1. 1. In mice receiving a single injection of sodium pentobarbital, 75 mg/kg, i.p., the whole brain catecholamine contents did not change. However, norepinephrine levels of the diencephalon and mesencephalon and dopamine contents of the cortex and the striatum were increased by acute pentobarbital treatment. The depletion of norepinephrine after the treatment of α-methyl- p ̄tyrosine, 250 mg/kg, 4 hr before sacrifice, was significantly smaller in the cortex, the pons plus medulla oblongata and the cerebellum in acute pentobarbital-treated animals. The rate of dopamine depletion after α-methyl- p ̄-tyrosine treatment in the striatum was also slower than that of the control group. 2. 2. In pentobarbital tolerant animals, decreases in norepinephrine level of the pons plus medulla oblongata and in dopamine content of the striatum were observed. The depletion of dopamine after α-methyl- p ̄-tyrosine treatment was significantly smaller than that of the control group. 3. 3. In pentobarbital dependent animals, changes of catecholamine steady state levels in discrete areas of the brain were returned to normal. The rates of norepinephrine depletion observed after α-methyl- p ̄-tyrosine treatment in the cortex and the pons plus medulla oblongata were significantly greater than that of the control groups. 4. 4. The present results suggest that acute pentobarbital causes a depression of catecholaminergic neuronal activity by a decrease of catecholamine turnover (degradation) and the development of tolerance to pentobarbital accompanies with the suppression of catecholamine synthesis. In contrast, the norepinephrine turnover increases after the occurrence of abrupt withdrawal.
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