title: The visceromotor responses to colorectal distension and skin pinch are inhibited by simultaneous jejunal distension.
abstract: Noxious stimuli that are applied to different somatic sites interact; often one stimulus diminishes the sensation elicited from another site. By contrast, inhibitory interactions between visceral stimuli are not well documented. We investigated the interaction between the effects of noxious distension of the colorectum and noxious stimuli applied to the jejunum, in the rat. Colorectal distension elicited a visceromotor reflex, which was quantified using electromyographic (EMG) recordings from the external oblique muscle of the upper abdomen. The same motor units were activated when a strong pinch was applied to the flank skin. Distension of the jejunum did not provoke an EMG response at this site, but when it was applied during colorectal distension it blocked the EMG response. Jejunal distension also inhibited the response to noxious skin pinch. The inhibition of the visceromotor response to colorectal distension was prevented by local application of tetrodotoxin to the jejunum, and was markedly reduced when nicardipine was infused into the local jejunal circulation. Chronic sub-diaphragmatic vagotomy had no effect on the colorectal distension-induced EMG activity or its inhibition by jejunal distension. The nicotinic antagonist hexamethonium suppressed phasic contractile activity in the jejunum, had only a small effect on the inhibition of visceromotor response by jejunal distension. It is concluded that signals that arise from skin pinch and colorectal distension converge in the central nervous system with pathways that are activated by jejunal spinal afferents; the jejunal signals strongly inhibit the abdominal motor activity evoked by noxious stimuli.
authors.affiliation: Department of Anatomy and Cell Biology and Centre for Neuroscience, University of Melbourne, Parkville, Vic., 3010, Australia.
authors.forename: Anthony D
authors.initials: AD
authors.lastname: Shafton
authors.forename: John B
authors.initials: JB
authors.lastname: Furness
authors.forename: Dorota
authors.initials: D
authors.lastname: Ferens
authors.forename: Goce
authors.initials: G
authors.lastname: Bogeski
authors.forename: Shir Lin
authors.initials: SL
authors.lastname: Koh
authors.forename: Nicholas P
authors.initials: NP
authors.lastname: Lean
authors.forename: Peter D
authors.initials: PD
authors.lastname: Kitchener
mesh_terms: D000009:Abdominal Muscles / Q000503:physiopathology*; D000344:Afferent Pathways / Q000503:physiopathology*; D000698:Analgesia; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects; D002404:Catheterization; D003106:Colon / Q000294:innervation*; D004108:Dilatation, Pathologic / Q000503:physiopathology; D004576:Electromyography; D018738:Hexamethonium / Q000494:pharmacology; D007583:Jejunum / Q000294:innervation*; D008297:Male; D009529:Nicardipine / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D011312:Pressure / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012007:Rectum / Q000294:innervation*; D012867:Skin / Q000294:innervation*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013116:Spinal Cord / Q000503:physiopathology; D013779:Tetrodotoxin / Q000494:pharmacology; D014160:Transducers, Pressure; D014628:Vagotomy
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D018733:Nicotinic Antagonists; D026941:Sodium Channel Blockers; D018738:Hexamethonium; D013779:Tetrodotoxin; D009529:Nicardipine