On catalepsy and catatonia and the predictability of the catalepsy test for neuroleptic activity

Morphine catatonia was more susceptible to inhibition by the amygdaloid lesions than the catalepsy/catatonia induced by the other agents tested, and was potentiated by lesions destroying the extrapyramidal/mesolimbic innervation, caudate-putamen and globus pallidus.

Abstract

The neuroleptic agents peromide and spiroxatrine induced an immobility in the rat which, in appearance, more resembled morphine catatonia than haloperidol catalepsy. Therefore, in a attempt to differentiate the behavioural states termed catalepsy and catatonia, haloperidol and morphine were closely compared using drug interaction and brain lesion studies. Atropine abolished or reduced the effects of haloperidol, peromide and spiroxatrine but not morphine, whilst morphine and spiroxatrine were similarly modified by nalorphine. The spiroxatrine effect was completely abolished by atropine and nalorphine combined. The cholinergic agent RS 86 synergised with haloperidol, peromide and spiroxatrine but not with morphine. Lesion of the dopaminergic extrapyramidal and/or mesolimbic innervation, of the caudate-putamen, globus pallidus and nucleus amygdaloideus centralis each reduced or abolished haloperidol, peromide and spiroxatrine catalepsy/catatonia. In contrast, morphine catatonia was only partially reduced by ablating the mesolimbic input, and was potentiated by lesions destroying the extrapyramidal/mesolimbic innervation, caudate-putamen and globus pallidus. Morphine catatonia was more susceptible to inhibition by the amygdaloid lesions than the catalepsy/catatonia induced by the other agents tested.