Synapse Structure and Function

Transmission of an action potential across a chemical synapse involves a uni-directional release of molecules of neurotransmitter from pre-synaptic to post-synaptic membranes.

• Mitochondria are abundant in the synaptic button: release energy for refilling of synaptic vesicles and possibly for pumping of Ca2+ to re-establish Ca2+ concentration gradient across neurone membrane.
• Drugs and poisons may interfere with synaptic transmission by:

1. mimicry of neurotransmitter, e.g. nicotine mimics both acetylcholine (ACh) and noradrenaline
2. reduced degradation, e.g. cocaine inhibits re-uptake of noradrenaline
3. blocking receptors, e.g. Beta-blockers may help to control rapid heartbeat by blocking receptors on the heart muscle. These Beta-receptors are normally sensitive to adrenaline
4. reduced release of neurotransmitter, e.g. alcohol alters sleeping patterns by reducing release of serotonin

• Synaptic cleft represents a barrier to the direct passage of the wave of depolarisation from pre-synaptic to post-synaptic membranes.


1. Increase in local Ca2+ concentration: depolarisation of membrane at synaptic button affects 'calcium channels' so that Ca2+ ions flow quickly into synaptic button from tissue fluid.
2. Synaptic vesicles containing molecules of neurotransmitter move towards the presynaptic membrane. 
3. Neurotransmitter molecules diffuse across synaptic gap when synaptic vesicles fuse with pre-synaptic membrane. Molecules bind to stereospecific receptors in the post-synaptic membrane.
Catecholamines such as adrenaline are released from adrenergic nerve endings, acetylcholine from cholinergic nerve endings, and GABA (gamma-aminobutyric acid) and serotonin at synapses in the brain.
4. Chemically gated ion channels on post-synaptic membrane -- allow influx of Na+ and efflux of K+ --> depolarisation of post-synaptic membrane. Ion channels are 'opened' when triggered by binding of neurotransmitter.
5. Enzymes degrade neurotransmitter.
These degradative enzymes, which are released from adjacent glial cells or are located on the post-synaptic membrane, remove neurotransmitter molecules so that their effect on the chemically gated ion channels is only short-lived.
They include :
• monoamine oxidase (degrades catecholamines)
• acetylcholine esterase (degrades acetylcholine)

6. Reabsorption of neurotransmitter or products of degradation.
Molecules are resynthesised and reincorporated into synaptic vesicles.
Catecholamines are often reabsorbed without degradation.


•  Excitatory post-synaptic potentials result if the neurotransmitter binding to the receptors on the post-synaptic membrane opens chemically gated ion channels, making depolarisation more likely.
• Inhibitory post-synaptic potentials result if the neurotransmitter binding to the receptors on the post-synaptic membrane keeps chemically gated ion channels closed, promoting hyperpolarisation and making depolarisation less likely.