Pre-ischemic Treatment with Ampicillin Reduces Neuronal Damage in the Mouse Hippocampus and Neostriatum after Transient Forebrain Ischemia.
10.4196/kjpp.2008.12.6.287
- Author:
Kyung Eon LEE
1
;
Seul Ki KIM
;
Kyung Ok CHO
;
Seong Yun KIM
Author Information
1. Department of Pharmacology, Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea. syk@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Ampicillin;
Neuroprotection;
Hippocampus;
Neostriatum;
Global forebrain ischemia;
Mice
- MeSH:
Ampicillin;
Animals;
Carotid Artery, Common;
Glutamic Acid;
Halothane;
Hippocampus;
Humans;
Ischemia;
Male;
Mice;
Neostriatum;
Neurons;
Prosencephalon
- From:The Korean Journal of Physiology and Pharmacology
2008;12(6):287-291
- CountryRepublic of Korea
- Language:English
-
Abstract:
Ampicillin, a beta-lactam antibiotic, has been reported to induce astrocytic glutamate transporter-1 which plays a crucial role in protecting neurons against glutamate excitotoxicity. We investigated the effect of ampicillin on neuronal damage in the mouse hippocampus and neostriatum following transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery for 40 min. Ampicillin was administered post-ischemically (for 3 days) and/or pre-ischemically (for 3~5 days until one day before the onset of ischemia). Pre- and post-ischemic treatment with ampicillin (50 mg/kg/day or 200 mg/kg/day) prevented ischemic neuronal death in the medial CA1 area of the hippocampus as well as the neostriatum in a dose-dependent manner. In addition, ischemic neuronal damage was reduced by pre-ischemic treatment with ampicillin (200 mg/kg/day). In summary, our results suggest that ampicillin plays a functional role as a chemical preconditioning agent that protects hippocampal neurons from ischemic insult.
