Abstract
DOPA is believed to be an inert amino acid that affects Parkinson’s disease via conversion to dopamine (DA) by aromatic L-amino acid decarboxylase (AADC). We proposed that DOPA is a transmitter and/or modulator as well as a DA precursor.1 DOPA seems to be a transmitter of the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS).2 In the NTS, neurons showing immunocytochemically tyrosine hydroxylase-(+), AADC-(-), DOPA-(+) and DA-(-)-reactivity exist.1,2 Such neurons may have DOPA as an end product. DOPA is released by aortic depressor nerve (ADN) stimulation.2 DOPA esters competitively antagonize hypotension and bradycardia by ADN stimulation and by DOPA microinjected.1–3 DOPA cyclohexyl ester (CHE) is the most potent and relatively stable competitive antagonist among DOPA esters.3 Responses to DOPA occur under inhibition of central AADC.1,2 KeywordsGlutamate ReleaseNucleus Tractus SolitariiTransient IschemiaDepressor ResponseIschemic NeuronThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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