Nerve conduction, synaptic transmission, neurotransmitters, sensory pathways, and reflexes — neurophysiology explains how the brain and nerves communicate. These memory tricks make the complex machinery of the nervous system stick.
Proven Mnemonics & Acronyms — fast to learn, hard to forget.
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Synaptic Transmission
SAVE — Synthesis · Action potential · Vesicle release · Effect on target
Four steps of synaptic transmission in order
How one neuron communicates with the next — step by step
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.
Synthesis
Neurotransmitter made and stored in presynaptic vesicles.
AP arrives
Depolarization → voltage-gated Ca2+ channels open → Ca2+ enters terminal.
Vesicle release
Ca2+ triggers exocytosis → NT into synaptic cleft.
Effect
NT binds postsynaptic receptor → ion channels open → EPSP or IPSP.
Termination
Reuptake (most NTs), enzymatic degradation (ACh by AChE), diffusion.
How synaptic potentials summate to determine if a neuron fires
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.
Hyperpolarizing — K+ efflux or Cl- influx. Moves membrane away from threshold.
Spatial summation
Multiple synapses fire at same time — potentials add up.
Temporal summation
Same synapse fires rapidly — potentials accumulate before decaying.
Axon hillock
Integration zone — where summation is assessed and AP initiated if threshold reached.
Nerve Fiber Types
A-B-C — Large fast · Medium · Small slow
A fibers (myelinated, fast) · B fibers (myelinated, autonomic) · C fibers (unmyelinated, slow)
Three nerve fiber types — size, myelination, and conduction speed
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.
Aα fibers
Proprioception + motor. Fastest (70–120 m/s). Largest diameter.
Aδ fibers
Sharp fast pain + cold. Medium speed. First pain you feel after injury.
Blocks C fibers first → pain gone. A fibers last → touch/pressure preserved.
Salutatory Conduction
AP jumps node to node — faster than continuous conduction
Myelin speeds conduction by forcing AP to jump between nodes of Ranvier
Why myelinated nerves are faster — the saltatory conduction advantage
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.
Nodes of Ranvier
Gaps in myelin sheath — only place AP can occur in myelinated fibers.
Two pains — Fast sharp (Aδ) · Slow burning (C) · Both cross and ascend
Lateral spinothalamic tract carries pain and temperature signals
How pain signals travel from body to brain — and why this matters clinically
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.
Aδ fibers
Fast sharp pain — first sensation after injury. Precise localization.
C fibers
Slow burning pain — follows Aδ. Diffuse, harder to localize.
Crosses immediately
At spinal cord level → contralateral spinothalamic tract.
Gate control theory
Aβ (touch) fibers can inhibit pain in dorsal horn — why rubbing an injury helps.
Stretch Reflex
Tap → Stretch → Ia → Alpha motor → Contract — monosynaptic
Muscle spindle detects stretch → Ia afferent → alpha motor neuron → muscle contraction
The stretch reflex — the only monosynaptic reflex in the body
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.
LMN lesion (at or below spinal cord) — arc interrupted → absent or diminished reflexes.
Autonomic Nervous System
Sympathetic = Short pre, Long post · Parasympathetic = Long pre, Short post
Preganglionic and postganglionic fiber length differences
Structural differences between sympathetic and parasympathetic divisions
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.
Sympathetic origin
Thoracolumbar T1–L2. Short pre, long post. NE postganglionic.
Parasympathetic origin
Craniosacral CN III/VII/IX/X + S2–S4. Long pre, short post. ACh throughout.
Exception
Sweat glands — sympathetic but use ACh (not NE) as postganglionic NT.
Adrenal medulla
Modified sympathetic ganglion — releases epinephrine and NE directly to blood.
EEG Brain Waves
BDAT — Beta · Delta · Alpha · Theta — frequency order high to low