This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Herbert Y. Meltzer, MD; Craig A. Stockmeier, PhD
Department of Psychiatry Case Western Reserve University 2074 Abington Rd Cleveland, OH 44106

Arch Gen Psychiatry. 1992;49(7):588-589.

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

To the Editor. —

Clozapine hydrochloride, an atypical antipsychotic drug, has been reported to occupy fewer striatal D₂ dopamine receptors (DRD2) (38% to 63%) than typical neuroleptic drugs (>70%), as determined by positron emission tomography (PET) using raclopride labeled with carbon 11.^1-3 Furthermore, clozapine has been shown by PET studies using ₁₁CSchering 23390 as ligand to occupy more D₁ dopamine receptors (DRD1) than typical neuroleptics.^2,3

See also p 538.

Decreased DRD2 and increased DRD1 occupancy has been suggested as the explanation of why clozapine does not produce extrapyramidal symptoms in humans.³ We have offered an alternative theory, namely, that clozapine produces fewer extrapyramidal symptoms because of its higher serotonin₂ (5-HT₂) receptor-blocking properties compared with its DRD2-blocking properties.⁴ We have also suggested that the latter mechanism is relevant to the antipsychotic advantages of clozapine.⁵ Others^5,6 have suggested that the . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?