Synaptic transmission

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Synaptic transmission occurs when an action potential reaches an axon terminal, depolarising the presynaptic membrane. Voltage-gated Ca2+ channels in the presynaptic membrane open in response to the depolarisation[1]., allowing Ca2+ ions to enter the axon terminal down their concentration gradient. This causes vesicles containing neurotransmitter molecules (e.g. Acetylcholine molecules) to migrate towards the presynaptic membrane, and then fuse with the presynaptic membrane releasing neurotransmitter molecules into the synaptic cleft by the process of exocytosis. The molecules of neurotransmitter diffuse across the synaptic cleft and bind to their receptors on the postsynaptic membrane. The binding of neurotransmitter molecules causes ligand-gated Na+ channels in the postsynaptic membrane to open. Na+ ions subsequetly rush into the postsynaptic cell, and because these channels are non-specifc, K+ ions can also leave the postsynpatic cell down their concentration gradient. This particular movement of ions generates a graded_potential in the postsynaptic membrane. If that graded potential is suprathreshold when it arrives at the axon hillock then an action potential will fire in the postsynaptic neurone, if the graded potential is subthreshold when it arrives at the axon hillock then an action potential will not fire in the postsynaptic neurone.

There is a safety factor in the release of neurotransmitter, which ensures that many more vesicles that are required to release their neurotransmitter into the synaptic cleft. This is evident by measurable mini endplate potentials, which occur randomly when the nerve and muscle are at rest. A mini EPP is the result of one vesicle fusing with the plasma membrane to release neurotransmitter. The quantal nature of transmission ensures that each vesicle releases all or none of its contents. One endplate potential is approximately 100x the mini-EPP amplitude. This safety factor is important to ensure that action potential is stimulated in the postsynaptic neurone. Diseases such as Myasthenia Gravis are delayed due to the safety factor; antibodies destroy acetylcholine receptors which leads to reduced effectiveness of transmission, and the safety factor allows the transmission to not fail completely until antibodies have accumulated, which consequently leads to lack of action potential stimulation.


  1. Antranik (2012) Synaptic Transmission by Somatic Motorneurons, [Online], Available: accessed [27 Nov 2013].
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