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Calcium mobilization in platelets from schizophrenic and healthy subjects. Regulation by lithium and neuroleptics

Departments of Psychiatry and Biochemistry, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6, UK

I. Das

Departments of Psychiatry and Biochemistry, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6, UK

J. de Belleroche

Departments of Psychiatry and Biochemistry, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6, UK

S.R. Hirsch

Departments of Psychiatry and Biochemistry, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6, UK

Intracellular free calcium concentrations ([Ca²⁺]₁) were measured in platelets from healthy volunteers before and after adding thrombin, chlorpromazine, haloperidol and/or lithium, and in platelets from DSM-III-R diagnosed schizophrenic patients receiving neuroleptic medication. Thrombin increased [Ca²⁺] ₁ in a dose- dependent fashion. Chlorpromazine and haloperidol also mobilized Ca²⁺ in a dose-dependent fashion, and augmented the response to low doses of thrombin without changing the maximal response to thrombin. The effects of all three drugs were not additive, suggesting that they affected the same intraplatelet calcium pool; most likely the dense tubular system. Lithium also increased [Ca²⁺ ] but without affecting the response to thrombin, chlorpromazine or haloperidol. The effects of the latter three drugs were additive to that of lithium, suggesting that lithium was acting on a different calcium pool. The response to thrombin was significantly lower in platelets from schizophrenic patients than in platelets from healthy volunteers. Further studies are required to explore potential causes for this observation. Such causes include schizophrenia per se and chronic neuroleptic treatment.

Key Words: calcium mobilization • platelets • schizophrenia • lithium • neuroleptics

Journal of Psychopharmacology, Vol. 6, No. 3, 389-394 (1992)
DOI: 10.1177/026988119200600308


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