Neurotrophic factors and reactive oxygen species (ROS) modulate neuronal plasticity. In a model of a lower motor neuron lesioned bladder, somatic nerve transfer was used as a reinnervation strategy. Levels of neurotrophins, ROS, and TNF-α in bladder mucosa and muscle layers collected from three groups of adult female dogs: (1) Decentralized, via bilateral transection of coccygeal and sacral spinal roots, lumbar 7 dorsal roots, and hypogastric nerves, then 6–21 mo recovery; (2) reinnervated (ObNT-Reinn), after similar decentralization for 12 mo, then bilateral obturator-to-vesical nerve transfer and 8–12 mo recovery; and (3) Controls. In mucosa, BDNF and ROS levels were highest in ObNT-Reinn bladders, GDNF and TNF-α levels were restored to Control levels in ObNT-Reinn bladders (lowest in Decentralized). NT-3 and ARTN were lower in ObNT-Reinn and Decentralized bladders versus Controls. In muscle, ROS was lower in ObNT-Reinn muscle versus Controls. BDNF mucosa levels correlated with bladder axonal density and detrusor layer thickness; and GDNF mucosal correlated with bladder contraction after vesical or transferred obturator nerve electrical stimulation, as did BDNF and GDNF muscle levels. The increased BDNF and GDNF in bladders that underwent somatic nerve transfer with subsequent recovery suggest that BDNF and GDNF may help promote the reestablishment of bladder innervation.

Chronic sleep disturbance is postulated to enhance pain and inflammatory responses, although systemic inflammation has been primarily investigated to date. We sought to examine the effects of chronic intermittent sleep disturbance on pain-related behaviors and peripheral forelimb neural- and myofascial tissues in the context of aging. Uninjured young adult and mature female rats (3 mo. and 9–10 mo. of age) were exposed to either normal or disturbed sleep for 9 h/day on 4 d/week (using in-cage environmental stimulation), for 6 weeks. Compared to rats with normal sleep, sleep disturbed rats of both ages displayed: (1) mild declines in grip strength; (2) low-grade elevations in immune cells and collagen in forepaw neural- and myofascial tissues; and (3) higher protein expression of collagen type I, CTGF, and phosphorylated AKT in forearm flexor muscles. Young adult sleep disturbed also showed increased TGF-beta. Mature sleep disturbed rats also displayed low-grade yet greatest forepaw mechanical sensitivity, muscle and serum TNF-α, and peripheral immune cell numbers. These data suggest that chronic intermittent sleep disruption can enhance pain-related behaviors, inflammation, and fibrosis-related changes in peripheral neural- and myofascial tissues in uninjured rats. These effects occurred in both age groups, yet were more pronounced in the older rats.