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.