Nesfatin-1 signaling in the basom聽edial amygdala modulates the gastric distension-sensitive neurons discharge and decreases gastric motility via melanocortin 3/4 receptors and modified by the arcuate nucleus

详细信息    查看全文

• 作者：Luo Xu^a ; ^{xu.luo@163.com" class="auth_mail" title="E-mail the corresponding author} ; Qiaoling Wang^a ; Feifei Guo^a ; Mingjie Pang^c ; Xiangrong Sun^a ; Shengli Gao^a ; Yanling Gong^b
• 关键词：Nesfatin-1 ; Amygdala ; Arcuate nucleus ; Gastric distension responsive neurons ; Gastric motility
• 刊名：European Journal of Pharmacology
• 出版年：2015
• 出版时间：5 October 2015
• 年：2015
• 卷：764
• 期：Complete
• 页码：164-172
• 全文大小：3418 K

文摘

Nesfatin-1 is a novel anorexigenic peptide that regulates feeding behavior and gastrointestinal function. This study aimed to explore the effects of nesfatin-1 on gastric distension (GD)-sensitive neurons in the basomedial amygdala (BMA) and the potential mechanism for nesfatin-1 to regulate gastric motility through the arcuate nucleus (Arc). The projection of nerve fiber and expression of nesfatin-1 were observed by retrograde tracing and fluo-immunohistochemistry staining. Single-unit discharges in the BMA were recorded extracellularly, and gastric motility in conscious rats was monitored. Results showed that the nesfatin-1/ fluorogold-double labeled neurons were observed in the Arc. Nesfatin-1 could excite the GD-excitatory neurons and inhibit the GD-inhibitory neurons in the BMA. Gastric motility and gastric emptying were significantly reduced by nesfatin-1 administration to the BMA in a dose-dependent manner. The effects of nesfatin-1 could be partially blocked by melanocortin 3/4 receptors antagonist, SHU9119. Electrical stimulation of the Arc significantly excited the response of GD neurons to nesfatin-1 and promoted gastric motility. Nevertheless, these effects could be mitigated by pretreatment with anti-NUCB2/nesfatin-1 antibody. It is suggested that nesfatin-1 in the BMA plays an important role in decreasing gastric motility and the Arc may be involved in this regulation process.