Original Author(s): Jess Speller
Last updated: 23rd August 2021
Revisions: 26
Original Author(s): Jess Speller
Last updated: 23rd August 2021
Revisions: 26
This is the first step of synaptic transmission. Some neurotransmitters (eg acetylcholine, ACh) are synthesised in the axon, while others (eg neuropeptides) are made in the cell body. Once
synthesised, neurotransmitters are stored in vesicles within the synaptic terminal until an action potential arrives, causing their release. Neurotransmitters such as acetylcholine are stored within the small synaptic vesicles, whereas neuropeptides reside within large dense-core vesicles. Action potentials depolarising
the synaptic terminal lead to the opening of voltage-gated calcium channels. This allows an influx of calcium in the terminal and fusion of the synaptic vesicles with the cell membrane (exocytosis). Consequently, the neurotransmitter is released into the synaptic cleft. By OpenStax [CC BY 4.0 (//creativecommons.org/licenses/by/4.0)], via Wikimedia CommonsSynthesis and Storage of Neurotransmitters
Neurotransmitter Release
Fig 2 – Diagram showing exocytosis, the process by which neurotransmitters are released into the synaptic cleft.
Postsynaptic Receptors
The neurotransmitter in the synaptic cleft diffuses across the gap to the post-synaptic membrane. Here, they can bind to two types of post-synaptic receptors.
Name | Inotropic receptors | Metabotropic receptors |
Type | Ligand-gated ion channels | G protein-coupled receptors |
Response | Channel allows ion flux to change the cellular voltage | Receptor acts through secondary messengers to cause cellular effects |
Speed of response | Rapid | Slow |
Length of response | Short-acting | Prolonged response |
This can cause either depolarisation to promote or hyperpolarisation to inhibit the action potential generation in the post-synaptic neurone.
Inactivation/Removal of Neurotransmitters
Once the post-synaptic membrane has responded the neurotransmitter in the synaptic cleft; it is either inactivated or removed. This can be done in several ways:
- Re-uptake – serotonin is taken back into the pre-synaptic neurone by the transporter proteins in the neuronal membrane. These neurotransmitters are subsequently either recycled by re-packaging into vesicles or broken down by enzymes.
- Breakdown – acetylcholine is broken down by acetylcholinesterase present in the synaptic cleft, inactivating the neurotransmitter.
- Diffusion into surrounding areas
Clinical Relevance – Acetylcholinesterase Inhibitors
Acetylcholinesterase inhibitors are a class of drug that inhibits the activity of acetylcholinesterase within the synaptic cleft. This increases cholinergic transmission as more acetylcholine is present within the synaptic cleft for longer periods of time.
These drugs, such as pyridostigmine, rivastigmine, and donepezil, can be used to treat various conditions:
- Myasthenia gravis – the inhibition of acetylcholinesterase works at the neuromuscular junction rather than at the synaptic cleft to mitigate the effects of loss of nicotinic acetylcholine receptors.
- Alzheimer’s disease
- Glaucoma
- To reverse the effect of non-depolarising muscle relaxants, such as rocuronium.
As cholinergic transmission is widespread throughout the body, particularly mediating the actions of parasympathetic nervous system, these drugs can cause many side effects such as bradycardia, hypotension, diarrhoea, excessive salivation or blurry vision.
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