Neurophysiological control of urinary bladder storage and voiding-functional changes through development and pathology

The effective storage of urine and its expulsion relies upon the coordinated activity of parasympathetic, sympathetic, and somatic innervations to the lower urinary tract (LUT). At birth, all mammalian neonates lack the ability to voluntary regulate bladder storage or voiding. The ability to control urinary bladder activity is established as connections to the central nervous system (CNS) form through development. The neural regulation of the LUT has been predominantly investigated in adult animal models where comparatively less is known about the neonatal and postnatal neurophysiological development that facilitate urinary continence. Furthermore, congenital neurological or anatomical defects can adversely affect both storage and voiding functions through postnatal development and into adulthood, leading to secondary conditions including vesicoureteral reflux, chronic urinary tract infections, and end-stage renal disease. Therefore, the aim of the review is to provide the current knowledge available on neurophysiological regulation of the LUT through pre- to postnatal development of human and animal models and the consequences of congenital anomalies that can affect LUT neural function.

Automated summary

Research on human and animal models shows that the effective storage and expulsion of urine rely on the coordinated activity of the parasympathetic, sympathetic, and somatic nervous systems. However, congenital neurological or anatomical defects can impact the development of urinary control, leading to various urinary tract-related complications.