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食欲素A影响大鼠海马中胃扩张敏感神经元以及穹窿周区对胃动力和调节的作用。

Orexin-A affects gastric distention sensitive neurons in the hippocampus and gastric motility and regulation by the perifornical area in rats.

作者信息

Sun Shu, Xu Luo, Sun Xiangrong, Guo Feifei, Gong Yanling, Gao Shengli

机构信息

Department of Pathophysiology, Medical College of Qingdao University, Qingdao 266021, China.

Department of Pathophysiology, Medical College of Qingdao University, Qingdao 266021, China.

出版信息

Neurosci Res. 2016 Sep;110:59-67. doi: 10.1016/j.neures.2016.04.001. Epub 2016 Apr 11.

Abstract

Orexin-A is mainly produced in the lateral hypothalamus (LHA) and the perifornical area (PeF). Here, we aim to elucidate the effects of orexin-A in the hippocampus (Hi) on gastric distention (GD)-sensitive neurons and gastric motility, and potential regulation mechanisms by the PeF. Retrograde tracing and fluorescent-immunohistochemical staining were used to determine orexin-A neuronal projections. Single unit discharges in the Hi were recorded extracellularly and gastric motility in conscious rats was monitored during administration of orexin-A to the Hi or electrical stimulation of the PeF. Orexin-A administration to the Hi excited most of the GD-excitatory (GD-E) neurons and GD-inhibitory (GD-I) neurons, and increased gastric motility in a dose-dependent manner. All of effects induced by orexin-A could be partly blocked by pretreatment with orexin-A antagonist, SB-334867. Electrical stimulation of the PeF excited the majority of the orexin-A-responsive GD neurons in the Hi and promoted gastric motility. Additionally, pretreatment with SB-334867 in the Hi increased the firing rate of GDI and GDE neurons following electrical stimulation of the PeF. These findings suggest that orexin-A could regulate activities of GD-sensitive neurons and gastric motility. Furthermore, the PeF may be involved in this regulatory pathway.

摘要

食欲素A主要在下丘脑外侧区(LHA)和穹窿周区(PeF)产生。在此,我们旨在阐明海马体(Hi)中食欲素A对胃扩张(GD)敏感神经元和胃动力的影响,以及PeF的潜在调节机制。采用逆行追踪和荧光免疫组织化学染色来确定食欲素A神经元投射。在向Hi注射食欲素A或电刺激PeF期间,细胞外记录Hi中的单单位放电,并监测清醒大鼠的胃动力。向Hi注射食欲素A可兴奋大多数GD兴奋性(GD-E)神经元和GD抑制性(GD-I)神经元,并以剂量依赖方式增加胃动力。食欲素A诱导的所有效应均可被食欲素A拮抗剂SB-334867预处理部分阻断。电刺激PeF可兴奋Hi中大多数对食欲素A有反应的GD神经元并促进胃动力。此外,在Hi中用SB-334867预处理可增加电刺激PeF后GDI和GDE神经元的放电频率。这些发现表明,食欲素A可调节GD敏感神经元的活动和胃动力。此外,PeF可能参与了这一调节途径。

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