Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, USA.
Peptides. 2011 Aug;32(8):1600-5. doi: 10.1016/j.peptides.2011.06.023. Epub 2011 Jul 2.
We and others have shown that gastrin-releasing peptide (GRP) reduces food intake. In this study, we determined the activation of the gastrointestinal and dorsal vagal complex (DVC) neurons by various forms of GRP to determine the pathway involved in this reduction. We found the following: (1) GRP-10, -27 and -29 (2.1 nmol/kg, i.p.) increased the Fos-like immunoreactivity (Fos-LI, a marker for neuronal activation) in the myenteric neurons of the stomach and the area postrema (AP) of the DVC; (2) GRP-27 and GRP-29 increased the Fos-LI in the myenteric plexus of the duodenum; and (3) only GRP-29 increased the Fos-LI in the submucosal plexus of the duodenum. In conclusion, GRP may reduce food intake by activating the area postrema. The enteric neurons may have a potential role in this reduction through the direct activation of the AP or exerting local gut actions, such as the stimulation of gut motility or secretions.
我们和其他人已经表明,胃泌素释放肽(GRP)可减少食物摄入。在这项研究中,我们确定了各种形式的 GRP 对胃肠道和迷走神经背侧复合体(DVC)神经元的激活作用,以确定参与这种减少的途径。我们发现:(1)GRP-10、-27 和-29(2.1 nmol/kg,腹腔内注射)增加了胃的肌间神经元和 DVC 的后极(AP)中的 Fos 样免疫反应性(Fos-LI,神经元激活的标志物);(2)GRP-27 和 GRP-29 增加了十二指肠肌间神经丛中的 Fos-LI;(3)只有 GRP-29 增加了十二指肠黏膜下神经丛中的 Fos-LI。总之,GRP 可能通过激活后极来减少食物摄入。肠神经元可能通过直接激活 AP 或发挥局部肠道作用,如刺激肠道蠕动或分泌,在这种减少中发挥潜在作用。