Is L-Dopa a Neurotransmitter of the Primary Baroreceptor Afferents Terminating in the Nucleus Tractus Solitarii of Rats?

Abstract

Transmitter-like Dihydroxyphenylalanine (DOPA) is released from rat striata and blood pressure regulation centers in the lower brain stem. Exogenous DOPA itself elicits in vitro presynaptic and in vivo postsynaptic responses. All are stereoselective, and most are antagonized by DOPA methyl ester, a competitive DOPA antagonist. DOPA does not displace selective binding of α 2 , β , D 1 , and D 2 ligands in brain membrane preparations. It is possible to cooperate for effectiveness in Parkinson's disease. Meanwhile, DOPA induces DOPA ester-sensitive neuronal glutamate release from slices, even under inhibition of aromatic L-amino acid decarboxylase (AADC). The release by baroreceptor stimulation with phenylephrine has been abolished by bilateral sinoaortic denervation without modification of hypertension. DOPA microinjected into depressor sites of the medial nucleus tractus solitarii (NTS) identified by prior glutamate leads to dose-dependent decreases in blood pressure and heart rate (HR) in untreated rats and in those treated with central AADC inhibitor. The discussion also includes interactions between DOPAergic and GABAergic systems. GABA is an inhibitory neuromodulator for baroreflex at the level of NTS. GABA functions tonically via GABA A receptors to elicit increases in blood pressure and HR and to inhibit decreases in those by electrical aortic nerve stimulation. The third topic under discussion in this chapter is altered functions of the DOPA system in the NTS of adult spontaneously hypertensive rats (SHR). Basal DOPA release is lower in SHR than age-matched Wistar-Kyoto (WKY) rats. This release has been reduced by tetrodotoxin (TTX) to the same absolute levels in the two strains.