Role of nitric oxide in altered nociception and memory following chronic stress

Chronic stress alters sensory and cognitive function of mankind and animals. Sub-chronic swim stress is known to induce a prolonged hyperalgesia which is mediated through the NMDA and opioid systems. Nitric oxide is a soluble gas which acts as a retrograde messenger that modulates the release of the mentioned neurotransmitters. It is also involved in nociception and memory. The objective of the current study was to evaluate the role of NO pathway in nociception and memory impairments induced by sub-chronic swim stress.

A three session forced swimming stress protocol was administered to the rats. Pretreatment with l-NAME (10mg/kg, i.p.), l-Arginine (10mg/kg, i.p.) or saline was made before each swimming session. Anxiety-like behavior, nociception and passive avoidance (PA) learning were evaluated 24h after the last swim stress session.

Swim stress altered locomotion and anxiety-like behaviors in the open field test. Reduced thermal threshold was observed in the nociceptive measurement after swim stress. Pretreatment with l-NAME could reverse the reduced threshold. A decreased step through latency was observed in the PA paradigm after swim stress, which could be inhibited by pretreatment with l-NAME.

The results of this study indicate that sub-chronic swim stress impairs nociception and PA learning. NO pathway seems to have a modulatory role in these alterations. Further studies are suggested to examine the protective effect of NOS inhibitors on stress-induced impairments in sensory and cognitive function.