Fig. 2.

Proposed mechanism for interaction of IC-mediated spontaneous contractions and spinal reflex pathways. Urine is expelled from the fetal bladder via the urachus in utero. In neonates, IC forms a syncytium through gap junctions that allow for coordinated activation of detrusor smooth muscle. These large magnitude contractions can stimulate mechanosensitive afferents that activate a bladder-to-bladder spinal pathways that triggers micturition. The spinal reflex pathway is lost in adulthood and voiding becomes regulated entirely by the CNS. Along with neural remodeling in the spinal cord, there is decreased connectivity between bladder IC and spontaneous activity. In neuropathologies, a spinal reflex loop similar to that in neonates can form, along with increased bladder IC connectivity. This may be a initially compensatory mechanism to allow voiding in the absence of CNS input. However, in conditions such as spinal cord injury this can lead to detrusor sphincter dyssynergia due to uncontrolled neural remodeling.