Memory tricks for neurophysiology

Neurotransmitter Synthesis: produced in the presynaptic neuron and stored in vesicles. Action potential arrives at axon terminal → depolarization opens voltage-gated Ca2+ channels → Ca2+ flows in. Vesicle fusion: calcium triggers vesicle fusion with presynaptic membrane → neurotransmitter released into synaptic cleft. Effect: neurotransmitter binds postsynaptic receptors → EPSP (excitatory) or IPSP (inhibitory). Neurotransmitter then removed by reuptake, enzymatic degradation, or diffusion.

GABA: main inhibitory NT in CNS — benzodiazepines and alcohol enhance GABA. Acetylcholine (ACh): NMJ, parasympathetic, basal ganglia — Alzheimer's = ACh deficiency. Dopamine: reward, movement, motivation — Parkinson's = low dopamine, schizophrenia = excess. Serotonin: mood, sleep, appetite — SSRIs block reuptake for depression. Epinephrine/Norepinephrine: fight or flight, alertness. Glutamate: main excitatory NT in CNS — excess causes excitotoxicity.

EPSPs depolarize the postsynaptic membrane (bring it closer to threshold). IPSPs hyperpolarize the membrane (move it away from threshold). Neither alone usually causes an action potential — summation is required. Spatial summation: multiple synapses firing simultaneously. Temporal summation: same synapse fires repeatedly in rapid succession. If combined summation reaches threshold (-55 mV) at the axon hillock → action potential fires. Neurons integrate hundreds of EPSPs and IPSPs simultaneously — the balance determines output.

Nerve conduction velocity depends on diameter and myelination. A fibers (largest, heavily myelinated): Aα = proprioception and motor (fastest, 70–120 m/s), Aβ = touch and pressure, Aδ = sharp/fast pain and temperature. B fibers: preganglionic autonomic, moderately myelinated. C fibers (smallest, unmyelinated, slowest 0.5–2 m/s): slow/burning pain, temperature, postganglionic autonomic. Local anesthetics block C fibers first (pain gone) before A fibers (touch preserved) — explains why you feel pressure but not pain after injection.

In unmyelinated fibers, the action potential must regenerate at every point along the membrane — slow and energy intensive. In myelinated fibers, myelin insulates the membrane between nodes of Ranvier. The action potential depolarizes one node → electrical current flows through the axoplasm to the next node → action potential regenerates at the next node. This "jumping" (saltus = jump in Latin) dramatically increases conduction speed and reduces ATP consumption. Multiple sclerosis destroys myelin → slowed or blocked conduction → motor and sensory deficits.

Pain receptors (nociceptors) → Aδ fibers (fast, sharp pain) or C fibers (slow, burning pain) → dorsal horn of spinal cord → cross the midline immediately → ascend in the lateral spinothalamic tract → thalamus → somatosensory cortex. Because pain fibers cross at the spinal level, a spinal cord lesion on one side causes pain/temperature loss on the OPPOSITE side — while fine touch (DCML) is lost on the SAME side. This dissociation helps localize spinal cord lesions. Opioids act on receptors in the dorsal horn to reduce pain transmission.

The stretch reflex (myotatic reflex) is the simplest reflex arc — only one synapse between afferent and efferent. Tendon tap stretches the muscle → muscle spindle (intrafusal fiber) detects stretch → Ia afferent fiber fires → directly synapses on alpha motor neuron in ventral horn → muscle contracts. Simultaneously, Ia fiber sends inhibitory signal to antagonist muscle (reciprocal inhibition). Clinically tests the integrity of the reflex arc. Hyperreflexia = upper motor neuron lesion. Hyporeflexia = lower motor neuron or sensory lesion.

Both divisions have a two-neuron chain: preganglionic → ganglion → postganglionic → effector. Sympathetic: preganglionic neurons in thoracolumbar (T1–L2) spinal cord. Short preganglionic fibers synapse in paravertebral ganglia close to spinal cord. Long postganglionic fibers reach effectors. Neurotransmitters: ACh (preganglionic), norepinephrine (postganglionic, except sweat glands which use ACh). Parasympathetic: craniosacral outflow (CN III, VII, IX, X and S2–S4). Long preganglionic fibers reach ganglia near or in effector organ. Short postganglionic fibers. Both pre and postganglionic use ACh.

Beta waves (13–30 Hz): alert, active thinking, problem solving — low amplitude, high frequency. Alpha waves (8–12 Hz): relaxed, eyes closed, calm — classic "meditation waves." Theta waves (4–7 Hz): drowsiness, early sleep, deep meditation. Delta waves (0.5–3 Hz): deepest sleep (stages 3–4 NREM) — highest amplitude, lowest frequency. Clinical note: spike-and-wave discharges on EEG indicate epilepsy. Burst suppression pattern indicates deep anesthesia or severe brain injury. Alpha waves disappear when eyes are opened (alpha block).

Glutamate: main excitatory NT in CNS. GABA: main inhibitory NT in CNS (benzodiazepines enhance it). Acetylcholine: NMJ, ANS, memory (Alzheimer's involves ACh loss). Dopamine: reward, movement (Parkinson's = dopamine loss). Serotonin: mood, sleep (SSRIs target it). Norepinephrine: fight-or-flight arousal.

SNS (fight-or-flight): ↑ HR, ↑ BP, dilate pupils, bronchodilation, inhibit digestion, release glucose. Uses NE at effectors. PNS (rest-and-digest): ↓ HR, ↓ BP, constrict pupils, bronchoconstriction, promote digestion, conserve energy. Uses ACh at all synapses.

Receptor detects stimulus → afferent (sensory) neuron carries signal → integration center (spinal cord for simple reflexes) → efferent (motor) neuron carries response → effector (muscle/gland) acts. Monosynaptic reflex (patellar) has no interneuron; polysynaptic reflex does.

Frontal: motor cortex, executive function, Broca's area (speech production). Temporal: auditory cortex, Wernicke's area (language comprehension), memory (hippocampus). Parietal: somatosensory cortex, spatial awareness. Occipital: primary visual cortex.