Homeβ€ΊPhysiologyβ€ΊπŸ§  Neurophysiology
🧠 Physiology · Neuro

Memory tricks for neurophysiology

Action potentials, synaptic transmission, neurotransmitters, and sensory coding.

Community
πŸ“‹
Neuro Forum
Ask questions Β· Share techniques
πŸ’¬
Neuro Study Room
Live Β· Study together now
🧠 Neurophysiology

Memory Tricks

Proven Mnemonics & Acronyms β€” fast to learn, hard to forget.

Synaptic Transmission
SAVE β€” Synthesis Β· Action potential Β· Vesicle release Β· Effect on target
Four steps of synaptic transmission in order
How one neuron communicates with the next β€” step by step
Neurotransmitter Synthesis: produced in the presynaptic neuron and stored in vesicles. Action potential arrives at axon terminal β†’ depolarization opens voltage-gated Ca2+ channels β†’ Ca2+ flows in. Vesicle fusion: calcium triggers vesicle fusion with presynaptic membrane β†’ neurotransmitter released into synaptic cleft. Effect: neurotransmitter binds postsynaptic receptors β†’ 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 β†’ voltage-gated Ca2+ channels open β†’ Ca2+ enters terminal.
Vesicle release
Ca2+ triggers exocytosis β†’ NT into synaptic cleft.
Effect
NT binds postsynaptic receptor β†’ ion channels open β†’ EPSP or IPSP.
Termination
Reuptake (most NTs), enzymatic degradation (ACh by AChE), diffusion.
Difficulty: Intermediate
Key Neurotransmitters
GADSEND β€” GABA Β· ACh Β· Dopamine Β· Serotonin Β· Epinephrine Β· Norepinephrine Β· Glutamate
Seven major neurotransmitters and their primary roles
The major neurotransmitters β€” function, location, and clinical significance
GABA: main inhibitory NT in CNS β€” benzodiazepines and alcohol enhance GABA. Acetylcholine (ACh): NMJ, parasympathetic, basal ganglia β€” Alzheimer's = ACh deficiency. Dopamine: reward, movement, motivation β€” Parkinson's = low dopamine, schizophrenia = excess. Serotonin: mood, sleep, appetite β€” SSRIs block reuptake for depression. Epinephrine/Norepinephrine: fight or flight, alertness. Glutamate: main excitatory NT in CNS β€” excess causes excitotoxicity.
GABA
Main CNS inhibitory NT. Benzos, barbiturates, alcohol all enhance GABA.
ACh
NMJ + parasympathetic. Alzheimer's = low ACh. Blocked by anticholinergics.
Dopamine
Reward + movement. Low = Parkinson's. High = schizophrenia.
Serotonin
Mood + sleep + appetite. Low = depression. SSRIs most prescribed antidepressants.
Glutamate
Main excitatory NT. Excess β†’ excitotoxicity β†’ neuronal death (stroke, TBI).
Difficulty: Intermediate
EPSP vs IPSP
EPSP Excites (depolarizes) Β· IPSP Inhibits (hyperpolarizes)
Excitatory postsynaptic potential Β· Inhibitory postsynaptic potential
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 β€” 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 β†’ action potential fires. Neurons integrate hundreds of EPSPs and IPSPs simultaneously β€” the balance determines output.
EPSP
Depolarizing β€” Na+ or Ca2+ influx. Moves membrane toward threshold (-55 mV).
IPSP
Hyperpolarizing β€” K+ efflux or Cl- influx. Moves membrane away from threshold.
Spatial summation
Multiple synapses fire at same time β€” potentials add up.
Temporal summation
Same synapse fires rapidly β€” potentials accumulate before decaying.
Axon hillock
Integration zone β€” where summation is assessed and AP initiated if threshold reached.
Difficulty: Intermediate
Nerve Fiber Types
A-B-C β€” Large fast Β· Medium Β· Small slow
A fibers (myelinated, fast) Β· B fibers (myelinated, autonomic) Β· C fibers (unmyelinated, slow)
Three nerve fiber types β€” size, myelination, and conduction speed
Nerve conduction velocity depends on diameter and myelination. A fibers (largest, heavily myelinated): AΞ± = proprioception and motor (fastest, 70–120 m/s), AΞ² = touch and pressure, AΞ΄ = 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) β€” explains why you feel pressure but not pain after injection.
AΞ± fibers
Proprioception + motor. Fastest (70–120 m/s). Largest diameter.
AΞ΄ fibers
Sharp fast pain + cold. Medium speed. First pain you feel after injury.
C fibers
Slow burning pain + warmth. Slowest (0.5–2 m/s). Unmyelinated.
Local anesthetic
Blocks C fibers first β†’ pain gone. A fibers last β†’ touch/pressure preserved.
Difficulty: Advanced
Salutatory Conduction
AP jumps node to node β€” faster than continuous conduction
Myelin speeds conduction by forcing AP to jump between nodes of Ranvier
Why myelinated nerves are faster β€” the saltatory conduction advantage
In unmyelinated fibers, the action potential must regenerate at every point along the membrane β€” slow and energy intensive. In myelinated fibers, myelin insulates the membrane between nodes of Ranvier. The action potential depolarizes one node β†’ electrical current flows through the axoplasm to the next node β†’ 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 β†’ slowed or blocked conduction β†’ motor and sensory deficits.
Nodes of Ranvier
Gaps in myelin sheath β€” only place AP can occur in myelinated fibers.
Speed advantage
Myelinated: 70–120 m/s. Unmyelinated: 0.5–2 m/s. ~100Γ— faster.
Energy advantage
Fewer ion pumps needed β€” Na+/K+ ATPase only works at nodes.
Multiple sclerosis
Autoimmune demyelination β†’ conduction slows/blocks β†’ weakness, vision loss, sensory changes.
Difficulty: Intermediate
Pain Pathways
Two pains β€” Fast sharp (AΞ΄) Β· Slow burning (C) Β· Both cross and ascend
Lateral spinothalamic tract carries pain and temperature signals
How pain signals travel from body to brain β€” and why this matters clinically
Pain receptors (nociceptors) β†’ AΞ΄ fibers (fast, sharp pain) or C fibers (slow, burning pain) β†’ dorsal horn of spinal cord β†’ cross the midline immediately β†’ ascend in the lateral spinothalamic tract β†’ thalamus β†’ 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 β€” 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.
AΞ΄ fibers
Fast sharp pain β€” first sensation after injury. Precise localization.
C fibers
Slow burning pain β€” follows AΞ΄. Diffuse, harder to localize.
Crosses immediately
At spinal cord level β†’ contralateral spinothalamic tract.
Gate control theory
AΞ² (touch) fibers can inhibit pain in dorsal horn β€” why rubbing an injury helps.
Difficulty: Advanced
Stretch Reflex
Tap β†’ Stretch β†’ Ia β†’ Alpha motor β†’ Contract β€” monosynaptic
Muscle spindle detects stretch β†’ Ia afferent β†’ alpha motor neuron β†’ muscle contraction
The stretch reflex β€” the only monosynaptic reflex in the body
The stretch reflex (myotatic reflex) is the simplest reflex arc β€” only one synapse between afferent and efferent. Tendon tap stretches the muscle β†’ muscle spindle (intrafusal fiber) detects stretch β†’ Ia afferent fiber fires β†’ directly synapses on alpha motor neuron in ventral horn β†’ 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.
Muscle spindle
Intrafusal fibers β€” detect muscle length change. Runs parallel to muscle.
Ia afferent
Fastest sensory fiber β€” carries stretch info to spinal cord.
Monosynaptic
Only one synapse β€” Ia directly onto alpha motor neuron. Fastest reflex.
Hyperreflexia
UMN lesion (above spinal cord) β€” removes descending inhibition β†’ exaggerated reflexes.
Hyporeflexia
LMN lesion (at or below spinal cord) β€” arc interrupted β†’ absent or diminished reflexes.
Difficulty: Intermediate
Autonomic Nervous System
Sympathetic = Short pre, Long post Β· 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 β†’ ganglion β†’ postganglionic β†’ 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 β€” sympathetic but use ACh (not NE) as postganglionic NT.
Adrenal medulla
Modified sympathetic ganglion β€” releases epinephrine and NE directly to blood.
Difficulty: Advanced
EEG Brain Waves
BDAT β€” Beta Β· Delta Β· Alpha Β· Theta β€” frequency order high to low
Beta (alert) Β· Alpha (relaxed) Β· Theta (drowsy) Β· Delta (deep sleep)
Four EEG wave types β€” what each state of consciousness looks like
Beta waves (13–30 Hz): alert, active thinking, problem solving β€” low amplitude, high frequency. Alpha waves (8–12 Hz): relaxed, eyes closed, calm β€” 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) β€” 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).
Beta (13–30 Hz)
Active thinking, alert, anxious. Low amplitude. Frontal lobe dominant.
Alpha (8–12 Hz)
Relaxed, eyes closed. Blocked by eye opening or mental activity.
Theta (4–7 Hz)
Drowsiness, early sleep, deep meditation. Children have more theta.
Delta (0.5–3 Hz)
Deep NREM sleep. Growth hormone released during delta sleep.
Difficulty: Intermediate
Neurotransmitter Types
GABS β€” Glutamate Β· Acetylcholine Β· GABA Β· Serotonin/Dopamine
πŸ“Œ Synaptic Signaling
Key neurotransmitters and whether they excite or inhibit postsynaptic neurons
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.
GGlutamate β€” main excitatory CNS
AACh β€” NMJ, memory, ANS
BGABA β€” main inhibitory CNS
SSerotonin/Dopamine β€” mood/reward
Sympathetic vs Parasympathetic
Fight-or-Flight vs Rest-and-Digest
πŸ“Œ Autonomic NS
SNS prepares for danger; PNS restores homeostasis β€” opposite effects on most organs
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.
SSNS = Stress β€” NE at effectors
PPNS = Peace β€” ACh throughout
Reflex Arc Components
SARIE β€” Stimulus Β· Afferent Β· Reflex center Β· Integration Β· Efferent response
πŸ“Œ Spinal Reflexes
A reflex arc has five components β€” no brain required for simple spinal reflexes
Receptor detects stimulus β†’ afferent (sensory) neuron carries signal β†’ integration center (spinal cord for simple reflexes) β†’ efferent (motor) neuron carries response β†’ effector (muscle/gland) acts. Monosynaptic reflex (patellar) has no interneuron; polysynaptic reflex does.
SStimulus triggers receptor
AAfferent = sensory neuron
RReflex center = integration
IIntegration β†’ decision
EEfferent β†’ effector response
Brain Lobes and Functions
FTOP β€” Frontal thinks Β· Temporal hears Β· Occipital sees Β· Parietal touches
πŸ“Œ Cerebral Cortex
Four cerebral lobes and their primary functions for the boards
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.
FFrontal β€” thinking, motor, Broca's
TTemporal β€” hearing, Wernicke's
OOccipital β€” vision
PParietal β€” touch, spatial
🎓 Common Exam Questions
Q: Describe the ionic basis of the action potential β€” what happens at each phase?
A: Resting membrane potential: ~βˆ’70 mV (K+ leaks out, Na+/K+ ATPase maintains gradient). Threshold: ~βˆ’55 mV. Depolarization: voltage-gated Na+ channels open β†’ Na+ rushes in β†’ membrane potential shoots to ~+30 mV. Repolarization: Na+ channels inactivate (absolute refractory) + voltage-gated K+ channels open β†’ K+ rushes out β†’ potential falls. Hyperpolarization (afterhyperpolarization): K+ channels slow to close β†’ membrane briefly more negative than resting β†’ relative refractory period. Return to rest: Na+/K+ ATPase restores gradients.
Q: What is the difference between upper motor neuron (UMN) and lower motor neuron (LMN) lesions?
A: Lower Motor Neuron (LMN) lesion: damages the nerve directly innervating the muscle. Signs: flaccid paralysis, muscle atrophy, fasciculations, hyporeflexia/areflexia, decreased muscle tone. Example: polio, ALS (LMN component), peripheral nerve injury. Upper Motor Neuron (UMN) lesion: damages corticospinal tract above the anterior horn. Signs: spastic paralysis, hyperreflexia, Babinski sign (upgoing plantar reflex), increased muscle tone, no significant atrophy. Example: stroke, MS, spinal cord compression. Key: UMN controls LMN β€” lose UMN inhibition β†’ LMN overactive β†’ spasticity.
Q: How do the sympathetic and parasympathetic nervous systems differ in anatomy and neurotransmitters?
A: Sympathetic (thoracolumbar, T1–L2): short preganglionic (ACh β†’ nicotinic) β†’ paravertebral/prevertebral ganglia β†’ long postganglionic (NE β†’ adrenergic receptors). Exception: adrenal medulla directly innervated β†’ releases EPI/NE into blood. Parasympathetic (craniosacral, CN III/VII/IX/X + S2–S4): long preganglionic (ACh β†’ nicotinic) β†’ ganglia near/in target organ β†’ short postganglionic (ACh β†’ muscarinic). Both preganglionic use ACh at nicotinic receptors β€” only postganglionic SNS uses NE. Sweat glands are SNS but use ACh (muscarinic) β€” the exception.
Q: What are the major ascending and descending spinal cord tracts and what do they carry?
A: Ascending (sensory): Dorsal columns/medial lemniscus: fine touch, vibration, proprioception β€” ipsilateral until medulla, then cross. Spinothalamic tract: pain and temperature β€” cross within 1–2 levels of entry (contralateral). Descending (motor): Corticospinal tract (pyramidal): voluntary motor control β€” crosses in medulla (pyramidal decussation) β†’ contralateral. Clinical: Brown-SΓ©quard syndrome (hemisection): ipsilateral motor loss + proprioception loss, contralateral pain/temp loss. Syringomyelia: central cord lesion β†’ bilateral loss of pain/temp at that level (anterior white commissure damaged).
Q: What are the major neurotransmitter systems and their associated diseases/drugs?
A: Dopamine: nigrostriatal (movement) β€” Parkinson's = loss of dopamine neurons; mesolimbic (reward) β€” schizophrenia = excess dopamine; treated with antipsychotics (D2 blockers). Serotonin: mood, sleep, appetite β€” depression treated with SSRIs. Norepinephrine: arousal, attention β€” depleted in depression; SNRIs increase both NE and serotonin. ACh: NMJ (nicotinic) β€” myasthenia gravis = antibodies against AChR; CNS (muscarinic) β€” Alzheimer's = loss of cholinergic neurons in basal forebrain. GABA: inhibitory β€” benzodiazepines enhance GABA (↑ frequency of Clβˆ’ channel opening); barbiturates enhance GABA (↑ duration). Glutamate: excitatory β€” NMDA receptor blocked by Mg2+ (removed by depolarization) β€” role in LTP and memory.