The effect of acute ethanol on dopamine metabolism and other neurotransmitters in the hypothalamus and the corpus striatum of mice

Abstract

The effect of acute ethanol on the levels of NE, DA and its metabolites DOPAC and HVA, as well as on the levels of GABA, in the corpus striatum and hypothalamus were investigated in mice in the first two hours after acute ethanol administration. There was a marked increase in the concentration of DOPAC and HVA in the corpus striatum from 30 to 120 minutes after a dose of 3.5 g/kg of ethanol even though the concentration of DA was only elevated at 60 minutes after ethanol. A dose of 1.75 g/kg of ethanol did not increase DA levels 60 minutes after administration although it did increase the concentration of DOPAC and HVA at this time. In the hypothalamus a dose of 3.5 g/kg of ethanol did not change the concentration of NE or DA but did produce a marked increase in the levels of DOPAC and HVA at 60 and 120 minutes post ethanol. A lower dose of ethanol, 1.75 g/kg, produced the same effect 60 minutes after ethanol. Ethanol caused a dose-dependent accumulation of DOPA in the corpus striatum after inhibition of DOPA-decarboxylase suggesting an increased synthesis of DA. These data suggest that the increased concentrations of DA metabolites after ethanol is secondary to enhanced DA synthesis and turnover. The concentration of NE and GABA in the hypothalamus and the corpus striatum was unchanged at any time period after ethanol.

A Critical Evaluation of Influence of Ethanol and Diet on Salsolinol Enantiomers in Humans and Rats

“…The central dopaminergeric system is a well-recognized target for addiction behavior (Dar and Wooles, 1984; Heinz et al, 2005). We found lower basal DA levels in the STR or NAC of P-rats in comparison to NP-rats.…”

“…Effects of ethanol on DA levels have been shown to vary depending on many parameters such as dose or duration of ethanol treatment or the brain regions examined (Dar and Wooles, 1984; Murphy et al, 1983; Myers et al, 1985a; Sjöquist et al, 1982). A decreasing trend of DA levels in both NAC and STR observed in our study is in agreement with previous findings.…”

Invertebrate models of drug abuse

“…Consistent with this notion are observations that some of the neural circuits and neurochemical systems, such as the mesolimbic dopamine pathway, that are central to drug reinforcement also influence acute stimulant effects. Although this has been studied primarily for psychostimulants such as cocaine and methamphetamine, acute ethanol exposure also increases dopamine release and locomotor activity in rodents (Dar and Wooles, 1984;Imperato and Di Chiara, 1986). Genetic or pharmacologic manipulations that interfere with mesolimbic dopamine systems block not only the stimulant effects of ethanol, but also the rewarding properties (Phillips and Shen, 1996;Phillips et al, 1998;Cunningham et al, 2000;Risinger et al, 2000); however, other neurochemic systems and brain regions are also involved in drug reinforcement (reviewed in Wise, 2000).…”

Inhibition of phosphorylated tyrosine hydroxylase attenuates ethanol-induced hyperactivity in adult zebrafish (Danio rerio)

“…However, the precise mechanism by which dopamine (DA) regulates acute alcohol responses and addiction remains elusive. Acute alcohol exposure has been shown to increase extracellular brain DA concentrations in rats (Di Chiara & Imperato, 1988) and levels of DA and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in mice (Saeed & Wooles, 1984). The increase in DA levels has been proposed to underlie the stimulating properties of alcohol, as DA depletion and DA receptor antagonists block alcohol-induced locomotor activity (Bainton et al, 2000; Camarini et al, 2011).…”

“…The increase in DA levels has been proposed to underlie the stimulating properties of alcohol, as DA depletion and DA receptor antagonists block alcohol-induced locomotor activity (Bainton et al, 2000; Camarini et al, 2011). Furthermore, alcohol causes a dose-dependent accumulation of 3, 4-dihydroxyphenylalanine (DOPA) after inhibition of DOPA decarboxylase in the brains of mice (Saeed & Wooles, 1984). …”