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Abstract
Normal lower urinary tract (LUT) function requires coordination between the bladder and the external urethral sphincter (EUS). Phasic EUS relaxation during bladder contractions, necessary for efficient voiding in rats, is lost initially after complete spinal cord transection (txSCI), but re-emerges chronically in some rats. The bladder becomes hypertrophied and hyperreflexic after initial areflexia. Bladder afferent neurons become hypertrophied and terminals of sensory afferents extend deeper into the dorsal horn in the lumbosacral cord. While most spinal cord injury (SCI) patients suffer from incomplete SCI, there have been few studies on LUT function after a clinically relevant incomplete contusive SCI (iSCI). Thus, I compared LUT function between iSCI and txSCI rats, hypothesizing that iSCI rats would exhibit better LUT function than txSCI rats due to spared supraspinal connections. Urodynamic assessments were performed in awake rats, as anesthesia can adversely affect micturition. As expected, iSCI rats were less impaired in some aspects of LUT function (bladder weight, contraction duration and voiding pressure). However, some rats in both injury groups were surprisingly normal in terms of exhibiting phasic EUS relaxation (Phasic rats) and high voiding efficiencies. Other rats exhibited only tonic EUS activity (Tonic rats) and low voiding efficiencies. Further, retrogradely traced bladder afferent neurons had increased soma size and the distribution of sensory afferent terminals in the L6-S1 dorsal horns was expanded after both iSCI and txSCI. Immunoreactivity for descending monoaminergic pathways was absent after txSCI. Serotonin immunoreactivity was decreased initially after iSCI but partially returned chronically. However, there were no differences between Phasic and Tonic iSCI rats in terms of distal plasticity in lumbosacral cord, suggesting that plasticity in serotonin and sensory afferents may not play a key role in the recovery of phasic EUS activity after ISCI. Instead, alterations in local circuitry, such as central pattern generators, may be more important for the recovery of this specific aspect of LUT function. Finally, 8-OHDPAT, a 5HT1a receptor agonist, improved LUT function in iSCI and txSCI rats by easing bladder-EUS dyssynergia although it did not elicit phasic EUS relaxation, suggesting that therapeutic targets other than increasing EUS relaxation time should be considered.
