Increase of p75 immunoreactivity in rat urinary bladder following inflammation.
Previous studies suggest that NGF may function as a mediator of inflammatory pain. Here, we examined the effect of inflammation on expression of the low affinity neurotrophin receptor p75, using the model of cyclophosphamide-induced cystitis in rats. In control rats, p75-positive thick fibre bundles were scattered in the muscle layer. At 2 and 3 days after injection of cyclophosphamide, numbers of p75-positive fine fibres in the muscle layer were dramatically increased. Electron microscopy revealed that p75 immunoreactivity was localized on the surface of Schwann cells and at the sites where they were apposed to axons. Results show that p75 is up-regulated in inflamed tissues, suggesting that p75 may bind to and take up nerve growth factor (NGF), thus participating in NGF-induced hyperalgesia.
Wakabayashi
Y
Y
Department of Physiology, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Maeda
T
T
Kwok
Y N
YN
D000818:Animals; D003520:Cyclophosphamide; D003556:Cystitis / Q000139:chemically induced / Q000378:metabolism*; D007124:Immunoenzyme Techniques; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism*; D001743:Urinary Bladder / Q000737:chemistry*
D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D003520:Cyclophosphamide