NROSCI 0081 Lecture Notes - Lecture 11: Tryptophan Hydroxylase, Tyrosine Hydroxylase, Monoamine Oxidase
12 Feb 2018
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Document Summary
Synthesized in the axon terminal from products derived from diet. Made from choline and acetyl coa by chat. Signaling terminated be degradation of ach within the synapse, by the enzyme acetylcholinesterase (ache) Levels are crucial: too much or too little is lethal, many insecticies, venoms, nerve gases work by blocking ache, leading to paralysis (because ach works in your muscles) Ionotropic: cns and pns, primary nt of muscles. Muscarinic: slow, metabotropic, cns, vital role in the synaptic plasticity (ability of synapses to learn new things grow and die) Loaded into vesicles by vesicle monoamine transporter (vmat: all metabotropic, both excitatory and inhibitory effects. Signaling inactivated by dopamine transporter reuptake (dat) and degradation by monoamine oxidase (mao) Drugs like cocaine and methylphenidate (ritalin) block or reverse dat. Synthesis controlled by tyrosine hydroxylase (th) the rate limiting step (determines how much you can make: we also use this to identify dopaminergic cells. Made from dopamine by dopamine beta-hydroxylase (dbh: also uses vmat.
