Elsevier

Biological Psychiatry

Volume 34, Issues 1–2, 1–15 July 1993, Pages 119-121
Biological Psychiatry

Brief report
Antipsychotic drugs block phencyclidine receptor-mediated neurotoxicity

https://doi.org/10.1016/0006-3223(93)90265-FGet rights and content

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Cited by (96)

  • Evidence for Neuroprotective Effects of Antipsychotic Drugs: Implications for the Pathophysiology and Treatment of Schizophrenia

    2007, International Review of Neurobiology
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    For example, the dizocilpine‐induced delayed alteration impairment in rats was prevented by pretreatment with clozapine (Hauber, 1993). Also clozapine protected against NMDA‐antagonist neurotoxicity reaction in rats (Farber et al., 1993; Hashimoto et al., 2000). Although traditional antipsychotics (e.g., loxapine, haloperidol, and thioridazine) showed similar effects, their neuroprotective action was not attributed to the drugs’ binding affinity to dopamine receptors, as sulpiride, an agent that binds to dopamine receptors only, did not significantly reduce MK‐801 neurotoxicity at doses up to 30 mg/kg.

  • Acute D<inf>2</inf>/D<inf>3</inf> Dopaminergic Agonism but Chronic D<inf>2</inf>/D<inf>3</inf> Antagonism Prevents NMDA Antagonist Neurotoxicity

    2006, Biological Psychiatry
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    This loss of protection with chronic dosing of a D2/D3 agonist suggested the possibility that chronic administration of a D2/D3 antagonist, through some mechanism (e.g., receptor upregulation), might have the opposite effect and be protective. To test this possibility haloperidol, a D2/D3 antagonist, was given daily for 0 (i.e., one acute injection), 1, 3, or 5 weeks at a dopaminergic dose (1 mg/kg, ip), which does not have significant acute protective effects against NRHypo neurotoxicity (Farber et al 1993). Control groups received DMSO daily for the same amount of time.

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Supported in part by NIH grants DA 05072, DA 06454, AG 05681 and Research Scientist Award MH 38894 (JWO).

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