Volume 23, Issue 2 (June 2019)                   Physiol Pharmacol 2019, 23(2): 82-90 | Back to browse issues page

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Hamidizad Z, Ababzadeh S, Heidari F, Haeri N, Eslami Farsani M, Sadegh M. Cobalamin modulate neurotoxic effects of trimethyltin chloride on hippocampus neural cells and cognitive function. Physiol Pharmacol. 2019; 23 (2) :82-90
URL: http://phypha.ir/ppj/article-1-1460-en.html
Abstract:   (492 Views)
Introduction: Cobalamin (vitamin B12) is essential for metabolism of the nervous system and its supplementation attenuate neuropathic and neuroinflammatory diseases. We designed to investigate the neuroprotective effects of cobalamin against the trimethyltin chloride (TMT) induced structural and functional damages in the hippocampus. Methods: Adult male Wistar rats were divided into four groups: 1) control: received saline; 2) TMT: received a single dose of TMT (8mg/kg; ip) to induce hippocampal damages; 3) cobalamin: received cobalamin (18mg/kg; ip) for five consecutive days and 4) TMT+cobalamin: received single ip injection of TMT then were treated with cobalamin for five consecutive days. In day six of the experiments, behavioral effects of TMT and cobalamin were evaluated through shuttle box and novel object recognition task. After the behavioral tests, animals were perfused transcardially and Nissl staining was used on hippocampus to assess neural cell damages. Results: Novel object exploring time was significantly decreased in TMT treated rats and treatment with cobalamin after TMT injection significantly recompensed this effect of TMT. In passive avoidance, TMT significantly decreased latency to enter the dark box, while cobalamin administration after the TMT injection significantly abolished this effect of TMT. Neural cell counted in the areas of hippocampus was significantly decreased in the TMT group and cobalamin treatment after the TMT injection significantly prevented neural cell loss. Conclusion: These results indicate a neuroprotective role for cobalamin against the TMT induced memory impairment and hippocampal neuronal loss.
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Types of Manuscript: Original Research | Subject: Learning and memory