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“School of Cognitive Sciences”

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Paper   IPM / Cognitive Sciences / 9606
School of Cognitive Sciences
  Title:   The amygdala modulates morphine-induced state-dependent memory retrieval via muscarinic acetylcholine receptors
1.  A. Rezayof
2.  L. Khajehpour
3.  M.R. Zarrindast
  Status:   Published
  Journal: Neuroscience Letters
  Vol.:  160
  Year:  2009
  Pages:   255-263
  Supported by:  IPM
The current study was conducted to examine the involvement of muscarinic acetylcholine receptors of the amygdala in morphine-induced state-dependent memory retrieval. Male Wistar rats implanted bilaterally with cannulas in the amygdala were submitted to a step-through type passive avoidance task, and tested 24 h after training to measure step-through latency. Post-training s.c. administration of morphine at the doses of 5 and 7.5 mg/kg impaired the memory on the test day, which was restored when the same doses of morphine were used as a pre-test drug. This phenomenon is well known as morphine-induced state-dependent memory retrieval. Bilateral microinjection of the non-selective muscarinic acetylcholine receptor agonist, pilocarpine (0.25 and 0.5 ug/side), into the amygdala with an ineffective dose of morphine (0.5 mg/kg s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of morphine. It should be noted that in the animals that received saline after training and tested following intraamygdala administration of pilocarpine (0.125, 0.25 and 0.5 ug/side) and those which received post-training morphine(7.5 mg/kg s.c.) and pre-test intra-amygdala microinjection of the same doses of pilocarpine, no significant change was observed in the step-through latencies. On the other hand, pre-test intra-amygdala microinjection of a selective muscarinic acetylcholine receptor antagonist scopolamine(0.125 and 0.25 ug/side) inhibited morphine-induced statedependent memory retrieval. In addition, no significant changes were seen in memory retrieval of the animals trained before saline treatment and tested following intraamygdala microinjection of the same doses of scopolamine (0.0625, 0.125 and 0.25 ug/side). Bilateral microinjection of scopolamine into the amygdala reversed the pilocarpine-induced potentiation of the morphine response.In view of the known actions of the drugs used, the present data point to the involvement of amygdala muscarinic muscarinic acetylcholine receptors in morphine-induced state-dependent memory retrieval.

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