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1: Proc Natl Acad Sci U S A. 1997 Oct 28;94(22):12157-61.Click here to read Click here to read Links

Loss of haloperidol induced gene expression and catalepsy in protein kinase A-deficient mice.

Adams MR, Brandon EP, Chartoff EH, Idzerda RL, Dorsa DM, McKnight GS.

Department of Pharmacology, University of Washington, Seattle, WA 98195, USA.

The antipsychotic drug, haloperidol, elicits the expression of neurotensin and c-fos mRNA in the dorsal lateral region of the striatum and produces an acute cataleptic response in rodents that correlates with the motor side effects of haloperidol in humans. Mice harboring a targeted disruption of the RIIbeta subunit of protein kinase A have a profound deficit in cAMP-stimulated kinase activity in the striatum. When treated with haloperidol, RIIbeta mutant mice fail to induce either c-fos or neurotensin mRNA and the acute cataleptic response is blocked. However, both wild-type and mutant mice become cataleptic when neurotensin peptide is directly injected into the lateral ventricle, demonstrating that the kinase deficiency does not interfere with the action of neurotensin but rather its synthesis and release. These results establish a direct role for protein kinase A as a mediator of haloperidol induced gene induction and cataleptic behavior.

PMID: 9342379 [PubMed - indexed for MEDLINE]

PMCID: PMC23735

Patient Drug Information

  • Haloperidol

    Haloperidol is used to treat psychotic disorders (conditions that cause difficulty telling the difference between things or ideas that are real and things or ideas that are not real). Haloperidol is also used to control ...

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