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Paper   IPM / Cognitive / 8958
School of Cognitive Sciences
  Title:   Nicotinic acetylcholine receptors of the ventral tegmental area are involved in mediating morphine-state-dependent learning
  Author(s): 
1.  Ameneh Rezayof
2.  Niloufar Darbandi
3.  Mohammad-Reza Zarrindast
  Status:   Published
  Journal: Neurobiology of Learning and Memory
  Vol.:  90
  Year:  2008
  Pages:   255-260
  Supported by:  IPM
  Abstract:
In the present study, the possible role of nicotinic acetylcholine (nACh) receptors of the ventral tegmental area (VTA) on morphine-state-dependent learning was studied in adult male Wistar rats. As a model of memory, a step-through type passive avoidance task was used. All animals were bilaterally implanted with chronic cannulae in the VTA, trained using a 1 mA foot shock, and tested 24 h after training to measure step-through latency. Post-training subcutaneous (s.c.) injection of morphine (0.5�5 mg/kg) dosedependently reduced the step-through latency, showing morphine-induced amnesia. Amnesia induced by post-training morphine was significantly reversed by pre-test administration of morphine (2.5� 5 mg/kg, s.c.) and induced morphine-state-dependent learning. Pre-test injection of nicotine (0.25� 1 lg/rat) into the VTA plus an ineffective dose of morphine (0.5 mg/kg) significantly restored the memory retrieval. It should be noted that pre-test intra-VTA injection of the same doses of nicotine (0.25�1 lg/rat) alone cannot affect memory retention. Furthermore, pre-test intra-VTA injection of the nicotinic acetylcholine receptor antagonist, mecamylamine (1�3 lg/rat) 5 min before the administration of morphine (5 mg/kg, s.c.) dose-dependently inhibited morphinestate- dependent learning. Pre-test injection of the higher dose of mecamylamine (3 lg/rat) into the VTA by itself decreased the step-through latency and induced amnesia. On the other hand, mecamylamine (0.5 and 1 lg/rat, intra-VTA) reversed the effect of nicotine on morphine response. The results indicate that nACh receptors in the VTA participate in the modulation of morphine-induced recovery of memory, on the test day.

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