Plasticity of Na+ channels in afferent neurones innervating rat urinary bladder following spinal cord injury.

1. Whole-cell patch-clamp recordings in combination with axonal tracing techniques were used to investigate the effects of chronic spinal cord injury on the electrical properties of dorsal root ganglion neurones innervating the urinary bladder or colon of the adult rat. 2. In spinal intact animals, the majority (73-74%) of bladder and colon neurones which were small in size exhibited high-threshold humped spikes mediated by tetrodotoxin (TTX)-resistant Na+ channels, whereas large neurones had low-threshold narrow spikes mediated by TTX-sensitive Na+ channels. 3. In chronic spinal transected animals, 60% of bladder afferent neurones exhibited TTX-sensitive low-threshold spikes. The average diameter and input capacitance of the cells were significantly larger than those of cells obtained from spinal intact animals. 4. In bladder afferent neurones from chronic spinal transected rats, the density of TTX-resistant Na+ currents significantly decreased from 60.5 to 17.9 pA pF-1, whereas that of TTX-sensitive currents increased from 32.1 to 80.6 pA pF-1. 5. These changes in action potential and Na+ current characteristics were not detected in colon afferent neurones following spinal cord injury. 6. The results indicate that spinal cord injury increases bladder afferent neurone excitability by shifting the expression of Na+ channels from a high-threshold TTX-resistant type to a low-threshold TTX-sensitive type. This change in properties may occur in response to alterations in neurotrophic signals originating in the hypertrophied bladder.