ACTIVATION OF ALPHA(1)-ADRENOCEPTORS TO LOWER CEREBROCORTICAL NEUROPEPTIDE-Y (NPY)-LIKE IMMUNOREACTIVITY IN RATS RECEIVING PARGYLINE TREATMENT

Role of neuropeptide Y (NPY) in noradrenergic neurotransmission has be en mentioned as co-transmitter in both central and peripheral nervous system. Cerebral NPY content was changed by drugs influencing endogeno us norepinephrine (NE) in rats. In an attempt to understand this mecha nism, the present study was carried out using the radioimmunoassay of NPY. Values of NPY-like immunoreactivity (NPY-ir) were reduced in rats receiving the treatment of pargyline, the inhibitor of monoamine oxid ase, with an elevation of catecholamine in parallel. This action was a bolished by pretreatment with a mixture of phentolamine, propranolol a nd haloperidol at concentration sufficient to block the receptors. How ever, it was not influenced by treatment with haloperidol alone. Cereb rocortical NPY-ir was lowered in rats receiving an intracerebroventric ular (i.c.v.) injection of methoxamine, the agonist of alpha(1)-adreno ceptors, This action was prevented by prazosin via an i.c.v. injection at the dose sufficient to block alpha(1)-adrenoceptors. Moreover, dec rease of cerebrocortical NPY-ir by pargyline was also reversed by simi lar treatment of prazosin. The data obtained suggests that activation of alpha(1)-adrenoceptors by endogenous NE which was increased by parg yline may lower the contents of NPY in cerebrocortex of the rat.