Effects of experimental colitis on the expressions of calcitonin gene-related peptide and vanilloid receptor 1 in rat spinal cord sensory neurons.
- Author:
Xia YANG
1
;
Jun-Qing HAN
;
Ran LIU
Author Information
1. Department of Cancer Research and Treatment Center, Shandong Provincial Hospital, Shandong University, Jinan 250021, China. freetree1126@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Calcitonin Gene-Related Peptide;
metabolism;
Colitis;
physiopathology;
Colon;
innervation;
Ganglia, Spinal;
cytology;
Inflammation;
physiopathology;
Neurons, Afferent;
cytology;
Rats;
Rats, Sprague-Dawley;
Sensory Receptor Cells;
cytology;
Spinal Cord;
cytology;
TRPV Cation Channels;
metabolism
- From:
Acta Physiologica Sinica
2008;60(1):143-148
- CountryChina
- Language:English
-
Abstract:
To study the acute and long-term effects of local gut inflammation on the sensitivity of the spinal sensory neurons, the expressions of vanilloid receptor 1 (VR1) and calcitonin gene-related peptide (CGRP) in the colon-innervated primary sensory neurons in dorsal root ganglia (DRG) were examined in rats with trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. The neurons projecting to the distal colon were identified by DiI(3) retrograde labelling. Macroscopic examination, mean damage score and myeloperoxidase (MPO) activity were determined to assess the inflammatory status of the colon tissue. The number of CGRP and VR1 immunoreactive neurons at different stages of inflammation (on days 7, 21 and 42 after TNBS treatment) were compared. On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38±9.45)% vs (42.86±.02)% for CGRP, (89.23±8.21)% vs (32.54±4.58)% for VR1]. When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25±8.21)%, (68.28±7.12)% vs (42.86±5.02)% for CGRP; (67.22±6.52)%, (56.25±4.86)% vs (32.54±4.58)% for VR1]. These results suggest that the local gut inflammation increases the expressions of CGRP and VR1 in gut-innervated DRG sensory neurons. More importantly, this abnormal status persists even after the gut inflammatory reaction has been resolved for certain time.
