Abstract
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.