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| Paper IPM / Cognitive / 8999 |
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| Abstract: | |||||||
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The present study evaluated the possible role of nicotinic acetylcholine receptors
of the dorsal hippocampus on morphine-induced amnesia and morphine statedependent
memory in adult male Wistar rats. The animals were bilaterally
implanted with chronic cannulas in the CA1 regions of the dorsal hippocampi,
trained in a step-through type passive avoidance task, and tested 24 h after
training to measure step-through latency.Results indicate that post-training
subcutaneous (s.c.) administration of morphine (2.5�7.5 mg/kg) dosedependently
reduced the step-through latency, showing an amnestic response.
Post-training intra-CA1 microinjection of nicotine (0.5�1 μg/rat) decreased
significantly the amnesia induced by post-training morphine (7.5 mg/kg).
Moreover, co-treatment of mecamylamine (0.5 and 1 μg/rat, intra-CA1) with an
ineffective dose of morphine (2.5 mg/kg), immediately after training, caused
inhibition of memory retrieval. On the other hand, amnesia produced by posttraining
morphine (7.5 mg/kg) was reversed by pre-test administration of the
opioid that is due to a state-dependent effect. Interestingly, pre-test intra-CA1
microinjection of nicotine (0.25 and 0.5 μg/rat) improved post-training morphine
(7.5 mg/kg)-induced retrieval impairment. Moreover, pre-test administration of the
same doses of nicotine in combination with a lower dose of morphine (0.5
mg/kg), which had no effects alone, synergistically improved memory
performance impaired by post-training morphine. Pre-test injection of
mecamylamine (0.5�2 μg/rat) prevented the restoration of memory by pre-test
morphine. It is important to note that post-training or pre-test intra-CA1
administration of the same doses of nicotine or mecamylamine, alone did not
affect memory retrieval. These results suggest that nicotinic acetylcholine
receptors of the hippocampal CA1 regions may play an important role in morphine-induced amnesia and morphine state-dependent memory.
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