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This document was created by Alex Yartsev ([email protected]); if I have used your data or images and forgot to reference you, please email me. Neurotransmitters and Neuromodulators The important names MONOAMINES: Acetylcholine Serotonin CATECHOLAMINES: Dopamine Noradrenaline Adrenaline AMINO ACIDS: Glutamate GABA (gamma-aminobutyric acid) Glycine Neuropeptides: Co-localised with the neurotransmitters; i.e. they coexist in the same synapses Neuromodulators: released into synapses to modify synaptic transmisison Adenosine, adenosine triphosphate, nitric oxide Receptors - Every ligand has many subtypes of receptors Neurotransmitters have presynaptic as well as postsynaptic elements - Prolonged exposure to ligands tends to make receptors less responsive, i.e. undergo desensitization Presynaptic “autoreceptors” typically INHIBIT FURTHER RELEASE of the neurotransmitter for example, noradrenaline acts on its own alpha-2 receptors to inhibit itself receptors tend to cluster near the nerve endings that release their neurotransmitter HOMOLOGOUS desensitization is when the cell is ONLY desensitized to that one neurotransmitter HETEROLOGOUS desensitization causes the cell to become less responsive to all other ligands Reuptake - Neurotransmitters are recycled out of the synapse by reuptake mechanisms, getting sucked back into the cytoplasm of the neuron which secreted them There are two families of transporters: o One co-transports noradrenaline, dopamine, GABA, glycine etc- co-transport with Na+ and Clo The other family transports only glutamate, and is coupled to co-transport of Na+ and countertransport of K+ - Inside the cell, there are two vesicular monoamine transporters: VMAT1 and VMAT2 They transfer the reabsorbed neurotransmitter back into the vesicles They have little specificity- they will just take anything and drag it back into the vesicles They are inhibited by RESERPINE: an old-school antihypertensive and antipsychotic - Reuptake is the main way of getting neurotransmitters to stop working Inhibition of reuptake causes increased neurotransmitter effects