Neuroscience letters
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Hand dominancy (i.e. handedness) is a factor that should be considered for further characterizing individual variations in sensitivity to pain. The aim of the present study was to examine the contribution of handedness and gender to sensitivity to tonic cold pain in healthy subjects. Participants were 109 healthy volunteers (52 males and 57 females), of whom 65 were right-handed and 44 left-handed. ⋯ No significant differences were found among the left-handed males or among the females. The results provide further evidence that handedness is one vital feature that should be considered more often when designing a psychophysical study. This may lead towards improving the translation of laboratory research findings to the clinical setting.
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Neuroscience letters · Dec 2009
Acute bladder inflammation differentially affects rat spinal visceral nociceptive neurons.
The present investigation examined the effect of inflammation produced by intravesical zymosan on spinal dorsal horn neuronal responses to urinary bladder distension (UBD). Extracellular single-unit recordings of neurons excited by UBD were obtained in spinalized female Sprague-Dawley rats. Neurons were classified as Type I-inhibited by heterotopic noxious conditioning stimuli (HNCS) or as Type II-not inhibited by a HNCS. ⋯ No significant changes were noted in neuronal activity in control experiments. Inflammation differentially affects subpopulations of spinal dorsal horn neurons excited by UBD that can be differentiated according to the effect of HNCS. This results in an altered pattern of spinal sensory transmission that may serve as the mechanism for the generation of visceral nociception.
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Neuroscience letters · Dec 2009
NMDA receptors are involved in upstream of the spinal JNK activation in morphine antinociceptive tolerance.
N-methyl-d-aspartate (NMDA) receptors and c-Jun N-terminal kinase (JNK) have been shown to be involved in morphine antinociceptive tolerance. However, whether chronic morphine-induced activation of the spinal JNK is NMDA receptor-dependent is unknown. The present study investigated the link between the spinal NMDA receptor NR2B subunit and the JNK activation during morphine antinociceptive tolerance in rats. ⋯ SP600125, a selective inhibitor of JNK, significantly attenuated morphine tolerance. MK-801, a noncompetitive NMDA receptor antagonist, not only suppressed morphine antinociceptive tolerance and the increase in NR2B, but also reduced the spinal JNK activation induced by chronic morphine treatment. These findings demonstrated for the first time that NMDA receptor-dependent activation of the spinal JNK contributes to morphine antinociceptive tolerance and that MK-801 attenuates morphine tolerance partly due to its inhibition on the spinal JNK activation.
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Neuroscience letters · Dec 2009
Nitric oxide mechanism in protective effect of imipramine and venlafaxine against acute immobilization stress-induced behavioral and biochemical alteration in mice.
Frequent and persistent stressful events caused depressive illness. Stress is an aversive stimulus which disturbs physiological homeostasis and reflects a variety of biological systems. The present study was designed to investigate the nitric oxide mechanism in the protective effect of imipramine and venlafaxine against acute immobilization stress-induced behavioral and biochemical alterations in mice. ⋯ Pretreatment with imipramine (10 and 20mg/kg) and venlafaxine (5 and 10mg/kg) significantly reversed immobilized stress-induced behavioral and biochemical alterations. l-arginine (100mg/kg) pretreatment with imipramine (10mg/kg) and venlafaxine (5mg/kg) significantly attenuated the protective effect of imipramine and venlafaxine. However, l-NAME (10mg/kg) and/or methylene blue (10mg/kg) pretreatment with lower dose of imipramine and venlafaxine significantly potentiated their protective effects which were significant as compared to their effect per se respectively. Present study highlights the involvement of nitric oxide mechanism in the protective effect of imipramine and venlafaxine against acute immobilization-induced behavioral and biochemical alterations in mice.