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The effects of temazepam 20 mg and temazepam 20 mg plus whisky 100 ml on sleep and performance were investigated in 5 healthy volunteers in comparison with placebo. In the sleep laboratory, after temazepam there was a trend for reduction of sleep latency, stage wake and stage 1 sleep, and for an increase in REM sleep. The addition of alcohol to the regimen reduced the sleep latency still further, and diminished REM sleep. In subjective assessments, temazepam received the highest score for quality of sleep and the temazepam/alcohol combination that for ease of falling asleep. None of the observed changes reached statistical significance. No morning hangover, as measured by effects on wakefulness, performance or affective state, was seen after the combined treatment. Its effect on blood pressure was negligible. It is concluded that the combined administration of temazepam and alcohol in the doses used here does not result in excessive additive, but in moderate pharmacological effects. [ABSTRACT FROM AUTHOR]

Following interruption of the nerve impulse flow in the dopamine neurons by treatment with gammabutyrolactone, the selective dopamine autoreceptor agonist B-HT 920 reduced the DOPA accumulation after DOPA decarboxylase inhibition and the 3,4-dihydroxyphenylacetic acid concentration in the corpus striatum, the nucleus accumbens, the olfactory tubercle, the limbic cortex and the rostral part of the cerebral cortex of rats. The effects were completely inhibited by the dopamine receptor antagonist haloperidol, indicating that they were caused by stimulation of dopamine autoreceptors. In the caudal part of the cerebral cortex and the cerebellum, B-HT 920 somewhat reduced the concentration of dihydroxyphenylacetic acid via a haloperidol-sensitive mechanism, suggesting that there are a few dopamine neurons with autoreceptors in these regions. No evidence was obtained for the presence of autoreceptors on the dopamine neurons in the hypothalamus. The gammabutyrolactone-induced elevation of the dopamine concentration was not reduced by B-HT 920 in any region, suggesting that this effect of gammabutyrolactone was caused by decreased release rather than increased synthesis of dopamine under our experimental circumstances. [ABSTRACT FROM AUTHOR]

The α-methyltyrosine-induced disappearance of dopamine was inhibited by the selective dopamine autoreceptor agonist B-HT 920 in the corpus striatum, the nucleus accumbens, the olfactory tubercle, the limbic cortex, and the rostral part of the cerebral cortex of the rat. These inhibitory actions of B-HT 920 were almost completely reversed by the dopamine receptor antagonist haloperidol, indicating that they were caused by a stimulation of dopamine autoreceptors. In the caudal cortex and the cerebellum, the effects of B-HT 920 and haloperidol were less clear, perhaps due to a low concentration of dopamine and to the occurrence of this dopamine in both dopamine and noradrenaline neurons. In the hypothalamus, B-HT 920 and haloperidol did not change the α-methyltyrosine-induced disappearance of dopamine in agreement with previous findings that the tubero-infundibular dopamine neurons are not regulated via dopamine receptors. [ABSTRACT FROM AUTHOR]