PSYCO275 Lecture Notes - Autoreceptor, Reuptake, Acetylcholine
11 Mar 2014
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Document Summary
1- nt molecules are synthesized from precursors under the influence of enzymes. 3- nt molecules that leak from their vesicles are destroyed by enzymes. 4- action potentials cause vesicles to fuse with the presynaptic membrane and release their nt molecules into the synapse. 5- released nt molecules bind with auto receptors and inhibit subsequent nt release. 6- released nt molecules bind to postsynaptic receptors. 7- released nt molecules are deactivated by either reuptake or enzymatic degradation (or both with the exception of acetylcholine which only undergoes degradation and has no reuptake. ) Drug increases the synthesis of nt molecules: e. g. by increasing the amount of the precursor. Drug increases the number of nt molecules by destroying the degrading enzymes. Drug increases the release of nt molecules from terminal buttons. Drug binds to autoreceptors and blocks their inhibitory effect on nt release. Drug binds to postsynaptic receptors and either activates them or increases the effect on them of nt.
