Activation of this second class of neurotransmitter receptor elicits a cascade of molecular events within the postsynaptic neurone that in turn mediate the effects of the neurotransmitter
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There is a great deal diversity in the types of intracellular events that are activated by metabotropic receptors and the detailed biochemistry of these events is beyond the scope of this subject. However one fairly common mechanism involves a G-protein that acts as an intermediary between the receptor and an enzyme. Binding of the neurotransmitter to the receptor activates the G-protein which in turn stimulates the enzyme to produce a small molecule second messenger such as cAMP, cGMP, Ca2+ or nitric oxide. These second messengers are able to freely diffuse through the cytoplasm of the postsynaptic neurone and in turn produce a number of indirect effects including enzyme activation, regulation of gene transcription, ion channel opening and modification of the sensitivity of ionotropic receptors. |
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A good example of this type of system is the muscarinic acetylcholine receptor that is found on cardiac muscle cells. When acetylcholine binds to this receptor it activates a G protein complex that leads to the formation of a second messenger that acts intracellularly to open a K+ ion channel. Potassium ions leave the cell along their concentration gradient, the membrane hyperpolarises and cardiac muscle is inhibited.
Because of the series of biochemical events that are required to produce the second messenger and its effects, synaptic transmission mediated by metabotropic receptors is fairly slow in onset (around 100 ms). Consequently these types of receptors are not involved in neuronal circuits that require rapid communication. However because these neurotransmitters can result in changes to the metabolism of neurones, their effects are generally much more persistent to those produced by ionotropic receptors.