title: The expression of Fos-labeled spinal neurons in response to colorectal distension is enhanced after chronic spinal cord transection in the rat.
abstract: The present study used Fos-like immunoreactivity to examine neuronal activation in response to colorectal distension in rats at 1 day or 30 days following spinal cord transection or sham transection. Fifty-five Wistar rats were anesthetized and an incision was made to expose the T(5) spinal segment. The dura was reflected away in all rats and a complete transection at the rostral end of the T(5) segment was given to the lesioned group. At 1 day (acute) or 30 days (chronic) post-surgery, conscious rats were subjected to a 2 h period of intermittent colorectal distension. Rats were perfused and spinal segments L(5)-S(2) were removed and processed for Fos-like immunoreactivity. Spinal cord transection alone had no effect on Fos-labeling in either acute or chronic rats. In acute rats, colorectal distension produced significant increases in Fos-labeling in the superficial and deep dorsal horn regions. In chronic rats, colorectal distension produced a three-fold increase in Fos-labeled neurons that was manifest throughout all laminar regions. These results indicate that the number of neurons expressing Fos in response to colorectal distension is much greater after a chronic spinal cord transection than after an acute transection. Since Fos is an indicator of neuronal activation, the results show that many more neurons become active in response to colorectal distension following a chronic spinal injury. This suggests that a functional reorganization of spinal circuits occurs following chronic spinal cord transection. This may ultimately result in altered visceral and somatic functions associated with spinal cord injury in humans.
authors.affiliation: Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA.
authors.forename: L M
authors.initials: LM
authors.lastname: Landrum
authors.forename: S L
authors.initials: SL
authors.lastname: Jones
authors.forename: R W
authors.initials: RW
authors.lastname: Blair
mesh_terms: D000818:Animals; D020211:Autonomic Dysreflexia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002908:Chronic Disease; D003106:Colon / Q000294:innervation* / Q000503:physiopathology; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D009619:Nociceptors / Q000166:cytology / Q000378:metabolism*; D010812:Physical Stimulation; D020671:Posterior Horn Cells / Q000166:cytology / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D013904:Thoracic Vertebrae; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology; D017833:Visceral Afferents / Q000503:physiopathology*
chemical_list: D016760:Proto-Oncogene Proteins c-fos