Volume 18, Issue 2 ( Summer 2014)                   Physiol Pharmacol 2014, 18(2): 236-248 | Back to browse issues page

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Abstract:   (7342 Views)
Introduction: Sub-chronic swim stress is known to induce a prolonged hyperalgesia, which is mediated through NMDA and opioid systems. Nitric oxide is a soluble gas, which acts as a retrograde messenger that modulates the release of mentioned neurotransmitters. It is also involved in nociception and memory. The aim of this study was to evaluate the role of NO pathway in nociception and memory disruption induced by sub-chronic swim stress. Methods: Three sessions forced swimming stress protocols were applied to rats. Before each swimming session, pretreatment with L-NAME (10 mg/kg, i.p.), L-Arginine (10 mg/kg, i.p.) or saline was made. Passive avoidance learning, nociception and anxiety-like behavior were evaluated 24 hours after last swim stress session. Results: Results showed that step through latency was decreased after swim stress and it could be inhibited by pretreatment with L-NAME. Swim stress increased anxiety-like behavior in the open field test, which could be inhibited by pretreatment with L-NAME and L-Arginine. Reduced thermal threshold was observed in the nociceptive measurement after swim stress. Pretreatment with L-NAME could reverse this reduced threshold. Conclusion: The results of this study indicate that sub-chronic swim stress impairs nociception and passive avoidance learning. It seems that NO pathway have a modulatory role in these alterations.
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