Yokoyama Toru, Minami Kouichiro, Terawaki Kiyoshi, Miyano Kanako, Ogata Junichi, Maruyama Takashi, Takeuchi Mamoru, Uezono Yasuhito, Ueta Yoichi
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan; Division of Cancer Pathophysiology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan; Department of Anesthesiology and Critical Care Medicine, Jichi Medical University, 3311-1 Yakishiji, Shimotsuke, Tochigi 329-0483, Japan.
Division of Cancer Pathophysiology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan; Tsumura Research Laboratories, Tsumura and Company, 3586 Yoshiwara, Ami-machi, Inashiki-gun, Ibaraki 300-1192, Japan.
Brain Res. 2014 Oct 2;1583:45-54. doi: 10.1016/j.brainres.2014.08.020. Epub 2014 Aug 15.
Kisspeptin is the natural ligand of the G protein-coupled receptor -54 and plays a major role in gonadotropin-releasing hormone secretion in the hypothalamus. Kisspeptin-10 is an endogenous derivative of kisspeptin and has 10 -amino acids. Previous studies have demonstrated that central administration of kisspeptin-10 stimulates the secretion of arginine vasopressin (AVP) in male rats. We examined the effects of kisspeptin-10 on- excitatory synaptic inputs to magnocellular neurosecretory cells (MNCs) including AVP neurons in the supraoptic nucleus (SON) by obtaining in vitro whole-cell patch-clamp recordings from slice preparations of the rat brain. The application of kisspeptin-10 (100 nM-1 μM) significantly increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in a dose-related manner without affecting the amplitude. The kisspeptin-10-induced potentiation of the mEPSCs was significantly attenuated by previous exposure to the kisspeptin receptor antagonist kisspeptin-234 (100 nM) and to the protein kinase C inhibitor bisindolylmaleimide I (20 nM). These results suggest that kisspeptin-10 participates in the regulation of synaptic inputs to the MNCs in the SON by interacting with the kisspeptin receptor.
亲吻素是G蛋白偶联受体54的天然配体，在下丘脑促性腺激素释放激素分泌中起主要作用。亲吻素-10是亲吻素的一种内源性衍生物，含有10个氨基酸。先前的研究表明，向雄性大鼠中枢给予亲吻素-10可刺激精氨酸加压素（AVP）的分泌。我们通过从大鼠脑切片制备物中进行体外全细胞膜片钳记录，研究了亲吻素-10对包括视上核（SON）中AVP神经元在内的大细胞神经分泌细胞（MNCs）兴奋性突触输入的影响。给予亲吻素-10（100 nM - 1 μM）以剂量相关方式显著增加了微小兴奋性突触后电流（mEPSCs）的频率，而不影响其幅度。先前暴露于亲吻素受体拮抗剂亲吻素-234（100 nM）和蛋白激酶C抑制剂双吲哚马来酰亚胺I（20 nM）后，亲吻素-10诱导的mEPSCs增强作用显著减弱。这些结果表明，亲吻素-10通过与亲吻素受体相互作用参与对SON中MNCs突触输入的调节。
