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| Paper IPM / Cognitive Sciences / 8958 |
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| Abstract: | |||||||
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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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