The dorsal column pathway facilitates visceromotor responses to colorectal distention after colon inflammation in rats
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, P.H.S.
Grantová podpora
NS 09743
NINDS NIH HHS - United States
NS 11255
NINDS NIH HHS - United States
PubMed
12927622
DOI
10.1016/s0304-3959(03)00075-7
PII: 00006396-200308000-00009
Knihovny.cz E-zdroje
- MeSH
- buňky zadních rohů míšních fyziologie MeSH
- elektromyografie metody MeSH
- katetrizace MeSH
- kolitida patofyziologie MeSH
- kolon inervace patologie patofyziologie MeSH
- krysa rodu Rattus MeSH
- nuclei ventrales thalami MeSH
- potkani Sprague-Dawley MeSH
- rektum inervace patologie patofyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
Recent clinical studies have demonstrated that a midline lesion of the dorsal columns (DC, limited midline myelotomy) reduces pain of visceral origin in patients with pelvic cancer. Animal experiments showed that a DC lesion leads to decreased activation of thalamic neurons by visceral stimuli, lowers the impact of noxious colon stimulation in behavioral tests and suggested that the effect is mediated mainly by postsynaptic DC neurons. In the present experiments we examined the effect of bilateral DC or ventrolateral (VL) spinal cord lesions on visceromotor reflex EMG activity evoked by graded colorectal distention (30, 60, 80 mmHg) under control conditions and after colon inflammation with mustard oil. The colon inflammation increased significantly the visceromotor responses so that the response to a 30 mmHg distention was larger than that produced by 80 mmHg before inflammation. The DC lesion did not affect the visceromotor reflex response under control conditions but reduced the increased responses after colon inflammation back to control levels and prevented the potentiation of the reflex responses by colon inflammation when performed before the inflammation. Our results suggest that the role of the DC pathway in transmission of visceral pain is augmented under inflammatory conditions when symptoms of visceral allodynia and hyperalgesia may be present. The VL lesions eliminated the visceromotor reflex, presumably by interrupting a facilitatory pathway that involves the brain stem.
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