Abstract

Administration of acetaldehyde to rats following an intracisternal injection of [ 3H]norepinephrine (NE) produced a decrease in brain endogenous NE with a concurrent increase in disappearance rate of [ 3H]NE. In contrast, acute ethanol administration appears to decrease both the rate of disappearance of [ 3H]NE and endogenous NE in brain. The pattern of NE metabolites in the brain was changed by acetaldehyde but not by ethanol. In experiments where ethanol was given prior to i.e. injection of [ 3H]NE, a small decrease in retention of [ 3H]NE observed at 15 min was followed by an increase at 90 min exposure to [ 3H]NE. There was a non-significant increase in [ 3H]normetanephrine formation at 15 min. These results suggest ethanol has a dual action on NE, initially increasing the release of NE and at the same time decreasing the neuronal uptake which may decrease the turnover rate of NE. However, acetaldehyde affects only the release of NE, thus increasing its turnover rate in the brain.

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