Increased expression of neuronal nitric oxide synthase in bladder afferent and spinal neurons following spinal cord injury

Changes in the distribution of neuronal nitric oxide synthase immunoreactivity (NOS-IR) after chronic (5-6 weeks) spinal cord injury (SCI) were examined in bladder afferent and spinal neurons in the region of the sacral parasympathetic nucleus (SPN) in the L6-S1 spinal segments. Bladder afferent neurons in the L1, L2, L6 and S1 dorsal root ganglia (DRG) were identified by retrograde axonal transport following injection of fluorogold (FG) into the urinary bladder, A differential distribution of NOS-IR was detected in DRG cells at different segmental levels of spinal cord intact animals with significantly greater numbers of NOS-IR cells present in thoracic (T8, T12; 30-40 NOS-IR cell profiles/section) and rostral lumbar(L1) DRGs(18 NOS-IR cell profiles/section) compared to caudal lumbosacral(L5-S1) DRGs (0.2-0.4 NOS-IR cell profiles/section), A significant increase in the number of NOS-IR cells was detected in the L6-S1 DRG (p less than or equal to 0.001; 12-20 NOS-IR cell profiles/section) and in the L1-L2 DRG(15-40 NOS-IR cell profiles/section) but not in the L5 DRG following SCI, In these ganglia, an average of 41.2 +/- 7.8 % (L6) and 36.3 +/- 0.9% (S1) of FG-labeled bladder afferent neurons were NOS-IR. In contrast, in spinal cord intact animals, no FG-labeled bladder afferent neurons were NOS-IR. Following SCI, NOS-IR fibers were detected along the lateral edge of the dorsal horn extending from Lissauer's tract to the region of the SPN (lateral collateral pathway of Lissauer) of the L6 and S1 spinal segments. These NOS-IR fibers were not detected in adjacent spinal segments (L5, S2). SCI also significantly (p less than or equal to 0.001) increased the number of spinal neurons in the region of the SPN (presumptive preganglionic neurons) in the L6-S1 spinal segments exhibiting NOS-IR. These results indicate that NOS-IR in bladder afferent and spinal neurons is plastic and can be up-regulated by chronic SCI. Changes in the neurochemical properties of these neurons after SCI may be mediated by pathological changes in the target organ (i.e., urinary bladder) and/or spinal cord.