Simultaneous impairment of passive avoidance learning and nociception in rats following chronic swim stress

Authors

1 Department of Neuroscience, Neuroscience Research Center, Institute of Neuropharmacology; Department of Neuroscience, Medical Students Research Committee, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

2 Department of Neuroscience, Neuroscience Research Center, Institute of Neuropharmacology, Kerman, Iran

3 Department of Neuroscience, Medical Students Research Committee, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

Abstract

Background: Stress can alter response to nociception. Under certain circumstances stress enhances nociception, a phenomenon which is called stress-induced hyperalgesia (SIH). While nociception has been studied in this paradigm, possible alterations occurring in passive avoidance (PA) learning after exposing rats to this type of stress has not been studied before.
Materials and Methods: In the current study, we evaluated the effect of chronic swim stress (FS) or sham swim (SS) on nociception in both spinal (tail-flick) and supraspinal (53.5°C hot-pate) levels. Furthermore, PA task was performed to see whether chronic swim stress changes PA learning or not. Mobility of rats and anxiety-like behavior were assessed using open-field test (OFT).




Results: Supraspinal pain response was altered by swim stress (hot-plate test). PA learning was impaired by swim stress, rats in SS group did not show such impairments. Rats in the FS group showed increased mobility (rearing, velocity, total distant moved (TDM) and decreased anxiety-like behavior (time spent in center and grooming) compared to SS rats.
Conclusions: This study demonstrated the simultaneous impairment of PA and nociception under chronic swim stress, whether this is simply a co-occurrence or not is of special interest. This finding may implicate a possible role for limbic structures, though this hypothesis should be studied by experimental lesions in different areas of rat brain to assess their possible role in the pathophysiology of SIH.

Keywords

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