Effect of butaclamol, a new neuroleptic, on serotoninergic mechanisms.
Butaclamol (1.0-0.1 mg kg-1, i.p.) and spiroperidol (1-0-0-5 mg kg-1, i.p.) but not (-)-butaclamol (15 mg kg-1, i.p.), blocked the hyperactivity induced in rats by tranylcypromine-L-tryptophan pretreatment. Neither butaclamol nor spiroperidol altered the accumulation of brain 5-HT following parglyine or the decline of brain 5-HT following inhibition with the tryptophan hydroxylase inhibitor alpha-propyldopacetamide thus indicating that butaclamol and spiroperidol do not affect either the synthesis or the turnover of brain 5-HT. It is concluded that the antagonism of the tranylcypromise-L-tryptophan-induced hyperactivity by butaclamol and spiroperidol is due to their blockade of dopaminergic receptors rather than an action on neuronal serotoninergic mechanisms.
Effect of butaclamol, a new neuroleptic, on serotoninergic mechanisms. Butaclamol (1.0-0.1 mg kg-1, i.p.) and spiroperidol (1-0-0-5 mg kg-1, i.p.) but not (-)-butaclamol (15 mg kg-1, i.p.), blocked the hyperactivity induced in rats by tranylcypromine-L-tryptophan pretreatment. Neither butaclamol nor spiroperidol altered the accumulation of brain 5-HT following parglyine or the decline of brain 5-HT following inhibition with the tryptophan hydroxylase inhibitor alpha-propyldopacetamide thus indicating that butaclamol and spiroperidol do not affect either the synthesis or the turnover of brain 5-HT. It is concluded that the antagonism of the tranylcypromise-L-tryptophan-induced hyperactivity by butaclamol and spiroperidol is due to their blockade of dopaminergic receptors rather than an action on neuronal serotoninergic mechanisms.