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Clozapine Reverses Phencyclidine-Induced Desynchronization of Prefrontal Cortex through a 5-HT(1A) Receptor-Dependent Mechanism.

Lucila Kargieman, Maurizio S Riga, Francesc Artigas, Pau Celada

Neuropsychopharmacology February 2012 DOI: 10.1038/npp.2011.249 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental animal study (genetic knockout and pharmacological antagonist design) Peer reviewed
Population Wild-type C57BL/6 mice and 5-HT1A and 5-HT2A receptor knockout mice on the same background
Interventions Phencyclidine (PCP) Clozapine WAY-100635
Dose PCP 10 mg/kg intraperitoneally; clozapine 0.5 mg/kg intraperitoneally
Measures Local field potentials (LFPs) in the prefrontal cortex; slow cortical oscillations (SCO; 0.15-4 Hz)
Topics Serotonin
Key findings PCP (10 mg/kg) reduced prefrontal slow cortical oscillations equally in wild-type, 5-HT2A knockout, and 5-HT1A knockout mice (to 58±4%, 42±7%, and 63±7% of pre-drug values; n=23, 13, 11). Clozapine (0.5 mg/kg) reversed the PCP effect in wild-type and 5-HT2A knockout mice but not in 5-HT1A knockout mice or in wild-type mice pretreated with the 5-HT1A antagonist WAY-100635, suggesting clozapine's action involves 5-HT1A receptor activation without requiring 5-HT2A blockade.

Abstract

The non-competitive NMDA receptor (NMDA-R) antagonist phencyclidine (PCP)-used as a pharmacological model of schizophrenia-disrupts prefrontal cortex (PFC) activity. PCP markedly increased the discharge rate of pyramidal neurons and reduced slow cortical oscillations (SCO; 0.15-4 Hz) in rat PFC. Both effects were reversed by classical (haloperidol) and atypical (clozapine) antipsychotic drugs. Here we extended these observations to mice brain and examined the potential involvement of 5-HT(2A) and 5-HT(1A) receptors (5-HT(2A)R and 5-HT(1A)R, respectively) in the reversal by clozapine of PCP actions. Clozapine shows high in vitro affinity for 5-HT(2A)R and behaves as partial agonist in vivo at 5-HT(1A)R. We used wild-type (WT) mice and 5-HT(1A)R and 5-HT(2A)R knockout mice of the same background (C57BL/6) (KO-1A and KO-2A, respectively). Local field potentials (LFPs) were recorded in the PFC of WT, KO-1A, and KO-2A mice. PCP (10 mg/kg, intraperitoneally) reduced SCO equally in WT, KO-2A, and KO-1A mice (58±4%, 42±7%, and 63±7% of pre-drug values, n=23, 13, 11, respectively; p<0.0003). Clozapine (0.5 mg/kg, intraperitoneally) significantly reversed PCP effect in WT and KO-2A mice, but not in KO-1A mice nor in WT mice pretreated with the selective 5-HT(1A)R antagonist WAY-100635.The PCP-induced disorganization of PFC activity does not appear to depend on serotonergic function. However, the lack of effect of clozapine in KO-1A mice and the prevention by WAY-100635 indicates that its therapeutic action involves 5-HT(1A)R activation without the need to block 5-HT(2A)R, as observed with clozapine-induced cortical dopamine release.

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