Effects of Ethanol In Vitro and In Vivo on the Release of Endogenous Catecholamines from Specific Regions of Rat Brain

Abstract

Blocks of tissue from the hypothalamus, olfactory bulb, or striatum of rats were incubated in vitro to study the basal and potassium-stimulated release of endogenous catecholamines. When ethanol (100-250 mM) was added to these preparations in vitro no changes in release were observed. When ethanol (3.0 g X kg-1) was injected intraperitoneally in vivo, however, and 3,4-dihydroxyphenylethylamine (DA, dopamine) release was measured in vitro at various times after drug administration, significant increases in the basal release and decreases in the potassium-stimulated release were observed in striatum and olfactory bulb. In striatum, these changes showed a more rapid onset and a longer duration than in olfactory bulb. In both brain regions, DA release did not differ from controls at 4-6 h after the ethanol injection, although blood ethanol concentrations remained elevated. This may imply the tissue's acquisition of acute functional tolerance to the drug. Similar increases and decreases in the basal and the potassium-induced release of DA from striatal tissues were also found at 1 h after injection of a lower dose of ethanol (1.0 g X kg-1). In terms of behavior, this lower dose of ethanol produced only mild intoxication and ataxia, in contrast to the loss of righting reflex following the higher dose.

Ethanol potentiates the function of the human dopamine transporter expressed inXenopusoocytes

“…We postulate that enhanced DAT function represents a compensatory mechanism involved in terminating the actions of the ethanol‐induced increases in synaptic dopamine. Based on our finding that DAT function increased dramatically with longer ethanol exposure times, this mechanism could contribute to the acute functional tolerance that is observed for dopamine‐mediated responses (Mullin and Ferko 1981, 1983; Holman and Snape 1985). Furthermore, enhanced DAT function at dopaminergic soma and terminals contribute to the pronounced decreases in mesolimbic dopaminergic activity (Shen and Chiodo 1993) and extracellular dopamine concentrations (Diana et al .…”

Effect of ethanol on [3H]Dopamine release in rat nucleus accumbens and striatal slices

“…Previous reports have suggested that ethanol either has no effect (12)(13)(14) or that it enhances the spontaneous release of DA (15,16) and inhibits the K + or electrically induced release of DA from rat striatal preparations (15,17). Previous reports have suggested that ethanol either has no effect (12)(13)(14) or that it enhances the spontaneous release of DA (15,16) and inhibits the K + or electrically induced release of DA from rat striatal preparations (15,17).…”

Ethanol‐Induced Increase in Endogenous Dopamine Release May Involve Endogenous Opiates

“…Acute administration of ethanol has been shown to increase the turnover (Fadda et al, 1980;Reggiani et al, 1980;Yamanaka and Egashira, 1982) and release of endogenous dopamine (DA) (Holman and Snape, 1985;Imperato and DiChiara, 1986;DiChiara and Imperato, 1988). However, the intensity and the time course of these effects of ethanol appear to be different for the various DA systems in the brain (Holman and Snape, 1985;Imperato and DiChiara, 1986). Such observations imply a specificity of the action of ethanol on neurotransmission, especially DA.…”