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: In an effort to understand the involvement of dorsal hippocampal nitric oxide system in ethanol (ETOH)-induced state-dependent memory, the effects of microinjection of L-arginine (a precursor of nitric oxide) and/or L-NAME (a nitric oxide synthase inhibitor) into the CA1 regions of dorsal hippocampus on this kind of memory were examined. In order to assess memory retrieval, a single trial step-down inhibitory avoidance task was used in mice. Pre-training intraperitoneal administration of ETOH (0.5 and 1 g/kg) dose dependently caused amnesia, while pre-test administration of the same doses of ETOH restored the retrieval and induced state-dependent memory. Pre-test microinjection of L-arginine (0.5, 0.75 and 1 [mu]g/mouse), into the CA1 region of dorsal hippocampus (intra-CA1) had no effect on memory retrieval. However, pre-test intra-CA1 microinjection of the same doses of L-arginine interestingly inhibited ETOH-induced state-dependent memory. The maximum response was obtained with 1 [mu]g/mouse of L-arginine. Furthermore, memory impairment was produced following pre-test intra-CA1 microinjection of L-NAME (0.5, 0.75 and 1 [mu]g/mouse). Pre-test co-administration of a higher dose of L-NAME (1 [mu]g/mouse, intra-CA1) with an ineffective dose of ETOH (0.25 g/kg), improved the memory retrieval. Pre-test intra-CA1 microinjection of L-arginine or L-NAME could not affect ETOH-induced amnesia. In addition, L-arginine-induced inhibition of the pre-test ETOH response was decreased by pre-test microinjection of L-NAME. The ensemble of these observations suggests that ETOH-induced state-dependent memory can be modulated through the dorsal hippocampal nitric oxide system.

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