Volume 9, Issue 3 (Autumn 2007)
Advances in Cognitive Sciences 2007, 9(3): 9-19 |
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Abstract: (2393 Views)
Objective: To examine the effects of bilateral injections of cholinergic agents into the hippocampal CA1 regions (intra-CA1) on ethanol state-dependent memory in mice.
Method: Male NMRI mice (20-30 g) were used in this research. The cannulas were implanted (bilaterally) in the CA1 of dorsal hippocampus by Stereotaxic instrument in animals. All animals were allowed one week to recover before behavioral experiments. A single-trial step-down passive avoidance task was used for the assessment of memory retention.
Results: Pre-test administration of ethanol (0.5 and 1 g/kg) induced state-dependent retrieval of the memory acquired under pre-training ethanol (1 g/kg) influence. Pre-test intra-CA1 injection of physostigmine and nicotine improved pre-training ethanol (1 g/kg)-induced retrieval impairment. Moreover, pre-test intra-CA1 administration of physostigmine and nicotine with an ineffective dose of ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol state-dependent memory. Pre-test intra-CA1, injection of the muscarinic receptor antagonist, atropine or the nicotinic receptor antagonist, mecamylamine along with the intra-peritoneal administration of ethanol (1 g/kg) inhibited ethanol state-dependent memory. Intra-CA1 pre-test administration of physostigmine, atropine, nicotine or mecamylamine alone did not affect memory retention.
Conclusion: These findings indicate that the cholinergic system is involved in ethanol state-dependent memory through muscarinic and nicotinic receptors of dorsal hippocampalCA1 regions.
Method: Male NMRI mice (20-30 g) were used in this research. The cannulas were implanted (bilaterally) in the CA1 of dorsal hippocampus by Stereotaxic instrument in animals. All animals were allowed one week to recover before behavioral experiments. A single-trial step-down passive avoidance task was used for the assessment of memory retention.
Results: Pre-test administration of ethanol (0.5 and 1 g/kg) induced state-dependent retrieval of the memory acquired under pre-training ethanol (1 g/kg) influence. Pre-test intra-CA1 injection of physostigmine and nicotine improved pre-training ethanol (1 g/kg)-induced retrieval impairment. Moreover, pre-test intra-CA1 administration of physostigmine and nicotine with an ineffective dose of ethanol (0.25 g/kg) significantly restored the retrieval and induced ethanol state-dependent memory. Pre-test intra-CA1, injection of the muscarinic receptor antagonist, atropine or the nicotinic receptor antagonist, mecamylamine along with the intra-peritoneal administration of ethanol (1 g/kg) inhibited ethanol state-dependent memory. Intra-CA1 pre-test administration of physostigmine, atropine, nicotine or mecamylamine alone did not affect memory retention.
Conclusion: These findings indicate that the cholinergic system is involved in ethanol state-dependent memory through muscarinic and nicotinic receptors of dorsal hippocampalCA1 regions.
Type of Study: Research |
Subject:
Special
Received: 2007/05/3 | Accepted: 2007/07/24 | Published: 2007/09/23
Received: 2007/05/3 | Accepted: 2007/07/24 | Published: 2007/09/23
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