Okamura H, Sugano T, Ibata Y
Department of Anatomy and Neurobiology, Kobe University School of Medicine, Kobe, Japan.
Neurochem Res. 1996 Feb;21(2):239-43. doi: 10.1007/BF02529140.
The effect of reserpine on neuropeptide Y immunoreactive (NPY-IR) neurons in the rat hypothalamic arcuate nucleus was examined by immunocytochemical techniques. Although only NPY-IR fibers and terminals were distributed in this nucleus in untreated and saline treated rats, single treatment of reserpine (10 mg/kg, i.p.) visualized abundant NPY-IR neuronal cell bodies: the increase began at 12 h of postinjection, reached its maximal level at 48 h, and returned to its normal level at 96 h. Pretreatment of nialamide, a monoamine oxidase inhibitor, prevented these acute reserpine-induced changes, suggesting reserpine acts on NPY neurons through monoaminergic mechanism. Chronic treatment of haloperidol (5 mg/kg, once daily for 5 days) a dopamine receptor antagonist, could induce the similar increase of NPY immunoreactivity. However, interruption of adrenergic and serotonergic neurotransmissions by chronic treatment of propranorol and methysergide, or chemical lesions of ascending noradrenergic and serotonergic pathways by 6-hydroxydopamine and 5,6-dihydroxytryptamine, could not induce any immunoreactive increase of NPY in arcuate neurons. These findings strongly suggest that reserpine-induced NPY increase occurs through dopaminergic afferents in hypothalamic arcuate neurons.
采用免疫细胞化学技术研究了利血平对大鼠下丘脑弓状核中神经肽Y免疫反应性（NPY-IR）神经元的影响。在未处理和生理盐水处理的大鼠中，该核内仅分布有NPY-IR纤维和终末，但单次注射利血平（10mg/kg，腹腔注射）后可见大量NPY-IR神经元胞体：注射后12小时开始增加，48小时达到最高水平，96小时恢复至正常水平。单胺氧化酶抑制剂尼亚酰胺预处理可防止利血平引起的这些急性变化，提示利血平通过单胺能机制作用于NPY神经元。多巴胺受体拮抗剂氟哌啶醇（5mg/kg，每日一次，共5天）慢性处理可诱导类似的NPY免疫反应性增加。然而，普萘洛尔和甲基麦角新碱慢性处理阻断肾上腺素能和5-羟色胺能神经传递，或6-羟基多巴胺和5,6-二羟基色胺对去甲肾上腺素能和5-羟色胺能上行通路进行化学损伤，均不能诱导弓状核神经元NPY免疫反应性增加。这些发现强烈提示，利血平诱导的NPY增加是通过下丘脑弓状核神经元中的多巴胺能传入实现的。
