Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

Abstract

Abstract-The effects of ethanol on the contents of norepinephrine (NE) and dopamine (DA) and the activities of related enzymes in the various regions of rat brains with different doses and mode of administration of ethanol were investigated. In acute ethanol intoxication, steady-state levels of NE were not altered. Continuous ethanol intoxication, however, significantly reduced NE contents and tended to decrease the activity of dopamine-Q-hydroxylase in the hippocampus. The decrease in NE con tents became more significant during ethanol withdrawal, especially in the medulla oblongata and the striatum. DA contents were increased in the brain-stem region in all ethanol-treated rats. The increase in DA contents correlated with the increase in tyrosine hydroxylase activity. The present data suggest that the dopaminergic system may contribute to the develop ment of physical dependence on ethanol.

Elevated Norepinephrine may be a Unifying Etiological Factor in the Abuse of a Broad Range of Substances: Alcohol, Nicotine, Marijuana, Heroin, Cocaine, and Caffeine

“…11 In another rat study, acute alcohol intoxication did not affect brain levels of NE, whereas continuous intoxication reduced brain NE and decreased the activity of the NE synthesizing enzyme, dopamine beta-hydroxylase, in the hippocampus. 2 Acute administration of alcohol to mice increased plasma NE, whereas chronic drinking of alcohol over 14 days resulted in NE returning to its baseline level, and acute withdrawal produced a significant increase in plasma NE. 12 Systemic or localized administration of alcohol to the rat locus coeruleus, a major noradrenergic cell nucleus in the brainstem, produced suppression in the firing rate of cells there, which could decrease release of NE.…”

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).…”

Noradrenergic targets for the treatment of alcohol use disorder

“…The acute effects of alcohol administration on NE levels are complex, and depend on alcohol dose, route of administration and anatomical specificity of different brain regions (Yamanaka, 1982). The systemic or localized administration of alcohol (1–2 g/kg) directly onto a single neuron in the rat locus coeruleus (a major brainstem noradrenergic cell nucleus) produces a suppression in the neuronal firing rate (Strahlendorf and Strahlendorf, 1983).…”

“…The systemic or localized administration of alcohol (1–2 g/kg) directly onto a single neuron in the rat locus coeruleus (a major brainstem noradrenergic cell nucleus) produces a suppression in the neuronal firing rate (Strahlendorf and Strahlendorf, 1983). In Wistar rats, acute alcohol administration (1.5 and 4.0 g/kg of ethanol 30 min prior to sacrifice for moderate and severe intoxication) significantly reduced NE levels, with a decrease in the activity of dopamine-beta-hydroxylase in the hippocampus (Yamanaka and Egashira, 1982). The decrease in NE levels became more significant during alcohol withdrawal, particularly in the medulla oblongata and the striatum (Yamanaka and Egashira, 1982).…”

“…In Wistar rats, acute alcohol administration (1.5 and 4.0 g/kg of ethanol 30 min prior to sacrifice for moderate and severe intoxication) significantly reduced NE levels, with a decrease in the activity of dopamine-beta-hydroxylase in the hippocampus (Yamanaka and Egashira, 1982). The decrease in NE levels became more significant during alcohol withdrawal, particularly in the medulla oblongata and the striatum (Yamanaka and Egashira, 1982). The large noradrenergic input in the bed nucleus of the stria terminalis seems to inhibit glutamate release via activation of alpha-2 receptors (Egli and Winder, 2003, Egli et al, 2005), and has been associated with activation of the hypothalamic–pituitary–adrenal s axis, anxiety and stress-induced relapse to drug seeking (Kash, 2012).…”