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Delayed stress-induced antinociceptive effect of nitric oxide synthase inhibition in the dentate gyrus of rats

Stimulation of the hippocampal formation can modulate nociceptive mechanisms, whereas painful stimuli can activate this structure. Stress exposure can produce plastic changes in the hippocampus. Nitric oxide (NO) is an important neuroregulatory agent present in the hippocampus. The objective of the...

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Published in:Pharmacology, biochemistry and behavior biochemistry and behavior, 2002-12, Vol.74 (1), p.149-156
Main Authors: Echeverry, Marcela B, Guimarães, Francisco S, Oliveira, Marina A, do Prado, William A, Del Bel, Elaine A
Format: Article
Language:English
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Summary:Stimulation of the hippocampal formation can modulate nociceptive mechanisms, whereas painful stimuli can activate this structure. Stress exposure can produce plastic changes in the hippocampus. Nitric oxide (NO) is an important neuroregulatory agent present in the hippocampus. The objective of the present study was to investigate the effects of intrahippocampal administration of N ω-nitro- l-arginine methyl ester hydrochloride ( l-NAME), an inhibitor of NO synthase (NOS), on nociceptive processes in stressed and nonstressed rats. Male Wistar rats ( n=6–11/group) received unilateral microinjection of l-NAME (50–300 nmol/0.2 μl) into the dentate gyrus (DG) of the dorsal hippocampus. Immediately after the injection tail-flick reflex latency was measured. Stressed animals were submitted to 2 h of restraint and tested immediately or 1, 2, 5 or 10 days later. l-NAME failed to modify nociception in nonstressed rats. However, 5 days after, restraint l-NAME, at all doses tested, produced an antinociceptive effect (ANOVA, P
ISSN:0091-3057
1873-5177
DOI:10.1016/S0091-3057(02)00964-4