OBJECTIVE: To evaluate the role of neuropeptide Y in the detrusor of patients with neurogenic detrusor overactivity (NDO), as it has an important role in the neural regulation of the lower urinary tract by exerting differential effects on the release of cholinergic and adrenergic transmitters via autoinhibition and heterosynaptic interactions. MATERIALS AND METHODS: Detrusor biopsies were obtained from 38 patients; 31 had video-urodynamically verified NDO, caused by meningomyelocele in 17 or spinal cord injury in 14. Seven had stress urinary incontinence (SUI) and this group served as a control. All specimens were fixed, paraffin wax-embedded, sectioned and stained with a monoclonal antibody against neuropeptide Y and a general nerve marker protein-gene-product 9.5 (PGP 9.5). The number of PGP 9.5- and neuropeptide Y-containing nerves was quantified by a standardized evaluation using image-analysis software. RESULTS: The median (range) number of neuropeptide Y-containing nerves in the neurogenic detrusor, at 0.273 (0.126-0.639) per muscle cell nucleus (MCN), was significantly lower (P = 0.014) than that in patients with SUI, at 0.383 (0.267-0.728). In the neurogenic detrusor the number of PGP 9.5-positive nerves, at 0.278 (0.054-0.641)/MCN was also lower (P = 0.111) than in patients with SUI, at 0.368 (0.258-0.497). The ratio of neuropeptide Y to PGP 9.5 counts per biopsy did not differ between the groups (P = 0.628). CONCLUSIONS: The number of PGP 9.5-positive nerves was not significantly and the number of neuropeptide Y-containing nerves was significantly reduced in patients with NDO. This may have been caused by transynaptic nerve degeneration of the detrusor, as described by in patients with spinal cord injury. As neuropeptide Y inhibits the contractile response of the detrusor the reduction of neuropeptide Y-containing nerves may play a role in the development and persistence of DO.
OBJECTIVE: To evaluate the role of neuropeptide Y in the detrusor of patients with neurogenic detrusor overactivity (NDO), as it has an important role in the neural regulation of the lower urinary tract by exerting differential effects on the release of cholinergic and adrenergic transmitters via autoinhibition and heterosynaptic interactions. MATERIALS AND METHODS: Detrusor biopsies were obtained from 38 patients; 31 had video-urodynamically verified NDO, caused by meningomyelocele in 17 or spinal cord injury in 14. Seven had stress urinary incontinence (SUI) and this group served as a control. All specimens were fixed, paraffin wax-embedded, sectioned and stained with a monoclonal antibody against neuropeptide Y and a general nerve marker protein-gene-product 9.5 (PGP 9.5). The number of PGP 9.5- and neuropeptide Y-containing nerves was quantified by a standardized evaluation using image-analysis software. RESULTS: The median (range) number of neuropeptide Y-containing nerves in the neurogenic detrusor, at 0.273 (0.126-0.639) per muscle cell nucleus (MCN), was significantly lower (P = 0.014) than that in patients with SUI, at 0.383 (0.267-0.728). In the neurogenic detrusor the number of PGP 9.5-positive nerves, at 0.278 (0.054-0.641)/MCN was also lower (P = 0.111) than in patients with SUI, at 0.368 (0.258-0.497). The ratio of neuropeptide Y to PGP 9.5 counts per biopsy did not differ between the groups (P = 0.628). CONCLUSIONS: The number of PGP 9.5-positive nerves was not significantly and the number of neuropeptide Y-containing nerves was significantly reduced in patients with NDO. This may have been caused by transynaptic nerve degeneration of the detrusor, as described by in patients with spinal cord injury. As neuropeptide Y inhibits the contractile response of the detrusor the reduction of neuropeptide Y-containing nerves may play a role in the development and persistence of DO.