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 been mentioned as co-transmitter in both central and peripheral nervous system. Cerebral NPY content was changed by drugs influencing endogenous norepinephrine (NE) in rats. In an attempt to understand this mechanism, 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 oxidase, with an elevation of catecholamine in parallel. This action was abolished by pretreatment with a mixture of phentolamine, propranolol and haloperidol at concentration sufficient to block the receptors. However, it was not influenced by treatment with haloperidol alone. Cerebrocortical NPY-ir was lowered in rats receiving an intracerebroventricular (i.c.v.) injection of methoxamine, the agonist of alpha(1)-adrenoceptors, This action was prevented by prazosin via an i.c.v. injection at the dose sufficient to block alpha(1)-adrenoceptors. Moreover, decrease of cerebrocortical NPY-ir by pargyline was also reversed by similar treatment of prazosin. The data obtained suggests that activation of alpha(1)-adrenoceptors by endogenous NE which was increased by pargyline may lower the contents of NPY in cerebrocortex of the rat.