The Effects of Glutamate NMDA Receptor Antagonist MK-801 on Gastrointestinal Motility after Middle Cerebral Artery Occlusion in Rats.
10.4196/kjpp.2010.14.3.151
- Author:
Nasir Hussin AMEER
1
;
Jae Hee LEE
;
Myoung Ae CHOI
;
Guang Shi JIN
;
Min Sun KIM
;
Byung Rim PARK
Author Information
1. Department of Physiology, Wonkwang University School of Medicine, and Brain Research Institute at Wonkwang University, Iksan 570-749, Korea. byungp@wku.ac.kr
- Publication Type:Original Article
- Keywords:
Glutamate;
Insular cortex;
Intestinal transit;
MCAO;
MK-801
- MeSH:
Animals;
Atropine;
Dizocilpine Maleate;
Gastrointestinal Motility;
Glutamic Acid;
Gyrus Cinguli;
Infarction, Middle Cerebral Artery;
Middle Cerebral Artery;
N-Methylaspartate;
Neurotransmitter Agents;
Rats;
Salicylamides
- From:The Korean Journal of Physiology and Pharmacology
2010;14(3):151-156
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
