Pre-ischemic Treatment with Ampicillin Reduces Neuronal Damage in the Mouse Hippocampus and Neostriatum after Transient Forebrain Ischemia
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Published on: July 25, 2011
Kyung-Eon Lee1, Seul-Ki Kim, Kyung-Ok Cho
1Department of Pharmacology, Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
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.
Insights
Ampicillin, a beta-lactam antibiotic, protects brain neurons from ischemic damage. This study shows ampicillin acts as a chemical preconditioning agent, reducing neuronal death in the hippocampus and neostriatum.
Area of Science:
- Neuroscience
- Pharmacology
- Ischemic Stroke Research
Background:
- Astrocytic glutamate transporter-1 (GLT-1) is crucial for neuronal protection against excitotoxicity.
- Beta-lactam antibiotics like ampicillin may induce GLT-1 expression.
- Ischemic stroke causes significant neuronal damage in brain regions like the hippocampus and neostriatum.
Purpose of the Study:
- To investigate the neuroprotective effects of ampicillin against ischemic neuronal damage.
- To determine if ampicillin acts as a chemical preconditioning agent.
- To evaluate the dose-dependent efficacy of ampicillin in preventing ischemic neuronal death.
Main Methods:
- Transient global forebrain ischemia was induced in male C57BL/6 mice via bilateral carotid artery occlusion.
- Ampicillin was administered either pre-ischemically or post-ischemically at doses of 50 mg/kg/day or 200 mg/kg/day.
- Neuronal survival in the hippocampus (medial CA1) and neostriatum was assessed after the ischemic event.
Main Results:
- Both pre- and post-ischemic ampicillin treatment dose-dependently prevented neuronal death in the hippocampus and neostriatum.
- A significant reduction in ischemic neuronal damage was observed with pre-ischemic ampicillin administration (200 mg/kg/day).
- Ampicillin demonstrated a clear neuroprotective effect against global forebrain ischemia.
Conclusions:
- Ampicillin exhibits significant neuroprotective properties against ischemic brain injury.
- The findings suggest ampicillin functions as a chemical preconditioning agent, enhancing neuronal resilience to ischemic insults.
- Ampicillin's ability to protect hippocampal neurons highlights its therapeutic potential in stroke recovery.
