Laboratory for Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.
Auton Neurosci. 2013 Apr;175(1-2):61-9. doi: 10.1016/j.autneu.2012.12.006. Epub 2013 Jan 10.
Glucoprivation is a strong signal for the initiation of gastrointestinal contractions. While this relationship between utilizable nutrient levels and gastric motility has been recognized for more than 100 years, the explanation of this phenomenon has remained incomplete. Using widely differing approaches, recent work has suggested that the hindbrain is responsible for this chemoreflex effect. Surprisingly, astrocytes may be the main glucodetector elements under hypoglycemic conditions. Our own work using in vitro live cell calcium imaging shows that astrocytes in the NST increase cytoplasmic calcium in a concentration dependent manner in reaction to reductions in glucose. This effect is reversed on restoration of normal glucose concentrations. In vivo single unit neurophysiological recordings show that brainstem neurons driving gastric motility are activated by glucoprivic stimuli. Studies in intact animals verify that both dorsal medullary and systemic glucoprivation significantly increases gastric motility. Astrocyte inactivation with fluorocitrate blocks the pro-motility effects of glucoprivation. Thus, it appears that intact astrocyte signaling may be essential to glucoregulatory control over gastric motility.
糖剥夺是启动胃肠道收缩的强烈信号。虽然这种可用营养水平与胃动力之间的关系已经被认识了 100 多年，但对这一现象的解释仍然不完整。最近的研究工作使用了广泛不同的方法，表明后脑是这种化学反射效应的负责者。令人惊讶的是，星形胶质细胞可能是低血糖条件下的主要葡萄糖检测元件。我们自己使用体外活细胞钙成像的工作表明，NST 中的星形胶质细胞以浓度依赖的方式增加细胞质钙，以响应葡萄糖的减少。当恢复正常葡萄糖浓度时，这种作用会逆转。体内单个单位神经生理学记录显示，驱动胃动力的脑干神经元被糖剥夺刺激激活。在完整动物中的研究证实，背侧延髓和全身糖剥夺都会显著增加胃动力。用氟柠檬酸使星形胶质细胞失活会阻断糖剥夺的促动力作用。因此，似乎完整的星形胶质细胞信号可能是对胃动力进行糖调节控制所必需的。
