REGULATION OF TRANSMITTER SYNTHESIS AND RELEASE IN MESOLIMBIC DOPAMINERGIC NERVE-TERMINALS - EFFECT OF ETHANOL

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dc.contributor.authorBUSTOS, G
dc.contributor.authorLIBERONA, JL
dc.contributor.authorGYSLING, K
dc.date.accessioned2025-01-23T19:44:12Z
dc.date.available2025-01-23T19:44:12Z
dc.date.issued1981
dc.description.abstractSlices from rat olfactory tubercle were incubated in freshly oxygenated Krebs-Ringer phosphate (KRP) and in the presence of L-tyrosine[14C-U [uniformly 14C-labeled]] as dopamine (DA) precursor. The newly synthesized [14C]DA and the [14C]DA released into the incubation media were isolated by Alumina column and ion-exchange chromatography. The presence of K+ depolarizing concentrations (25-70 mM) in the incubation media markedly increased the formation of [14C]DA from [14C]tyrosine, following a rather complex and biphasic pattern. Dibutyryl cAMP (dB-cAMP) and theophylline increased the formation of newly synthesized [14C]DA. Ethanol (0.2 to 0.4%, wt/vol) significantly blocked the stimulation of [14C]DA biosynthesis that was induced by low K+ depolarizing concentrations (25 mM) and by dB-cAMP (5 .times. 10-4 M) or theophylline (1 .times. 10-3 M. Only higher ethanol concentrations (0.8 to 1.1%, wt/vol) blocked the increase in DA formation induced by high K+ depolarizing concentrations (40 and 55 mM). K depolarization (40 mM) markedly evoked the release of newly synthesized [3H]DA or [3H]DA previously taken up by the slices. The release was dependent upon the presence of Ca2+ and inhibited by an excess of Mg2+ (12 mM). Ethanol (0.8-1.1%, wt/vol) produced no effect on K+-induced release of [3H]DA. The model described can be used as a simple experimental tool to study neurotransmitter synthesis and release from nerve terminals belonging to the mesolimbic dopaminergic system. At least 2 mechanisms exist by which neuronal depolarization increases transmitter formation 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.
dc.fuente.origenWOS
dc.identifier.eissn1873-2968
dc.identifier.issn0006-2952
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/99973
dc.identifier.wosidWOS:A1981MA93800018
dc.issue.numero15
dc.language.isoen
dc.pagina.final2164
dc.pagina.inicio2157
dc.revistaBiochemical pharmacology
dc.rightsacceso restringido
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleREGULATION OF TRANSMITTER SYNTHESIS AND RELEASE IN MESOLIMBIC DOPAMINERGIC NERVE-TERMINALS - EFFECT OF ETHANOL
dc.typeartículo
dc.volumen30
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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