Communication between cells is vital for the survival of any mulitcellular organism, and it is achieved by the transfer of chemical messengers from one cell to another. These messengers, which are known as neurotransmitters, are stored in vesicles within the cell and are released from neuronal cells upon membrane depolarisation during an action potential.
The binding of an agonist to the nicotinic ligand-gated ion channel induces a conformational change in the receptor-ionophore protein complex which allows the influx of sodium and some calcium into the cell. This influx of sodium causes cellular depolarisation with the opening of voltage-gated ion channels in the cell membrane. The depolarisation stimulates the opening of voltage-gated sodium channels, propogating the action potential, and also voltage-gated calcium channels.
The influx of calcium into the cell activates the enzyme protein kinase C (PKC) and this acts upon the cytoskeleton to break down the cytoskeletal barrier that prevents the neurotransmitter vesicles from fusing with the cell membrane and releasing their contents whilst the cell is at rest. Calcium also acts directly on the cytoskeleton to promote exocytosis.
The neurotransmitter vesicles then fuse with the cell membrane and exocytose their contents. The neurotransmitter then diffuses through the extracellular spaces and binds to nearby cellular receptors and the process continues.
CG and BGL, June-95
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