Abstract
The iminodibenzyl antipsychotic drugs, clocapramine, carpipramine and Y-516 were studied in order to elucidate their mechanisms of action. They all accelerated the accumulation of the dopamine (DA) metabolites, homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), in the striatum and nucleus accumbens of the rat brain. Only Y-516 antagonized in vivo the apomorphine-induced inhibition of DA synthesis as estimated from the accumulation of 3,4-dihydroxyphenylalanine (DOPA) in the decarboxylase-inhibited rat striatum after cessation of nerve impulse flow. All three drugs showed high affinity for DA receptors labelled by [ 3H]haloperidol and [ 3H]ADTN in the rat striatum in vitro, with the order of potency Y-516 > clocapramine > carpipramine. All accelerated the accumulation of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), in mouse brain. They showed high affinity for α 1-adrenoceptors labelled by [ 3H]WH 4101 and for α 2-adrenoceptors labelled by [ 3H] clonidine in the rat cerebral cortex in vitro. Although they all had the same level of affinity for the α 1-adrenoceptors, Y-516 had less affinity for the α 2-adrenoceptors than did clocapramine and carpipramine. The above results indicate that these drugs are potent DA antagonists which block α 1- and α 2-adrenoceptors in the brain.
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