Q: Name all 12 cranial nerves using the mnemonic, and give the function of each.
A: Mnemonic: 'Oh Oh Oh To Touch And Feel Very Good Velvet AH!' I Olfactory (smell), II Optic (vision β CN II damage β blindness), III Oculomotor (most eye movement, pupil constriction β damage β drooping eyelid/ptosis, dilated pupil), IV Trochlear (eye moves down and in), V Trigeminal (face sensation + chewing), VI Abducens (eye moves laterally β damage β can't look sideways), VII Facial (facial expression + taste front 2/3 tongue), VIII Vestibulocochlear (hearing + balance β damage β deafness or vertigo), IX Glossopharyngeal (taste + swallowing), X Vagus (parasympathetic to thorax/abdomen, voice β damage β hoarse voice, difficulty swallowing), XI Accessory (neck/shoulder muscles), XII Hypoglossal (tongue movements).
Q: Explain the action potential β what happens at each stage?
A: Resting potential (-70mV): Na+/K+ pump maintains 3 Na+ out, 2 K+ in per ATP. Depolarization: stimulus opens voltage-gated Na+ channels β Na+ rushes IN β membrane potential rises to +40mV (threshold = -55mV). Repolarization: Na+ channels close, voltage-gated K+ channels open β K+ rushes OUT β membrane returns toward -70mV. Hyperpolarization (undershoot): K+ channels close slowly β brief dip below -70mV. Refractory period: absolute (no AP possible β Na+ channels inactivated) then relative (strong stimulus can trigger AP). The Na+/K+ pump restores ion gradients. Saltatory conduction in myelinated axons: AP jumps node-to-node (nodes of Ranvier) β much faster than unmyelinated.
Q: What are the GASSED neurotransmitters and what is the role of each?
A: GASSED: GABA (gamma-aminobutyric acid β main inhibitory neurotransmitter; reduces neuronal excitability; benzodiazepines enhance GABA β anxiety relief). Acetylcholine (ACh β neuromuscular junction; learning/memory; parasympathetic; Alzheimer's involves ACh deficiency). Serotonin (mood, sleep, appetite, body temperature; SSRIs block its reuptake to treat depression). Substance P (pain signal transmission in spinal cord and brain). Endorphins (endogenous opioids β natural pain relief and euphoria; released by exercise). Dopamine (reward, motivation, motor control; Parkinson's = dopamine neuron loss in substantia nigra; cocaine blocks dopamine reuptake β euphoria).
Q: What is neuroplasticity and what is LTP (Long-Term Potentiation)?
A: Neuroplasticity is the brain's ability to reorganize by forming new neural connections throughout life β greatest in childhood but continues in adults. Hebbian learning: 'neurons that fire together, wire together' β simultaneous activity strengthens connections. LTP (Long-Term Potentiation) is the cellular mechanism of memory: repeated stimulation β NMDA receptors (N-methyl-D-aspartate β coincidence detectors requiring simultaneous pre- and postsynaptic activity) open β Ca2+ enters β AMPA receptors inserted into postsynaptic membrane β synapse becomes stronger and more responsive. LTP is blocked by alcohol (explaining memory blackouts) and enhanced by sleep (memory consolidation occurs during slow-wave and REM sleep).
Q: Compare the sympathetic and parasympathetic nervous systems.
A: Both are divisions of the autonomic nervous system (ANS) β part of the PNS (peripheral nervous system). Sympathetic (fight-or-flight): activated by stress/danger. Effects: increases heart rate, dilates airways, dilates pupils, redirects blood to muscles, inhibits digestion, releases adrenaline from adrenal medulla. Preganglionic neuron (short) β paravertebral ganglion β postganglionic (long). Neurotransmitters: ACh (preganglionic) β norepinephrine (postganglionic). Parasympathetic (rest-and-digest): active during rest. Effects: decreases heart rate, constricts pupils, promotes digestion, stimulates salivation. Preganglionic (long) β ganglion near target organ β postganglionic (short). Neurotransmitter: ACh at both synapses. Vagus nerve (CN X) carries most parasympathetic fibers.