# Synapse Physiology > Synapse physiology in MBBS Physiology: chemical transmission, EPSP IPSP properties, summation, inhibition types and toxin targets. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/synapse-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Synapse Physiology", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/synapse-physiology ## Direct answer A chemical synapse converts a presynaptic action potential into transmitter release and a graded postsynaptic response: calcium entry through voltage-gated channels triggers SNARE-mediated vesicle fusion, transmitter diffuses across the 20-30 nanometre cleft, and receptor binding opens ion channels that generate either an excitatory postsynaptic potential (EPSP, sodium-potassium influx, about 0.5-1 mV, depolarising) or an inhibitory postsynaptic potential (IPSP, chloride influx or potassium efflux, hyperpolarising). Because single potentials are subthreshold, the axon hillock — the lowest-threshold zone of the neuron — integrates hundreds of inputs by spatial and temporal summation. The 0.5 millisecond synaptic delay, one-way conduction, fatigue, and post-tetanic potentiation are defining properties with clinical and toxin logic attached. ## What you must remember - **Sequence at the terminal:** depolarisation opens calcium channels; calcium (the only trigger that matters) binds synaptotagmin; SNARE complexes (synaptobrevin, syntaxin, SNAP-25) fuse vesicles; transmitter releases in quanta. - **EPSP versus IPSP:** EPSP from nonspecific cation (mainly sodium) influx — glutamate centrally; IPSP from chloride influx or potassium efflux — GABA and glycine; both are graded, local, decremental potentials, not all-or-none. - **Summation:** spatial (many synapses at once) and temporal (rapid succession before decay) — the axon hillock fires when the sum reaches threshold; the neuron is a tiny computer voting on its inputs. - **Properties worth quoting:** one-way conduction, synaptic delay about 0.5 ms (used classically to estimate chain neuron numbers), susceptibility to fatigue (the basis of post-synaptic "filtering" and habituation), post-tetanic potentiation (residual calcium after high-frequency firing, a memory substrate), and occlusion with subliminal fringe in pool experiments. - **Inhibition types:** postsynaptic (IPSP via GABA-A or glycine), presynaptic (axo-axonic GABA-B reducing calcium entry into the primary terminal — no IPSP in the postsynaptic cell, just smaller EPSPs), recurrent or Renshaw cell inhibition (motor collateral excites the Renshaw cell, which glycine-inhibits the same motor neuron — lateral surround sharpening), and reciprocal inhibition in reflex arcs. - **Toxin map:** botulinum toxin cleaves SNAREs (synaptobrevin, SNAP-25) blocking acetylcholine release — flaccid paralysis; tetanus toxin travels retrogradely and cleaves synaptobrevin in inhibitory terminals of the cord — spastic paralysis from disinhibition; black widow spider alpha-latrotoxin pores the terminal and dumps transmitter. - **Plasticity:** long-term potentiation at hippocampal CA1 needs NMDA receptor calcium entry (coincidence detector: depolarisation plus glutamate), the cellular handmaiden of memory; conversely, low-frequency stimulation can depress a synapse. ## How to work through a synaptic pharmacology case Consider why tetanus and botulism look opposite while attacking the same machinery. Botulinum protease enters cholinergic terminals and stops vesicle fusion: no acetylcholine at the neuromuscular junction, so descending weakness, ptosis and dysphagia — flaccid. Tetanus toxin rides the same retrograde transport into the spinal cord but cleaves synaptobrevin inside inhibitory interneuron terminals releasing glycine and GABA: the motor neurons, released from Renshaw and reciprocal inhibition, fire unopposed — lockjaw, opisthotonus, spasms from trivial stimuli. One molecular action, two clinical universes, decided by which transmitter is silenced where. Now the anaesthetic bridge: benzodiazepines and barbiturates potentiate GABA-A (longer chloride channel opening, bigger IPSPs — anxiolysis, sedation, anticonvulsant action), while propofol acts on the same receptor's different site; neuromuscular blockers act at the far more accessible peripheral synapse. In status epilepticus, the physiology explains the ladder — benzodiazepines amplify inhibition; if the synapse is saturated, phenytoin attacks sodium channels to limit the high-frequency firing that summation requires. A patient with stiff-person syndrome (anti-GAD antibodies, less GABA synthesis) shows what the cord does when inhibition fails spontaneously: rigidity and painful spasms, improved by benzodiazepines and baclofen. ## Where students slip Students describe the IPSP as "less excitation"; it is an active hyperpolarisation or stabilisation toward the chloride equilibrium potential — a real signal, not an absence. The second slip is presynaptic versus postsynaptic inhibition: presynaptic inhibition produces no hyperpolarisation of the soma at all (the primary terminal simply releases less transmitter because its calcium entry is cut), so an intracellular electrode would show a smaller EPSP and nothing else — a classic figure interpretation. Finally, in the delay question, keep the arithmetic honest: a reflex taking 2 ms central time implies about four synapses at 0.5 ms each, the way Sherrington-era physiology actually estimated circuitry — quotable exam arithmetic. ## Frequently asked questions ### What triggers neurotransmitter release at the presynaptic terminal? Depolarisation opens voltage-gated calcium channels, and calcium entry — the one and only trigger — drives SNARE-complex vesicle fusion with the active zone membrane, releasing transmitter quanta. ### How do EPSPs and IPSPs differ in ionic basis? EPSPs arise from nonspecific cation (chiefly sodium) influx through glutamate-gated channels, depolarising towards threshold; IPSPs arise from chloride influx or potassium efflux through GABA-A or glycine channels, hyperpolarising or clamping the membrane. ### What is presynaptic inhibition and how does it differ from postsynaptic? Axo-axonic synapses (GABA-B) reduce calcium entry into the presynaptic terminal, shrinking transmitter release — no IPSP is recorded in the postsynaptic cell, unlike postsynaptic inhibition's hyperpolarisation. ### Why does tetanus toxin cause spasm while botulinum causes flaccidity? Both cleave SNARE proteins, but botulinum acts at the cholinergic neuromuscular junction (no acetylcholine, flaccid paralysis) while tetanus blocks glycine and GABA release in the spinal cord (loss of inhibition, spastic paralysis). ### What is post-tetanic potentiation? After high-frequency stimulation, residual calcium in the presynaptic terminal amplifies subsequent release for minutes — a short-term plasticity mechanism that contributes to memory formation at synapses like hippocampal CA1.