The Journal of Neuroscience, January 15, 2001, 21(2):559-569

Coordination of the Bladder Detrusor and the External Urethral Sphincter in a Rat Model of Spinal Cord Injury: Effect of Injury Severity
Victor Pikov1 and Jean R. Wrathall2

Departments of 1テつ*Cell Biology and 2テつ*Neuroscience, Georgetown University, Washington, DC 20007

Recovery of urinary tract function after spinal cord injury (SCI) is important in its own right and may also serve as a model for studying mechanisms of functional recovery after injury in the CNS. Normal micturition requires coordinated activation of smooth muscle of the bladder (detrusor) and striated muscle of the external urethral sphincter (EUS) that is controlled by spinal andsupraspinal circuitry. We used a clinically relevant rat model of thoracic spinal cord contusion injury to examine the effect of varying the degree of residual supraspinal connections on chronic detrusor-EUS coordination. Urodynamic evaluation at 8テつ*weeks after SCI showed that detrusor contractions of the bladder recovered similarly in groups of rats injured with a 10テつ*gm weight dropped 12.5,テつ*25,テつ*or 50テつ*mm onto the spinal cord. In contrast, the degree of coordinated activation of the EUS varied with the severity of initial injury and the degree of preservation of white matter at the injury site. The 12.5テつ*mm SCI resulted in the sparing of 20% of the white matter at the injury site and complete recovery of detrusor-EUS coordination. In more severely injured rats, the chronic recovery of detrusor-EUS coordination was very incomplete and correlated to decreased innervation of lower motoneurons by descending control pathways and their increased levels of mRNA for glutamate receptor subunits NR2A and GluR2. These results show that the extent of recovery of detrusor-EUS coordination depends on injury severity and the degree of residual connections with brainstem control centers.

Key words: bladder; urethral sphincter; dyssynergia; electromyography; urodynamics; spinal cord contusion; serotonin; corticotropin-releasing factor; glutamate receptors