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 paramet...
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 $66.3{\pm}7.5%$ and $62.3{\pm}5.7%$ 2 and 12 h after sham operation, respectively, and MCAO significantly decreased intestinal transit to $39.0{\pm}3.5%$ and $47.0{\pm}5.1%$ at 2 and 12 h after the occlusion, respectively (p<0.01). The geometric center was $5.6{\pm}0.4$ and $5.2{\pm}0.9$ at 2 and 12 h after sham operation, respectively, and MCAO significantly decreased geometric center to $2.9{\pm}0.8$ and $3.0{\pm}0.3$ at 2 and 12 h after the occlusion, respectively (p<0.01). In control animals, injection of atropine decreased intestinal transit to $35.9{\pm}5.2%$, and injection of glutamate NMDA receptor antagonist, MK-801, decreased intestinal transit to $28.8{\pm}9.5%$. Pretreatment with MK-801, a glutamate NMDA receptor antagonist, in the MCAO group decreased intestinal transit to $11.8{\pm}3.2%$, 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.
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 $66.3{\pm}7.5%$ and $62.3{\pm}5.7%$ 2 and 12 h after sham operation, respectively, and MCAO significantly decreased intestinal transit to $39.0{\pm}3.5%$ and $47.0{\pm}5.1%$ at 2 and 12 h after the occlusion, respectively (p<0.01). The geometric center was $5.6{\pm}0.4$ and $5.2{\pm}0.9$ at 2 and 12 h after sham operation, respectively, and MCAO significantly decreased geometric center to $2.9{\pm}0.8$ and $3.0{\pm}0.3$ at 2 and 12 h after the occlusion, respectively (p<0.01). In control animals, injection of atropine decreased intestinal transit to $35.9{\pm}5.2%$, and injection of glutamate NMDA receptor antagonist, MK-801, decreased intestinal transit to $28.8{\pm}9.5%$. Pretreatment with MK-801, a glutamate NMDA receptor antagonist, in the MCAO group decreased intestinal transit to $11.8{\pm}3.2%$, 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.
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문제 정의
One study showed that electrical stimulation of a certain area in the ventral insular cortex had no significant effect on heart and respiration rates but evoked changes in gastric motility [8]. This report supports the idea that the cerebral cortex takes part in modulation of gastrointestinal motility mediated through glutamate NMDA receptor system.
제안 방법
They were fasted for 48 h with free access to water only until use. Experimental animals were divided into control and MCAO groups. The control group was subdivided into control group for atropine injection or MK-801 injection and sham group for MCAO.
대상 데이터
Fifty-eight adult male Sprague-Dawley rats (Saemtaco Biokorea Co, Suwon, Korea) weighing 250 g were used. Animals were group-housed in a thermoregulated environment with a 12 h light/dark cycle.
데이터처리
All data are presented as the mean±SD. The statistical significance of the differences was assessed using one-way analysis of variance (ANOVA) followed by Tukey's post-hoc comparison matrix. Values of p<0.
성능/효과
In this study, both the intestinal transit and the geometric center in the MCAO group were significantly decreased compared to the sham group. Those results strongly suggest that gastrointestinal motility decreases after focal cerebral ischemia, explaining the high incidence of constipation after strokes.
Taken together, the findings of this study suggest that modulation of gastrointestinal motility after MCAO might be partially mediated through a glutamate NMDA receptor system. These results may provide a basic strategy for treatment of constipation in stroke patients.
0%. The reduction of intestinal transit in the atropine group was almost equal to the value of the MCAO group but was significantly decreased compared to the saline group (p < 0.01). After injection of MK-801 in control animals, the intestinal transit was 28.
참고문헌 (25)
Cheung RT, Hachinski V. The insula and cerebrogenic sudden death. Arch Neurol. 2000;57:1685-1688.
Harari D, Norton C, Lockwood L, Swift C. Treatment of constipation and fecal incontinence in stroke patients: Randomized controlled trial. Stroke. 2004;35:2549-2555.
Bracci F, Badiali D, Pezzotti P, Scivoletto G, Fuoco U, Di Lucente L, Petrelli A, Corazziari E. Chronic constipation in hemiplegic patients. World J Gastroenterol. 2007;13:3967-3972.
Aleksandrov VG, Bagaev VA, Nozdrachev AD, Panteleev SS. Identification of gastric related neurons in the rat insular cortex. Neurosci Lett. 1996;216:5-8.
Saito I, Segawa H, Shiokawa Y, Taniguchi M, Tsutsumi K. Middle cerebral artery occlusion: correlation of computed tomography and angiography with clinical outcome. Stroke. 1987;18:863-868.
Cabezos PA, Vera G, Castillo M, Fernandez-Pujol R, Martin MI, Abalo R. Radiological study of gastrointestinal motor activity after acute cisplatin in the rat. Temporal relationship with pica. Auton Neurosci. 2008;141:54-65.
Puig N, Davalos A, Adan J, Piulats J, Martinez JM, Castillo J. Serum amino acid levels after permanent middle cerebral artery occlusion in the rat. Cerebrovasc Dis. 2000;10:449-454.
Lee JH, Ameer AN, Choi MA, Lee MY, Kim MS, Park BR. Recovery of vestibulogastrointestinal symptoms during vestibular compensation after unilateral labyrinthectomy in rats. Otol & Neurotol. 2010;31:241-249.
Kim MS, Jin BK, Chun SW, Lee MY, Lee SH, Kim JH, Park BR. Effect of MK801 on cfos-like protein expression in the medial vestibular nucleus at early stage of vestibular compensation in uvulonodullectomized rats. Neurosci Lett. 1997;231:147-150.
Colivicchi F, Bassi A, Santini M, Caltagirone C. Cardiac autonomic derangement and arrhythmias in right-sided stroke with insular involvement. Stroke. 2004;35:2094-2098.
Schneider RJ, Friedman DP, Mishkin M. A modality-specific somatosensory area within the insula of the rhesus monkey. Brain Res. 1993;621:16-120.
Yasui Y, Breder CD, Saper CB, Cechetto DF. Autonomic responses and efferent pathways from the insular cortex in the rat. J Comp Neurol. 1991;303:355-374.
Collaco-Moraes Y, Aspey BS, de Belleroche JS, Harrison MJ. Focal ischemia causes an extensive induction of immediate early genes that are sensitive to mk-801. Stroke. 1994;25:1855-1860.
Estus S, Zaks WJ, Freeman RS, Gruda M, Bravo R, Johnson EM Jr. Altered gene expression in neurons during programmed cell death: Identification of c-jun as necessary for neuronal apoptosis. J Cell Biol. 1994;127:1717-1727.
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