Effect of ethanol on tyrosine hydroxylation in brain regions of long and short sleep mice

Abstract

The effect of ethanol on the in vivo rate of tyrosine hydroxylation in 6 brain regions was examined in two lines of mice selectively bred for a differential sensitivity to ethanol. The mice are designated long-sleep (LS) and short-sleep (SS) and lose their righting reflex for a duration of 100 minutes (LS) and 13 minutes (SS) following an intraperitoneal dose of ethanol of 4.0 g/kg. DOPA accumulation after NSD-1015 administration was measured in the absence and presence of ethanol (4.0 g/kg, IP) in the periods 5–35 minutes and 85–115 minutes after saline or ethanol. There were no differences between the lines in either basal catecholamine levels or basal tyrosine hydroxylation rates (as measured by DOPA accumulation) in any brain region except the cerebellum, where the norepinephrine content in the SS mice is 33% greater and the tyrosine hydroxylation rate is 25% higher than that in the LS mice. In the presence of ethanol, there was a differential effect on the in vivo tyrosine hydroxylation rate. In the cerebellum of both LS and SS mice there was a decreased rate of tyrosine hydroxylation in the early period after ethanol, but the rate in the cerebellum of SS mice returned to the control value at 85–115 min. At that time, the rate in LS mice is still decreased. In the locus ceruleus, hypothalamus and frontal cortex, ethanol has no effect on the rate of tyrosine hydroxylation in either LS or SS mice during the early period, but ethanol decreases the rate during the later period in the LS mice only. Ethanol-induced changes in the tyrosine hydroxylation rate in the hippocampus and striatum were not different in the two lines of mice. These data suggest that a differential effect of ethanol on brain catecholaminergic systems in the LS and SS mice may contribute to the differential sensitivity to ethanol in these lines of mice.