Serter Kocoglu Sema, Gok Yurtseven Duygu, Cakir Cihan, Minbay Zehra, Eyigor Ozhan
Department of Histology and Embryology, Balikesir University School of Medicine, 10145 Balikesir, Turkey.
Department of Histology and Embryology, Sanko University School of Medicine, 27090 Gaziantep, Turkey.
Brain Sci. 2020 Apr 6;10(4):217. doi: 10.3390/brainsci10040217.
Neuronostatin, a newly identified anorexigenic peptide, is present in the central nervous system. We tested the hypothesis that neuronostatin neurons are activated by feeding as a peripheral factor and that the glutamatergic system has regulatory influences on neuronostatin neurons. The first set of experiments analyzed the activation of neuronostatin neurons by refeeding as a physiological stimulus and the effectiveness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: the fasting group, refeeding group, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)+refeeding group. We found that refeeding increased the phosphorylated signal transducers and transcription activator-5 (pSTAT5) expression in neuronostatin-positive neurons and that the CNQX injection significantly suppressed the number of pSTAT5-expressing neuronostatin neurons. The second set of experiments analyzed the activation pathways of neuronostatin neurons and the regulating effects of the glutamatergic system on neuronostatin neurons. The animals received intraperitoneal injections of glutamate receptor agonists (kainic acid, α-amino-3-hydroxy-5methyl-4-isoazepropionic acid (AMPA), and N-methyl-D-aspartate (NMDA)) or 0.9% NaCl. The number of c-Fos-expressing neuronostatin neurons significantly increased following the AMPA and NMDA injections. In conclusion, we found that the neuronostatin neurons were activated by peripheral or central signals, including food intake and/or glutamatergic innervation, and that the glutamate receptors played an important role in this activation.
神经抑素是一种新发现的厌食肽，存在于中枢神经系统中。我们检验了以下假设：神经抑素神经元作为外周因素会因进食而被激活，并且谷氨酸能系统对神经抑素神经元具有调节作用。第一组实验分析了再进食作为一种生理刺激对神经抑素神经元的激活作用，以及谷氨酸能系统对这种生理刺激的有效性。实验对象被随机分为三组：禁食组、再进食组和6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）+再进食组。我们发现，再进食增加了神经抑素阳性神经元中磷酸化信号转导子和转录激活因子-5（pSTAT5）的表达，并且注射CNQX显著抑制了表达pSTAT5的神经抑素神经元的数量。第二组实验分析了神经抑素神经元的激活途径以及谷氨酸能系统对神经抑素神经元的调节作用。给动物腹腔注射谷氨酸受体激动剂（ kainic acid、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）和N-甲基-D-天冬氨酸（NMDA））或0.9%氯化钠。注射AMPA和NMDA后，表达c-Fos的神经抑素神经元数量显著增加。总之，我们发现神经抑素神经元会被外周或中枢信号激活，包括食物摄入和/或谷氨酸能神经支配，并且谷氨酸受体在这种激活过程中发挥了重要作用。
