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David Pickar, MD; Robert E. Litman, MD; Walter W. Hong, MD; Tom P. Su, MD; Ellen M. Weissman, MD; John K. Hsiao, MD; William Z. Potter, MD, PhD
Experimental Therapeutics Branch, DIRP, NIMH National Institutes of Health NIH 10/4N214 9000 Rockville Pike Bethesda, MD 20892

Arch Gen Psychiatry. 1994;51(2):159-160.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

One of the take-home messages from our recent report regarding the clinical and biological effects of the atypical neuroleptic, clozapine, was that the admixture of clozapine's effects on dopaminergic, serotonergic, and noradrenergic systems may underlie its unique efficacy in otherwise poorly responsive patients with schizophrenia.¹ We agree with a suggestion by R. W. Pies, MD, (unpublished communication to the ARCHIVES, May 1992) that clozapine's diverse pharmacologic properties indicate strategies for augmentation of neuroleptic drugs in treatment-resistant patients and that thioridazine or mesoridazine besylate may be particularly useful, given their relatively low incidence of extrapyramidal side effects.

Whereas much attention has been given to the 5-hydroxytryptamine₂ (5-HT₂) antagonism of clozapine, including the ratio of 5-HT₂ to D₂ affinities as a predictor of neuroleptic atypicality,² we have noted that clozapine's relatively potent ₂-antagonism (putatively contributing to observed increases in norepinephrine turnover) is distinct among . . . [Full Text PDF of this Article]

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