Changes in the number of nitric oxide-synthesizing neurones on both sides of a chronic transection of the rat spinal cord.
Pain after chronic transection of the spinal cord is hypothesized to develop because of a hyperactivity in nociceptive neurones rostral to the lesion. One of the key substances in central nervous nociceptive processing is nitric oxide (NO). It has been demonstrated to tonically inhibit the background activity of dorsal horn neurones. Here, we show that in rats with chronic transection of the spinal cord there is a reduction of NO-synthesizing neurones on both sides of the lesion. This reduction is likely to be associated with a local lack of NO which could lead to an increased background activity of nociceptive dorsal horn neurones. The increased background activity of nociceptive neurones just rostral to the lesion might cause spontaneous pain that is perceived in segments close to the level of the lesion.
Trudrung
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Ruprecht-Karls-University Heidelberg, Institute of Anatomy and Cell Biology III, Heidelberg, Germany.
Wirth
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U
Mense
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D000818:Animals; D002908:Chronic Disease; D005260:Female; D009252:NADPH Dehydrogenase / Q000032:analysis / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D009619:Nociceptors / Q000378:metabolism; D010146:Pain / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000166:cytology* / Q000201:enzymology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000378:metabolism*
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D009252:NADPH Dehydrogenase