Plasticity in the Micturition Circuit During Development and Following Spinal Cord Injury

Abstract

The micturition reflex relies on complex neural signaling to enable the coordination of the lower urinary tract. In neonates, this reflex is organized in the lumbosacral spinal cord and responds automatically to distension of the bladder or, in animals, to stimulation of the perigenital region by the mother. During development, competitive reorganization by supraspinal inputs places the reflex under conscious control and gives rise to the mature micturition reflex. Traumatic injury to the spinal cord that interrupts supraspinal inputs to the lumbosacral spinal cord can result in reversion to an automatic, spinal micturition reflex accompanied by lower urinary tract dysfunction such as neurogenic detrusor overactivity and detrusor–sphincter dyssynergia. This is accompanied by a number of changes in the anatomy and function of the lower urinary tract; various signaling pathways, including neurotrophins and neuropeptides; and reorganization of spinal circuitry. Evidence suggests that, following spinal cord injury, the bladder hypertrophies and urothelial and external urethral sphincter function are altered, giving rise to phasic spontaneous behavior and reduced bladder outlet bursting during voiding, respectively. Sensitization of Aδ-fiber afferents and “awakening” of C-fibers in the lumbosacral micturition pathway contribute to the emergence of a spinal micturition reflex and subsequent lower urinary tract dysfunction, with substantial evidence indicating a primary role for altered neurotrophin and neuropeptide signaling.