Mechanisms underlying the recovery of urinary bladder function following spinal cord injury.

Micturition in cats and rats with an intact neuraxis is dependent upon a spinobulbospinal reflex activated by A delta bladder afferents. This report describes changes in micturition reflexes 2 h to 14 weeks following spinal cord transection at the lower thoracic level. In acute spinal cats micturition reflexes were blocked, however, several weeks after transection, a long latency (180-200 ms) spinal reflex could be activated by C-fiber bladder afferents. This reflex was blocked by capsaicin in doses (20-30 mg/kg, s.c.) that did not affect micturition reflexes in intact cats. Micturition reflexes were unmasked in acute spinal and facilitated in chronic spinal cats by naloxone, an opioid antagonist. Spinal neurons and axons containing opioid peptides were more prominent below the level of transection in chronic spinal cats. VIP, a putative neurotransmitter in C-fiber bladder afferents, inhibited micturition reflexes when injected intrathecally (2-10 micrograms) in intact cats but facilitated micturition reflexes in spinal cats (doses 0.1-1 micrograms, i.t.). VIP-containing C-fiber afferent projections to lamina I of the sacral spinal cord expanded in spinal cats. Thus VIP afferents may have an important role in the recovery of bladder reflexes after spinal injury. Paraplegic animals also exhibit bladder-sphincter dyssynergia, which causes functional outlet obstruction. Studies in rats have revealed that outlet obstruction induced by partial urethral ligation facilitates spinal micturition reflex pathways and causes an expansion of HRP-labelled bladder afferent projections in the spinal cord. These findings raise the possibility that the alterations in central reflex connections in paraplegic animals may be induced in part by changes in peripheral afferent input secondary to outlet obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)