Korean J Cerebrovasc Dis.
2002 Mar;4(1):46-51.
Effect of Melatonin on Brain Polyamine Contents and Hippocampal Neuronal Damage after Transient Global Ischemia in Mongolian Gerbil
- Affiliations
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- 1Department of Family Medicine, School of Medicine, Keimyung University, Daegu, Korea.
- 2Department of Neurosurgery, School of Medicine, Keimyung University, Daegu, Korea.
- 3Department of Pharmacology, School of Medicine, Keimyung University, Daegu, Korea. srlee@dsmc.or.kr
Abstract
OBJECTIVES
This study was designed to examine whether melatonin has a neuroprotective effect against hippocampal neuronal damage following transient global ischemia in a gerbil. Polyamine is known to play a role in the pathophysiology of ischemic neuronal damage, we evaluated the influences of melatonin on the polyamine level as well as histology. MATERIAL AND METHODS: Male Mongolian gerbils (60-80 g) were used in this study. Transient global ischemia was induced by occlusion of the bilateral common carotid arteries for 3 min with microclips. Melatonin was administered immediately after occlusion. The animals were decapitated 24 h after the occlusion for polyamine measurement by a high performance liquid chromatography (HPLC) and 4 days after the occlusion for histological evaluation (hematoxylin and eosin staining). A histological examination was performed by a blinded investigator.
RESULTS
The hippocampal putrescine level increased compared to sham-operated animals and the increase of putrescine was attenuated by 20 mg/kg melatonin administration. Spermidine and spermine levels didn't show significant changes after ischemia. Hippocampal neuronal damage in the CA1 region was markedly observed in vehicle-treated animals compared to sham-operated animals. Melatonin administration (10 or 20 mg/kg) significantly inhibited hippocampal CA1 neuronal damage after ischemia compared to corresponding vehicle-treated animals (p<0.05 and p<0.01, respectively).
CONCLUSION
Melatonin attenuates the putrescine level after transient global ischemia and may have putative neuroprotective effects against global ischemia induced neuronal damage.
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