Immunohistochemical alterations in neuropeptide Y-positive nerve elements in rat cerebral cortex following acute phencyclidine treatment.

Acute administration of phencyclidine (PCP), an NMDA receptor antagonist, alters neuropeptide Y (NPY) immunoreactivity in the rat forebrain. Compared to controls, PCP treatment increased the number of NPY-positive cell bodies by 178% while decreasing the area of NPY-positive fibers and terminals by 38%. These changes occurred throughout the cerebral cortex, suggesting that the cortical NPY neuronal system is at least partly regulated by glutamatergic inputs through NMDA receptor-mediated mechanisms.

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Abstract

Phencyclidine (PCP) is a dissociative drug and has been known to be an antagonist of N-methyl-D-aspartate (NMDA) receptor. We examined possible effects of acute treatment with PCP on neuropeptide Y (NPY) immunoreactive nerve fibres and cell bodies in rat forebrain by immunocytochemistry combined with morphometric analysis. Following the treatment, significant alterations were observed throughout the cerebral cortex, compared with controls. NPY-positive perikarya were increased in number (178%) whereas NPY-positive fibres and terminals were decreased in area (38%). The result suggests that the cortical NPY neuronal system is controlled, at least partly, by glutamatergic inputs via NMDA receptor-mediated mechanisms.