Abstract

An acute dose of ethanol reduced the content of ³H-norepinephrine metabolites (after ³H-tyrosine injection) in both the brain (hypothalamus, brainstem, telencephalon) and in the heart and spleen. Endogenous norepinephrine levels were not significantly altered, except in the hypothalamus 2 hours after ethanol administration. After 2 weeks of chronic ethanol intake (in the form of a liquid diet), there was an acceleration of norepinephrine turnover in the brain, heart and adrenals. In the brain the largest effect was seen in the brainstem. Endogenous norepinephrine levels in the brain remained unaltered by chronic ethanol intake. In the adrenal glands, total catecholamines were 15% higher in the ethanol-treated rats. Upon ethanol withdrawal, there was a time-dependent acceleration of norepinephrine turnover, which was most evident in the brainstem, with a peak effect 8 hours after ethanol discontinuation (36% increase). These parameters were normal 48 hours after ethanol withdrawal. Endogenous norepinephrine levels were higher in the brainstem during early ethanol withdrawal and were normal 48 hours later. In the hypothalamus and telencephalon, endogenous norepinephrine was higher than the control levels at both 24 and 48 hours. It is concluded that both central and peripheral noradrenergic neurons are affected by ethanol. However, what role catecholamines play in the effects of ethanol and during ethanol withdrawal remains to be established.