS-001 emphasizes behavioral correlates while BIO-017 emphasizes cellular and anatomical detail.
• B/B (Endocrine System BIO-018): Overlap with Biology endocrine coverage — hormone classes, feedback loops, and gland functions; PS-001 focuses on behavioral effects of hormones (stress, reproduction, metabolism) and endocrine-disorder behavioral manifestations.
• B/B (Genetics BIO-012): Mendelian and population genetics from Biology underpin behavioral genetics; PS-001 extends to heritability, twin studies, and gene-environment interactions for behavioral traits.

Common confusions

• Confusing sympathetic and parasympathetic effects. Sympathetic triggers ‘fight-or-flight’ — pupils dilate, heart rate increases, digestion is inhibited. Parasympathetic triggers ‘rest-and-digest’ — pupils constrict, heart rate slows, digestion is stimulated. A common MCAT trap describes a physiological state and asks which branch is active.
• Thinking dopamine only does reward. Dopamine also controls motor function (substantia nigra degeneration = Parkinson’s) and prolactin inhibition. The MCAT will test whether you know that excess dopamine is linked to schizophrenia (positive symptoms) while dopamine loss causes Parkinson’s motor symptoms.
• Mixing up Broca’s and Wernicke’s areas. Broca’s = speech production (frontal lobe, ‘Broca’s Broken speech’ — non-fluent aphasia). Wernicke’s = language comprehension (temporal lobe, ‘Wernicke’s Word salad’ — fluent but meaningless speech). Both are typically in the left hemisphere.
• Forgetting that the hypothalamus controls the pituitary via the portal system for anterior pituitary but via direct neural connection for posterior pituitary. Anterior pituitary hormones are regulated by hypothalamic releasing/inhibiting hormones; posterior pituitary hormones (oxytocin, ADH) are synthesized in hypothalamic neurons and transported down axons.
• Misinterpreting heritability. h^2 = 0.8 for height does NOT mean 80% of an individual’s height comes from genes — it means 80% of the variance across individuals in that population is attributable to genetic differences. Heritability is population-specific and says nothing about an individual.
• Confusing absolute and relative refractory periods. During the absolute refractory period, NO stimulus can trigger an action potential because Na+ channels are inactivated. During the relative refractory period, a stronger-than-normal stimulus CAN trigger an action potential because K+ channels are still open (membrane is hyperpolarized) and some Na+ channels are available.
• Assuming excitatory neurotransmitters are ‘good’ and inhibitory are ‘bad’. Both are essential. GABA (inhibitory) prevents runaway excitation and seizures. Benzodiazepines and alcohol enhance GABA — their sedative effects come from increasing inhibition, not decreasing excitation.

Quick review

• Resting potential: -70 mV (Na+/K+ pump: 3 Na+ out, 2 K+ in). Threshold: ~-55 mV. Action potential phases: depolarization (Na+ in), repolarization (K+ out), hyperpolarization. Absolute refractory = Na+ channels inactivated, no firing possible.
• Key neurotransmitters: ACh (muscle, learning, autonomic), dopamine (reward, motor — Parkinson’s = low), serotonin (mood — SSRIs block reuptake), norepinephrine (alertness, sympathetic), GABA (inhibitory — benzos enhance), glutamate (excitatory — LTP), endorphins (pain).
• CNS = brain + spinal cord. PNS = somatic (voluntary) + autonomic (involuntary). Autonomic: sympathetic (fight-or-flight, NE) vs. parasympathetic (rest-and-digest, ACh). Sympathetic: pupils dilate, HR up, bronchi dilate, digestion inhibited.
• Brain lobes: frontal (executive function, Broca’s area, motor cortex), parietal (somatosensory, spatial), temporal (auditory, Wernicke’s, hippocampus), occipital (vision). Left hemisphere = language in most; right = spatial.
• Hippocampus = episodic memory (HM case). Amygdala = fear/emotion. Thalamus = sensory relay (all except smell). Hypothalamus = homeostasis, controls pituitary. Cerebellum = motor coordination, procedural memory. Basal ganglia = motor, habits.
• HPA axis: hypothalamus (CRH) -> anterior pituitary (ACTH) -> adrenal cortex (cortisol). Cortisol increases blood glucose, suppresses immune function. Chronic stress elevates cortisol. Anterior pituitary: GH, TSH, ACTH, FSH, LH, prolactin. Posterior pituitary: oxytocin, ADH.
• Insulin (beta cells, pancreas) = lowers blood glucose. Glucagon (alpha cells) = raises blood glucose. Type 1 DM = no insulin (autoimmune beta cell destruction). Type 2 DM = insulin resistance.
• Heritability (h^2) = proportion of phenotypic variance due to genetic variance — population-specific, not individual. Twin studies: compare MZ vs. DZ concordance. Polygenic = many genes, small effects. Epigenetics: DNA methylation (silences), histone acetylation (opens chromatin).
• LTP = cellular learning mechanism. High-frequency stimulation -> AMPA receptor phosphorylation + insertion -> stronger synapse. Hebb’s rule: ‘neurons that fire together, wire together.’ Synaptic pruning: use-dependent elimination during development.
• Broca’s aphasia: non-fluent, broken speech (frontal). Wernicke’s aphasia: fluent but meaningless, word salad (temporal). Split-brain: object in left visual field cannot be named (goes to right hemisphere, no language).
• Monoamine hypothesis of mood: depression linked to low serotonin, NE, and dopamine. SSRIs block serotonin reuptake transporter. Neurotransmitter clearance: enzymatic degradation (AChE), reuptake, diffusion.
• Somatic nervous system: one motor neuron from CNS to skeletal muscle, ACh, always excitatory. Autonomic: two-neuron chain (pre- and post-ganglionic). Sympathetic: short pre, long post (NE except sweat = ACh). Parasympathetic: long pre, short post (ACh).