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The present studies compared the effects of acute and chronic administration of haloperidol or clozapine on  c-fos  mRNA expression in the rat medial prefrontal cortex. Acute administration of clozapine, but not haloperidol, robustly increased  c-fos  mRNA expression in the infralimbic and prelimbic cortex of the rat. Even though most  c-fos  mRNA-expressing neurons in the clozapine-treated animals were localized in deep cortical layers, labeled neurons were found organized into several cell bridges connecting the superficial and deep layers of the cortex. After chronic treatment with clozapine,  c-fos  mRNA was reduced by−60% of that seen acutely; however, the columns of  c-fos  mRNA expressing neurons did not show the same magnitude of tolerance. Haloperidol had no significant effect even after chronic treatment. We examined further the role of dopamine D2 versus D3 receptors in  c-fos  gene induction in the infralimbic cortex by studying the acute effects of remoxipride and U-99194A. Remoxipride, a selective D2 antagonist  in vitro , induced  c-fos  mRNA at very low doses and lost its ability to alter  c-fos  mRNA levels at higher doses. Interestingly, U-991 94A, an antagonist with 20-fold selectivity for D3 over D2 receptors, also produced greater induction of  c-fos  mRNA at lower doses. We hypothesize that blockade of D3 receptors may enhance  c-fos  gene expression in the medial prefrontal cortex but that of D2 receptors may prevent the same.

Induction of c-fos mRNA in Rat Medial Prefrontal Cortex by Antipsychotic Drugs: Role of Dopamine D2 and D3 Receptors