Basic and Clinical Neuroscience Journal · 2018 · 77 citations · 26 references
MedicineNeurosciencePharmacologyMemoryNeurochemistryNeuropharmacologyCognitive ImpairmentHippocampal SystemsMemory AssessmentMemory ConsolidationNeural Basis Of MemoryNeuroprotectionHippocampal AmnesiaHippocampal Memory FunctionHippocampal PhysiologyHippocampal ToxicityHippocampus SubfieldsOxidative Stress In NeurodegenerationOxidative Stress InjuryRodent Memory
INTRODUCTION: Scopolamine, a muscarinic cholinergic receptor antagonist, is widely used to induce memory impairment in experimental animals. The present study aims to compare memory impairment and oxidative stress following single and repeated doses administration of scopolamine. METHODS: A group of rats received a single shot of scopolamine in different doses (0.5, 1, or 3 mg/kg, IP) 24 hours after the passive avoidance training. Then the memory retrieval test was performed 30 minutes and 7 days after the injection. In the other experiment, rats received similar doses of scopolamine for 7 consecutive days, 24 hours after the training session. Then the memory retrieval test was performed 30 minutes and 7 days after the last injection. Acetylcholinesterase (AChE) activity and lipid peroxidation were measured in their hippocampus tissue, too. RESULTS: Scopolamine administered in repeated doses caused more impairment in memory function compared to single dose injection based on the evaluation 30 minutes after injection. Moreover, the memory impairment persisted for 7 days only in repeated doses treated groups. Increase in acetylcholinesterase activity and lipid peroxidation in both groups was observed 30 minutes after scopolamine administration. These abnormal increases persisted for 7 days only in repeated doses treated groups. Increased AChE activity and lipid peroxidation was well correlated with behavioral deficit. Also AChE activity was well associated with lipid peroxidation. CONCLUSION: The results of present study showed that repeated administration of scopolamine induced results in memory impairment. This effect can be due to long-lasting oxidative stress which may damage the hippocampus tissue.
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