Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee AL36088, United States.
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee AL36088, United States.
Brain Res. 2019 Apr 1;1708:200-206. doi: 10.1016/j.brainres.2018.12.019. Epub 2018 Dec 17.
Recently, we reported that non-sulfated cholecystokinin-8 (NS CCK-8) reduces food intake by cholecystokinin-B receptors (CCK-BR). To examine a possible site of action for this peptide, and based on the fact that both NS CCK-8 and CCK-BR are found centrally and peripherally, in the current study we hypothesized that NS CCK-8 increases Fos-like immunoreactivity (Fos-LI, a neuronal activation marker) in the dorsal vagal complex (DVC) of the hindbrain and the myenteric and submucosal plexuses of the small intestine. We found that intraperitoneal NS CCK-8 (0.5 nmol/kg) increases Fos-LI in the DVC, the myenteric and the submucosal plexuses of the duodenum and the myenteric plexus of the jejunum. The findings suggest, but does not prove, a potential role for the DVC and the enteric neurons in the feeding responses evoked by NS CCK-8.
最近，我们报道了非硫酸化胆囊收缩素-8（NS CCK-8）通过胆囊收缩素-B 受体（CCK-BR）减少食物摄入。为了研究这种肽的可能作用部位，并且基于 NS CCK-8 和 CCK-BR 都在中枢和外周发现的事实，在当前研究中，我们假设 NS CCK-8 增加了后脑迷走神经复合体（DVC）和小肠肌间和黏膜下丛中的 Fos 样免疫反应性（Fos-LI，神经元激活标志物）。我们发现，腹腔内给予 NS CCK-8（0.5 nmol/kg）会增加 DVC、十二指肠肌间和黏膜下丛以及空肠肌间丛中的 Fos-LI。这些发现表明，但不能证明，DVC 和肠神经元在 NS CCK-8 引起的进食反应中可能发挥作用。
