Inflammation enhances reflex and spinal neuron responses to noxious visceral stimulation in rats

To improve understanding of sensory processes related to visceral inflammation, the effect of turpentine-induced inflammation on reflex (cardiovascular/visceromotor) and extracellularly recorded lumbosacral dorsal horn neuron responses to colorectal distension (CRD) was investigated. A 25% solution...

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Published inAmerican journal of physiology: Gastrointestinal and liver physiology Vol. 280; no. 4; pp. G649 - G657
Main Authors Ness, T J, Gebhart, G F
Format Journal Article
LanguageEnglish
Published United States 01.04.2001
Subjects
Animals
Electrophysiology
Enterocolitis - pathology
Enterocolitis - physiopathology
Inflammation - physiopathology
Male
Neurons - physiology
Pain - pathology
Pain - physiopathology
Physical Stimulation
Pressure
Proctitis - pathology
Proctitis - physiopathology
Rats
Rats, Sprague-Dawley
Reflex - physiology
Spinal Cord - pathology
Spinal Cord - physiopathology
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Summary:To improve understanding of sensory processes related to visceral inflammation, the effect of turpentine-induced inflammation on reflex (cardiovascular/visceromotor) and extracellularly recorded lumbosacral dorsal horn neuron responses to colorectal distension (CRD) was investigated. A 25% solution of turpentine, applied to the colorectal mucosa, produced inflammation, decreased compliance of the colonic wall, and enhanced reflex responses in unanesthetized rats within 2-6 h. At 24 h posttreatment, pressor responses to CRD (80 mmHg, 20 s) were 20% greater, and intraluminal pressures needed to evoke visceromotor reflexes were 30% lower than controls. Parallel electrophysiological experiments in spinal cord-transected, decerebrate rats demonstrated that two neuronal subgroups excited by CRD were differentially affected by turpentine administered 24 h before testing. During CRD, abrupt neurons were 70% less active and sustained neurons were 25% more active than similar neurons in controls. In summary, reflex and neuronal subgroup (sustained neurons) responses to CRD were both potentiated by chemical inflammation. This suggests that the neurophysiological basis for inflammation-induced increases in reflex responses to CRD is increased activity of this neuronal subgroup.
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ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.2001.280.4.g649