Pain
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Several studies have shown that male subjects report lower pain intensity to female compared to male experimenters. The present experiment examined whether experimenter gender also modulated autonomic pain responses. Sixty-four students (32 females) participated in a 2 Subject gender x 2 Experimenter gender x 15 Pain Tests mixed design. ⋯ Autonomic responses were heart rate variability and skin conductance levels. The results revealed significant interactions between experimenter gender and subject gender on pain intensity and arousal, but there were no interactions in the physiological data. In conclusion, the lower pain report in male subjects to female experimenters is not mediated by changes in autonomic parameters, and the effect of experimenter gender is probably due to psychosocial factors.
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The present study was undertaken to examine the effect of amitriptyline on the antinociceptive effect of morphine and its underlying mechanisms in regulating glutamate transporters trafficking in morphine-tolerant rats. Long-term morphine infusion induced antinociceptive tolerance and down-regulation of glutamate transporters (GTs), GLAST, GLT-1, and EAAC1, expression in the rat spinal cord dorsal horn. Acute amitriptyline treatment potentiated morphine's antinociceptive effect, with a 5.3-fold leftward shift of morphine's dose-response curve in morphine-tolerant rats, and this was associated with GLAST and GLT-1 trafficking onto the cell surface. ⋯ Furthermore, long-term morphine infusion up-regulated PKA and PKC protein expression in the spinal cord dorsal horn, while amitriptyline inhibited the increase in expression of phospho-PKA, PKCalpha, PKCbetaII, and PKCgamma. In morphine-tolerant rats, acute treatment with PKA inhibitor H89 and PKC inhibitor Gö6805 attenuated morphine tolerance and the morphine-induced CSF glutamate and aspartate elevation, and induced trafficking of GLAST and GLT-1 from cytosol onto the cell surface. These results show that acute amitriptyline treatment preserved morphine's antinociceptive effect in morphine-tolerant rats; the mechanisms may be involved in inhibition of phospho-PKA and PKC expression, and thus inducing the GLAST and GLT-1 trafficking onto glial cell surface which enhances the EAA uptake from the synaptic cleft and reduces EAA concentration in the spinal CSF.