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Orexin-A signaling in the paraventricular nucleus modulates spontaneous firing of glucose-sensitive neurons and promotes food intake via the NPY pathway in rats
- Wang, Cheng, Han, Xiaohua, Guo, Feifei, Sun, Xiangrong, Luan, Xiao, Xu, Luo
- Biochemical and biophysical research communications 2018 v.505 no.1 pp. 162-167
- antagonists, food intake, glucose, injection, neurons, neuropeptide Y, obesity, pathogenesis, rats
- Understanding the mechanisms regulating feeding is crucial to unraveling the pathogenesis of obesity. The study primary explored the effects of orexin-A and neuropeptide Y (NPY) signaling in the hypothalamic paraventricular nucleus (PVN) on feeding and glucose-sensitive (GS) neuron activity in rats. Microinjection of orexin-A into the PVN promoted feeding and modulated the spontaneous firing of GS neurons. Those effects were eliminated by pre-injection of the orexin-A receptor-1 (OX1R) antagonist SB-334867 and weaken by the NPY-1 receptor (NPY-1R) antagonist BMS-193885. After orexin-A administration into the PVN, the number of c-fos cells in the arcuate nucleus (ARC) was significantly higher than that in the group receiving normal saline. Furthermore, most cells exhibited co-expression of NPY and c-fos, indicating activation of NPY neurons in the ARC by PVN-administered orexin-A, which might be involved in feeding regulation. These findings indicate that orexin-A and NPY signaling in the PVN are essential to regulating GS neuronal excitability and feeding in rats.