Mechanisms underlying the recovery of lower urinary tract function following spinal cord injury.
The lower urinary tract has two main functions, the storage and periodic expulsion of urine, which are regulated by a complex neural control system in the brain and lumbosacral spinal cord. This neural system coordinates the activity of two functional units in the lower urinary tract: (1) a reservoir (the urinary bladder) and (2) an outlet (consisting of bladder neck, urethra and striated muscles of the pelvic floor). During urine storage the outlet is closed and the bladder is quiescent, thereby maintaining a low intravesical pressure over a wide range of bladder volumes. During micturition the outlet relaxes and the bladder contracts to promote the release of urine. This reciprocal relationship between bladder and outlet is generated by visceral reflex circuits, some of which are under voluntary control. Experimental studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through a coordination center (the pontine micturition center) located in the rostral brainstem. This reflex pathway is in turn modulated by higher centers in the cerebral cortex that are presumably involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary control of voiding as well as the normal reflex pathways that coordinate bladder and sphincter functions. Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. Studies in animals indicate that the recovery of bladder function after spinal cord injury is dependent in part on plasticity of bladder afferent pathways and the unmasking of reflexes triggered by capsaicin-sensitive C-fiber bladder afferent neurons. The plasticity is associated with changes in the properties of ion channels and electrical excitability of afferent neurons, and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs.
de Groat
William C
WC
Department of Pharmacology and Urology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. degroat@server.pharm.pitt.edu
Yoshimura
Naoki
N
D000320:Adrenergic Fibers / Q000378:metabolism; D000344:Afferent Pathways / Q000033:anatomy & histology / Q000502:physiology; D000818:Animals; D001921:Brain / Q000033:anatomy & histology / Q000502:physiology; D004525:Efferent Pathways / Q000033:anatomy & histology / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007395:Interneurons / Q000166:cytology / Q000378:metabolism; D009414:Nerve Growth Factors / Q000378:metabolism; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D012018:Reflex; D015222:Sodium Channels / Q000378:metabolism; D013116:Spinal Cord / Q000033:anatomy & histology / Q000473:pathology / Q000502:physiology; D013119:Spinal Cord Injuries / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology; D015320:Tachykinins / Q000378:metabolism; D001743:Urinary Bladder / Q000294:innervation / Q000502:physiology; D014555:Urination Disorders / Q000209:etiology / Q000503:physiopathology*; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism
D009414:Nerve Growth Factors; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D015221:Potassium Channels; D015222:Sodium Channels; D015320:Tachykinins; D014660:Vasoactive Intestinal Peptide; D018698:Glutamic Acid