title: Changes in afferent activity after spinal cord injury.
abstract: OBJECTIVE
  To summarize the changes that occur in the properties of bladder afferent neurons following spinal cord injury.
  
  
  METHODS
  Literature review of anatomical, immunohistochemical, and pharmacologic studies of normal and dysfunctional bladder afferent pathways.
  
  
  RESULTS
  Studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through coordination centers (periaqueductal gray and pontine micturition center) located in the rostral brain stem. This reflex pathway, which is activated by small myelinated (Adelta) bladder afferent nerves, is in turn modulated by higher centers in the cerebral cortex involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary voiding, as well as the normal reflex pathways that coordinate bladder and sphincter function. Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. The recovery of bladder function after spinal cord injury is dependent in part on the plasticity of bladder afferent pathways and the unmasking of reflexes triggered by unmyelinated, capsaicin-sensitive, C-fiber bladder afferent neurons. Plasticity is associated with morphologic, chemical, and electrical changes in bladder afferent neurons and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs.
  
  
  CONCLUSIONS
  Spinal cord injury at sites remote from the lumbosacral spinal cord can indirectly influence properties of bladder afferent neurons by altering the function and chemical environment in the bladder or the spinal cord.
authors.affiliation: Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. degroat@server.pharm.pitt.edu
authors.forename: William C
authors.initials: WC
authors.lastname: de Groat
authors.forename: Naoki
authors.initials: N
authors.lastname: Yoshimura
mesh_terms: D000344:Afferent Pathways / Q000378:metabolism / Q000503:physiopathology*; D000818:Animals; D002490:Central Nervous System / Q000378:metabolism / Q000503:physiopathology*; D005727:Ganglia, Spinal / Q000378:metabolism / Q000503:physiopathology*; D015316:Genetic Therapy / Q000379:methods; D006801:Humans; D040542:Mechanotransduction, Cellular; D009413:Nerve Fibers, Myelinated; D036421:Nerve Fibers, Unmyelinated; D020932:Nerve Growth Factor / Q000378:metabolism; D056347:Neuroanatomical Tract-Tracing Techniques; D009473:Neuronal Plasticity; D018408:Patch-Clamp Techniques; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D020127:Recovery of Function; D012018:Reflex; D015222:Sodium Channels / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D001743:Urinary Bladder / Q000294:innervation*; D001750:Urinary Bladder, Neurogenic / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D014554:Urination; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D015221:Potassium Channels; D015222:Sodium Channels; D005680:gamma-Aminobutyric Acid; D020932:Nerve Growth Factor