B-HT 958 stimulates dopamine autoreceptors but blocks noradrenaline autoreceptors in the brain

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Abstract
B-HT 958 (2-amino-6-(p-chlorobenzyl)-4H-5,6,7,8-tetrahydrothiazolo 5,4-d azepine) blocked the γ-butyrolactone-induced increase in the synthesis of dopamine and slowed down the α-methyltyrosine-induced disappearance of dopamine in the mouse brain by haloperidol-sensitive mechanisms. In reserpine-treated mice, B-HT 958 produced at most a weak locomotion and no change in the apomorphine-induced increase in motor activity. The motor activity of normal mice was reduced by B-HT 958. At high doses, B-HT 958 accelerated the α-methyltyrosine-induced disappearance of noradrenaline and it inhibited the effects of clonidine on the turnover and on the synthesis of noradrenaline in the mouse brain. The findings indicate that the dopamine autoreceptors can be selectively stimulated by B-HT 958 but that the α2-adrenoceptors can be blocked following high doses.

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