2010Advances in Cognitive ScienceRequires access

Effects of WIN55,212-2 in the Dorsal Hippocampus on Scopolamine State-Dependent Memory

Morteza Piri, Nasehi Mohammad, Shahin Maryam Sadat, Zarrindast Mohammad Reza

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Abstract

Objective: To assess the effects of the cannabinoid receptor agonist, WIN55, 212-2 on scopolamine induced state-dependent memory. Method: The step-down passive avoidance paradigm was used in the present study, which is an accepted model to examine long-term memory in mice. Results: Post-training intra-CA1 administration of scopolamine (2 and 4 µg/mouse) decreased the memory retrieval. Pre-test scopolamine administration restored the retrieval to the control level in the test day. This phenomenon is known as scopolamine state-dependent memory. Administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 5 min before test by itself decreased the memory retrieval. On the other hand, the animals in which memory retrieval was impaired due to scopolamine (2 µg/mouse) post-training administration, pre-test administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 24 hr after training on the day of the test restored memory. Moreover, pre-test co-administration of non-effective dose of scopolamine with ineffective dose of WIN55, 212-2 increased the restoration of memory by scopolamine. Conclusion: These results suggest that cannabinoid receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state- dependent memory.

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Objective: To assess the effects of the cannabinoid receptor agonist, WIN55, 212-2 on scopolamine induced state-dependent memory. Method: The step-down passive avoidance paradigm was used in the present study, which is an accepted model to examine long-term memory in mice. Results: Post-training intra-CA1 administration of scopolamine (2 and 4 µg/mouse) decreased the memory retrieval. Pre-test scopolamine administration restored the retrieval to the control level in the test day. This phenomenon is known as scopolamine state-dependent memory. Administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 5 min before test by itself decreased the memory retrieval. On the other hand, the animals in which memory retrieval was impaired due to scopolamine (2 µg/mouse) post-training administration, pre-test administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 24 hr after training on the day of the test restored memory. Moreover, pre-test co-administration of non-effective dose of scopolamine with ineffective dose of WIN55, 212-2 increased the restoration of memory by scopolamine. Conclusion: These results suggest that cannabinoid receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state- dependent memory.

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Available abstract

Objective: To assess the effects of the cannabinoid receptor agonist, WIN55, 212-2 on scopolamine induced state-dependent memory. Method: The step-down passive avoidance paradigm was used in the present study, which is an accepted model to examine long-term memory in mice. Results: Post-training intra-CA1 administration of scopolamine (2 and 4 µg/mouse) decreased the memory retrieval. Pre-test scopolamine administration restored the retrieval to the control level in the test day. This phenomenon is known as scopolamine state-dependent memory. Administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 5 min before test by itself decreased the memory retrieval. On the other hand, the animals in which memory retrieval was impaired due to scopolamine (2 µg/mouse) post-training administration, pre-test administration of WIN55, 212-2 (1 µg/mouse, intra-CA1) 24 hr after training on the day of the test restored memory. Moreover, pre-test co-administration of non-effective dose of scopolamine with ineffective dose of WIN55, 212-2 increased the restoration of memory by scopolamine. Conclusion: These results suggest that cannabinoid receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state- dependent memory.

Key concepts: Scopolamine, Amnesia, Hippocampal formation, Hippocampus, Agonist, Psychology, Cannabinoid, Neuroscience

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