The Effects of Glutamate NMDA Receptor Antagonist MK-801 on Gastrointestinal Motility after Middle Cerebral Artery Occlusion in Rats.

This study was performed to investigate the role of glutamate neurotransmitter system on gastrointestinal motility in a middle cerebral artery occlusion (MCAO) model of rats. The right middle cerebral artery was occluded by surgical operation, and intestinal transit and geometric center as a parameter of gastrointestinal motility and expression of c-Fos protein in the insular cortex and cingulate cortex were measured at 2 and 12 h after MCAO. Intestinal transit was 66.3±7.5% and 62.3±5.7% 2 and 12 h after sham operation, respectively, and MCAO significantly decreased intestinal transit to 39.0±3.5% and 47.0±5.1% at 2 and 12 h after the occlusion, respectively (p＜ 0.01). The geometric center was 5.6±0.4 and 5.2±0.9 at 2 and 12 h after sham operation, respectively, and MCAO significantly decreased geometric center to 2.9±0.8 and 3.0±0.3 at 2 and 12 h after the occlusion, respectively (p＜ 0.01). In control animals, injection of atropine decreased intestinal transit to 35.9±5.2%, and injection of glutamate NMDA receptor antagonist, MK-801, decreased intestinal transit to 28.8±9.5%. Pretreatment with MK-801, a glutamate NMDA receptor antagonist, in the MCAO group decreased intestinal transit to 11.8±3.2%, which was significantly decreased compared to MCAO group (p＜0.01). MCAO markedly increased the expression of c-Fos protein in the insular cortex and cingulate cortex ipsilateral to the occlusion 2 h after MCAO, and pretreatment with MK-801 produced marked reduction of c-Fos protein expression compared to MCAO group (p＜ 0.01). These results suggest that modulation of gastrointestinal motility after MCAO might be partially mediated through a glutamate NMDA receptor system.