Regulation of transmitter synthesis and release in mesolimbic dopaminergic nerve terminals: effect of ethanol
Author
dc.contributor.author
Bustos, Gonzalo
Author
dc.contributor.author
Liberona Leppe, José
Author
dc.contributor.author
Gysling, Katia
Admission date
dc.date.accessioned
2018-08-29T20:14:34Z
Available date
dc.date.available
2018-08-29T20:14:34Z
Publication date
dc.date.issued
1981
Cita de ítem
dc.identifier.citation
Biochemical Pharmacology Vol.30, No. 15, pp. 2157-2164, 1981
es_ES
Identifier
dc.identifier.other
10.1016/0006-2952(81)90237-9
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/151372
Abstract
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Abstract-Slices from rat olfactory tubercle were incubated in freshly oxygenated Krebs-Ringer phosphate
(KRP) and in the presence of L-tyrosine[“C-U] as dopamine (DA) precursor. Thereafter, the
newly synthesized [‘“C]DA and the [“C]DA released into the incubation media were isolated by
Alumina column, and ion-exchange, chromatography. The presence of K” depolarizing concentrations
(25-70mM) in the incubation media markedly increased the formation of [“C]DA from [“Cltyrosine.
following a rather complex and biphasic pattern. Dibutyryl cyclic AMP (dB-CAMP) and theophylline
also increased the formation of newly synthesized (“CIDA. Ethanol (0.2 to 0.4%. w/v) significantly
blocked the stimulation of [l’C]DA biosynthesis that was induced by low K’ depolarizing concentrations
(25 mM) and by dB-CAMP (5 x lo-’ M) or theophylline (I x IO ’ M). In contrast, only higher ethanol
concentrations (0.8 to 1.10/c, w/v) blocked the increase in DA formation induced by high K- depolarizing
concentrations (40 and 55 mM). Potassium depolarization (JO mM) markedly evoked the release of
newly synthesized [‘HIDA or [‘HIDA previously taken up by the slices. The release was shown to be
dependent upon the presence of Ca” and inhibited by an excess of Mg” (I2 mM). Ethanol (0.8 to
1.10/c, w/v) produced no effect on K’-induced release of [‘HIDA. The model described in this paper
can be used as a simple experimental tool to study neurotransmitter synthesis and release from nerve
terminals belonging to the mesolimbic dopaminergic system. The results reported suggest the existence
of at least two mechanisms by which neuronal depolarization increases transmitter lormation in
mesolimbic dopaminergic terminals. Ethanol. at relatively low concentrations. seems to produce a
specific inhibitory effect upon the mechanism that predominates under low depolarizing conditions.
The possibility is raised that the effects described for ethanol may play a role in the neuropharmacological
responses induced by this agent in vivo.