K. Pleger

Obesity and altered stress responsiveness in women with polycystic ovary syndrome: Implications for the long-term cardiovascular and diabetes risks associated with the diagnosis?

immediately before spared nerve injury (SNI) on neuropathic pain. Allodynia was assessed before and 24 h after a single period of restraint and was found to be similar between WT and KO mice. However, 1, 3, 5, and 7 days after SNI, allodynia (assessed by von Frey monofilaments) in the hindpaw ipsilateral to the injury was significantly enhanced in stressed KO mice as compared to stressed WT and non-stressed mice. In addition, mechanical allodynia in the hindpaw contralateral to the injury was enhanced in stressed KO mice compared to stressed WT mice. Cold allodynia (assessed by acetone application) was signficantly increased for stressed KO mice on days 3, 5, and 7 post-SNI in the hindpaw ipsilateral to the injury and overall post-SNI in the hindpaw contralateral to the injury compared to non-stressed KO mice. In summary, male CX3CR1-/mice exhibit enhanced ipsilateral mechanical allodynia with enhanced mirror image pain following SNI compared to wild-type mice. These effects were potentiated by stress. These data suggest that the absence of the CX3CR1 does not confer protection from the onset of allodynia after peripheral nerve injury. However, other factors (e.g., corticosterone) produced as a result of stress or concomitant injury may enhance neuropathic pain.