Synaptic Transmission

Synaptic Transmission and Neurotransmitters

What is a Synapse?

A synapse is the junction between two neurons (or between a neuron and a muscle/gland). Electrical signals cannot jump the gap — they are converted to chemical signals.

There are two types:

Chemical synapse (most common): uses neurotransmitter molecules
Electrical synapse (gap junctions): ions flow directly — faster but less flexible

Steps of Synaptic Transmission

Step 1 — Action potential arrives

The electrical signal (action potential) travels down the axon to the presynaptic terminal (axon terminal / bouton).

Step 2 — Ca²⁺ enters

Depolarisation opens voltage-gated Ca²⁺ channels. Ca²⁺ rushes into the terminal (concentration is 10,000× higher outside).

Ca²⁺ is the trigger — without it, no neurotransmitter is released.

Step 3 — Vesicle fusion (exocytosis)

Ca²⁺ binds to proteins (synaptotagmin) on synaptic vesicles. Vesicles fuse with the presynaptic membrane and release neurotransmitter (NT) into the synaptic cleft by exocytosis.

Release is quantal — each vesicle releases a fixed packet ("quantum") of NT. Miniature end-plate potentials (mEPPs) are spontaneous single-vesicle releases.

Step 4 — Diffusion across the cleft

NT molecules diffuse across the synaptic cleft (~20–40 nm wide) — takes <1 ms.

Step 5 — Receptor binding on postsynaptic membrane

NT binds to receptors on the postsynaptic cell:

Ionotropic receptors (fast): NT directly opens ion channels → immediate response
Metabotropic receptors (slow): NT activates G-proteins → second messenger cascade → slower, longer response

Step 6 — Postsynaptic potential

EPSP (Excitatory Postsynaptic Potential): Na⁺ flows in → depolarisation → moves toward action potential threshold
IPSP (Inhibitory Postsynaptic Potential): Cl⁻ flows in or K⁺ flows out → hyperpolarisation → moves away from threshold

Step 7 — NT Removal (termination)

NT must be cleared so the signal can end cleanly:

Reuptake — NT pumped back into the presynaptic neuron (most common for dopamine, serotonin, noradrenaline)
Enzymatic degradation — e.g., acetylcholinesterase breaks acetylcholine into choline + acetate in the cleft
Diffusion — NT drifts away from the synapse

Summation — How Signals Are Integrated

A single EPSP is rarely enough to fire a new action potential. The postsynaptic neuron adds up (integrates) inputs:

Type	Description
Temporal summation	Same presynaptic neuron fires rapidly → multiple EPSPs add up over time
Spatial summation	Multiple different presynaptic neurons fire simultaneously → EPSPs add up across space

If the membrane reaches threshold (typically −55 mV), an action potential fires.

Key Neurotransmitters

NT	Main role	Where
Acetylcholine	Excitatory at NMJ; both E and I in CNS	All motor neurons, many brain regions
Glutamate	Main excitatory NT in brain	Most CNS synapses
GABA	Main inhibitory NT in brain	Throughout CNS
Dopamine	Reward, movement	Substantia nigra, striatum
Serotonin	Mood, sleep	Raphe nuclei
Noradrenaline	Arousal, fight-or-flight	Locus coeruleus

Drugs and Toxins at the Synapse

Agent	Mechanism	Effect
SSRIs (Prozac)	Block serotonin reuptake	More serotonin in cleft → elevated mood
Caffeine	Blocks adenosine receptors	Prevents drowsiness signal
Nicotine	Binds acetylcholine receptors	Stimulates reward pathway
Botulinum toxin	Blocks vesicle release	No acetylcholine → muscle paralysis
Curare	Blocks acetylcholine receptor at NMJ	Flaccid paralysis (used in surgery)

NEET/JEE Focus Points

Ca²⁺ is the trigger for vesicle fusion — not depolarisation directly
EPSP vs IPSP: know which ions cause each and the direction of current flow
Temporal vs spatial summation — both needed for NEET MCQs
Acetylcholinesterase at NMJ — why myasthenia gravis and organophosphate poisoning are related
Reuptake inhibition → prolonged NT in cleft (basis of most psychiatric drugs)
Botulinum toxin blocks Ca²⁺-triggered exocytosis — not the channels themselves

Synaptic Transmission