Chang T K, Niu C S, Cheng J T
Department of Neurology, China Medical College, Taichung City, Taiwan, ROC.
Neurosci Lett. 1996 Nov 8;218(3):161-4. doi: 10.1016/s0304-3940(96)13142-6.
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.
神经肽Y（NPY）在去甲肾上腺素能神经传递中的作用已被提及，它在中枢和外周神经系统中均作为共递质。影响大鼠内源性去甲肾上腺素（NE）的药物可改变大脑中的NPY含量。为了理解这一机制，本研究采用NPY放射免疫分析法进行。接受单胺氧化酶抑制剂帕吉林治疗的大鼠，其NPY样免疫反应性（NPY-ir）值降低，同时儿茶酚胺升高。用足以阻断受体的酚妥拉明、普萘洛尔和氟哌啶醇混合物预处理可消除此作用。然而，单独用氟哌啶醇治疗对此无影响。接受脑室内（i.c.v.）注射α1肾上腺素能受体激动剂甲氧明的大鼠，其大脑皮质NPY-ir降低。通过i.c.v.注射足以阻断α1肾上腺素能受体剂量的哌唑嗪可防止此作用。此外，哌唑嗪的类似处理也可逆转帕吉林引起的大脑皮质NPY-ir降低。所获得的数据表明，帕吉林使内源性NE增加，从而激活α1肾上腺素能受体，可能会降低大鼠大脑皮质中NPY的含量。
