Fetissov S, Nicolaïdis S
Groupe de Neurobiologie des Regulations, IESGCA de Dijon, CNRS UPR 9054, Collège de France, Paris, France.
Neuropeptides. 1998 Feb;32(1):63-6. doi: 10.1016/s0143-4179(98)90018-x.
The obesity syndrome in Zucker rats is associated with an elevated neuropeptide Y (NPY) content in the hypothalamus. It is recognized that the axons of NPY-ergic neurons arriving from the arcuate nucleus and the midbrain are the major source of NPY in this area. In magnocellular hypothalamic neurosecretory neurons (MCN) of normal rats NPY is expressed only in response to hyperosmotic stimulation. This study used immunohistochemistry with colchicine treatment aimed at MCN to compare NPY localization in obese (fa/fa) and in lean (Fa/Fa) Zucker rats. It was found that the obese (fa/fa), in contrast to the lean (Fa/Fa) Zucker rat, displays NPY immunoreactivity in numerous MCN of the paraventricular, supraoptic as well as accessory neurosecretory nuclei. This finding suggests local synthesis of NPY in the MCN of obese (fa/fa) rats and involvement of hydro-osmotic disorders in the Zucker syndrome of obesity.
肥胖型 Zucker 大鼠的肥胖综合征与下丘脑神经肽 Y(NPY)含量升高有关。已知来自弓状核和中脑的 NPY 能神经元轴突是该区域 NPY 的主要来源。在正常大鼠的大细胞下丘脑神经分泌神经元(MCN)中,NPY 仅在高渗刺激下表达。本研究采用秋水仙碱处理的免疫组织化学方法针对 MCN,比较肥胖型(fa/fa)和瘦型(Fa/Fa)Zucker 大鼠中 NPY 的定位。结果发现,与瘦型(Fa/Fa)Zucker 大鼠不同,肥胖型(fa/fa)大鼠在室旁核、视上核以及附属神经分泌核的众多 MCN 中均显示 NPY 免疫反应性。这一发现提示肥胖型(fa/fa)大鼠的 MCN 中存在 NPY 的局部合成,且水渗透紊乱参与了 Zucker 肥胖综合征。