Free MCAT study guide — Psychological, Social, and Biological Foundations of Behavior
The biological basis of behavior is a foundational topic in MCAT psychology, connecting neuroscience to psychological phenomena. You need to understand the organization of the nervous system (central vs. peripheral, somatic vs. autonomic, sympathetic vs. parasympathetic), the structure and function of neurons (dendrites, soma, axon, myelin, nodes of Ranvier), the action potential (resting potential, depolarization, repolarization, refractory periods), synaptic transmission, and the major neurotransmitter systems. Brain anatomy is high-yield: you must know the functions of the major brain regions including the cerebral cortex (frontal, parietal, temporal, occipital lobes), subcortical structures (thalamus, hypothalamus, basal ganglia, limbic system including hippocampus and amygdala), the cerebellum, and the brainstem. The MCAT tests your ability to predict behavioral deficits from brain lesions, understand the effects of drugs that alter neurotransmitter function, and connect neural mechanisms to psychological phenomena like memory, emotion, and motivation.
Neurons are the functional units of the nervous system, consisting of dendrites (receive signals), the cell body/soma (contains the nucleus and integrates signals), the axon (conducts signals as action potentials), and axon terminals (release neurotransmitters). The resting membrane potential is approximately -70 mV, maintained by the Na+/K+ ATPase (3 Na+ out, 2 K+ in) and resting potassium leak channels. When a stimulus depolarizes the membrane to threshold (approximately -55 mV), voltage-gated sodium channels open, causing rapid depolarization to approximately +30 mV. Sodium channels then inactivate, and voltage-gated potassium channels open, causing repolarization. Hyperpolarization occurs briefly as potassium channels close slowly. The absolute refractory period (during depolarization and early repolarization) prevents firing regardless of stimulus strength; the relative refractory period allows firing only with a stronger-than-normal stimulus. Action potentials follow the all-or-none principle: they either fire fully or not at all. Signal strength is encoded by firing frequency, not amplitude. Myelination by oligodendrocytes (CNS) or Schwann cells (PNS) increases conduction velocity through saltatory conduction at nodes of Ranvier.
Synaptic transmission occurs at chemical synapses. When an action potential reaches the axon terminal, voltage-gated calcium channels open, and calcium influx triggers exocytosis of neurotransmitter-containing vesicles into the synaptic cleft. Neurotransmitters bind postsynaptic receptors, causing either excitatory postsynaptic potentials (EPSPs, depolarization toward threshold) or inhibitory postsynaptic potentials (IPSPs, hyperpolarization away from threshold). Temporal summation occurs when multiple signals arrive at the same synapse in quick succession; spatial summation occurs when signals arrive from multiple synapses simultaneously. If the summed potentials reach threshold at the axon hillock, an action potential fires. Neurotransmitter action is terminated by reuptake into the presynaptic neuron (via transporter proteins), enzymatic degradation in the cleft (e.g., acetylcholinesterase breaks down ACh), or diffusion away from the synapse. Understanding these mechanisms is essential for predicting drug effects: SSRIs block serotonin reuptake, increasing serotonin in the cleft; organophosphates inhibit acetylcholinesterase, prolonging ACh action.
Acetylcholine (ACh): excitatory at the neuromuscular junction (nicotinic receptors), involved in attention, arousal, and memory. Degeneration of cholinergic neurons in the basal forebrain is associated with Alzheimer disease. Dopamine: involved in reward/motivation (mesolimbic pathway), motor control (nigrostriatal pathway, degeneration causes Parkinson disease), and executive function (mesocortical pathway). Excess dopamine activity is associated with schizophrenia (dopamine hypothesis). Serotonin (5-HT): regulates mood, sleep, appetite, and pain. Low serotonin is associated with depression and anxiety; SSRIs are first-line antidepressants. Norepinephrine: arousal, alertness, fight-or-flight response. Released by the locus coeruleus and the adrenal medulla (as a hormone). GABA: the main inhibitory neurotransmitter in the CNS. Benzodiazepines and barbiturates enhance GABA action. Glutamate: the main excitatory neurotransmitter in the CNS. Involved in learning and memory (LTP). Excessive glutamate causes excitotoxicity. Endorphins: endogenous opioids that reduce pain and produce euphoria. Their receptors are targeted by opioid drugs (morphine, heroin).
The frontal lobe contains the primary motor cortex (precentral gyrus, voluntary movement), prefrontal cortex (executive functions: planning, decision-making, personality, working memory), and Broca's area (left hemisphere, speech production -- damage causes non-fluent/expressive aphasia). The parietal lobe contains the primary somatosensory cortex (postcentral gyrus, touch, pain, temperature, proprioception) and integrates sensory information for spatial awareness. The temporal lobe contains the primary auditory cortex, Wernicke's area (left hemisphere, language comprehension -- damage causes fluent/receptive aphasia), and the hippocampus (memory consolidation). The occipital lobe contains the primary visual cortex. Subcortical structures: the thalamus is the sensory relay station (all senses except olfaction); the hypothalamus regulates homeostasis, hunger, thirst, temperature, circadian rhythms, and controls the pituitary gland; the basal ganglia coordinate voluntary movement (damage causes Parkinson's or Huntington's); the amygdala processes fear and emotional memories; the hippocampus is critical for forming new declarative memories (damage causes anterograde amnesia, as in patient H.M.).
The autonomic nervous system (ANS) controls involuntary functions and has two divisions. The sympathetic nervous system (fight-or-flight) increases heart rate, dilates bronchioles, dilates pupils, inhibits digestion, stimulates glucose release, and redirects blood flow to skeletal muscles. It uses short preganglionic neurons (release ACh at nicotinic receptors) and long postganglionic neurons (release norepinephrine at adrenergic receptors). The exception is sweat glands, which receive sympathetic innervation but use ACh. The parasympathetic nervous system (rest-and-digest) decreases heart rate, constricts bronchioles, constricts pupils, stimulates digestion and salivation, and promotes energy storage. It uses long preganglionic neurons (ACh at nicotinic receptors) and short postganglionic neurons (ACh at muscarinic receptors). The vagus nerve (cranial nerve X) is the main parasympathetic nerve, innervating the heart, lungs, and GI tract. The two divisions generally have opposing effects, maintaining homeostasis through tonic control (both are active at baseline, not just one or the other).
Neuroplasticity is the brain's ability to reorganize by forming new neural connections. It is greatest during critical periods in development (such as language acquisition before puberty) but continues throughout life. Long-term potentiation (LTP) is the strengthening of synaptic connections with repeated use, believed to be the cellular basis of learning and memory. LTP involves increased AMPA receptor insertion, increased neurotransmitter release, and dendritic spine growth. Brain lateralization refers to the specialization of the two cerebral hemispheres. The left hemisphere is typically dominant for language (Broca's and Wernicke's areas), logic, and analytical processing. The right hemisphere is associated with spatial processing, facial recognition, emotional expression, and prosody (emotional tone of speech). The corpus callosum connects the two hemispheres. Split-brain studies (by Roger Sperry) on patients with a severed corpus callosum revealed lateralized functions: objects presented to the right visual field (processed by left hemisphere) can be verbally identified, while objects in the left visual field (right hemisphere) can be identified by touch but not named.
Resting potential: -70 mV. Threshold: -55 mV. Peak depolarization: +30 mV.
Na+/K+ ATPase: 3 Na+ out, 2 K+ in. Maintains resting potential.
Myelination increases conduction velocity through saltatory conduction.
All-or-none: action potentials fire fully or not at all. Intensity coded by frequency.
GABA: main inhibitory NT (CNS). Glutamate: main excitatory NT (CNS). ACh: excitatory at NMJ.
Dopamine pathways: mesolimbic (reward), nigrostriatal (motor), mesocortical (cognition).
Low serotonin -> depression. Excess dopamine -> schizophrenia. Low dopamine -> Parkinson's.
Broca's area: speech production (non-fluent aphasia). Wernicke's area: language comprehension (fluent aphasia).
Hippocampus: memory consolidation. Amygdala: fear/emotion. Thalamus: sensory relay (except smell).
Sympathetic: fight-or-flight (norepinephrine). Parasympathetic: rest-and-digest (ACh).
The hypothalamus controls the autonomic nervous system and the pituitary gland.
LTP: cellular basis of learning. Involves NMDA/AMPA glutamate receptors.
Left hemisphere: language, logic. Right hemisphere: spatial, emotional, facial recognition.
Confusing the absolute refractory period (cannot fire) with the relative refractory period (can fire with stronger stimulus).
Thinking the Na+/K+ ATPase directly generates the action potential -- it maintains the resting potential; voltage-gated channels generate the action potential.
Confusing Broca's aphasia (non-fluent, knows what to say but cannot produce speech) with Wernicke's aphasia (fluent but nonsensical, cannot comprehend language).
Assuming the sympathetic and parasympathetic systems are simply on/off switches -- both are tonically active, and the balance determines the physiological state.
Mixing up afferent (sensory, toward CNS) and efferent (motor, away from CNS) neurons.
Forgetting that all senses EXCEPT olfaction relay through the thalamus.
Confusing the hippocampus (memory formation) with the hypothalamus (homeostasis, hormones).
Create a neurotransmitter table with columns for: neurotransmitter, type (excitatory/inhibitory), location, functions, associated disorders, and relevant drugs. The MCAT frequently describes a drug's mechanism (e.g., 'blocks reuptake of serotonin') and asks you to predict its clinical use (antidepressant) or side effects. Practice predicting the consequences of damage to specific brain regions -- this is one of the most common question types.
Study brain anatomy using labeled diagrams and functional descriptions. For each region, know its location, function, and what happens when it is damaged. Practice connecting brain structures to the psychological concepts you have learned: the amygdala to fear conditioning, the hippocampus to declarative memory, the prefrontal cortex to decision-making and personality (Phineas Gage case study). Understanding these brain-behavior relationships is essential for integrating neuroscience with psychology on the MCAT.
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