Neuroprotective Effects by Nimodipine Treatment in the Experimental Global Ischemic Rat Model : Real Time Estimation of Glutamate.
- Author:
Seok Keun CHOI
1
;
Gi Ja LEE
;
Samjin CHOI
;
Youn Jung KIM
;
Hun Kuk PARK
;
Bong Jin PARK
Author Information
- Publication Type:Original Article
- Keywords: Nimodipine; Glutamate; Eleven vessel occlusion ischemia model; Real-time monitoring; Nissl staining
- MeSH: Animals; Biosensing Techniques; Brain; Cell Death; Electroencephalography; Glutamic Acid; Glycosaminoglycans; Hippocampus; Ischemia; Microdialysis; Neurons; Neuroprotective Agents; Neurotransmitter Agents; Nimodipine; Rats; Salicylamides
- From:Journal of Korean Neurosurgical Society 2011;49(1):1-7
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVE: Glutamate is a key excitatory neurotransmitter in the brain, and its excessive release plays a key role in the development of neuronal injury. In order to define the effect of nimodipine on glutamate release, we monitored extracellular glutamate release in real-time in a global ischemia rat model with eleven vessel occlusion. METHODS: Twelve rats were randomly divided into two groups: the ischemia group and the nimodipine treatment group. The changes of extracellular glutamate level were measured using microdialysis amperometric biosensor, in coincident with cerebral blood flow (CBF) and electroencephalogram. Nimodipine (0.025 microg/100 gm/min) was infused into lateral to the CBF probe, during the ischemic period. Also, we performed Nissl staining method to assess the neuroprotective effect of nimodipine. RESULTS: During the ischemic period, the mean maximum change in glutamate concentration was 133.22+/-2.57 microM in the ischemia group and 75.42+/-4.22 microM (p<0.001) in the group treated with nimodipine. The total amount of glutamate released was significantly different (p<0.001) between groups during the ischemic period. The %cell viability in hippocampus was 47.50+/-5.64 (p<0.005) in ischemia group, compared with sham group. But, the %cell viability in nimodipine treatment group was 95.46+/-6.60 in hippocampus (p<0.005). CONCLUSION: From the real-time monitoring and Nissl staining results, we suggest that the nimodipine treatment is responsible for the protection of the neuronal cell death through the suppression of extracellular glutamate release in the 11-VO global ischemia model of rat.
