Effects of intestinal inflammation on specific subgroups of guinea-pig celiac ganglion neurons
Section snippets
Acknowledgements
This work was supported by project grant 400020 from the National Health and Medical Research Council (NHMRC) of Australia. Dr. Nurgali is supported by a NHMRC Peter Doherty (Biomedical) Fellowship. We thank Drs. Daniel Poole and Karina Needham for their insightful comments on the manuscript.
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2021, Brain ResearchCitation Excerpt :For example, it has been reported that the increased excitability of phasic, but not tonic, neurons contributes to cystitis-induced pain and hyperactivity of the urinary bladder (Sculptoreanu and de Groat, 2007; Yoshimura and de Groat, 1999). In contrast, Dong et al. (Dong et al., 2008) demonstrated that increased excitability of tonic, but not phasic, celiac ganglion neurons occurs under inflammatory intestinal conditions. Ditting et al. (Ditting et al., 2009) also suggested that a greater susceptibility of renal afferent neurons correlates with a higher rate of tonic firings, and further contributes to inflammatory process in the kidney.
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2014, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :In addition to patients with active inflammation, those with IBD in clinical remission also exhibit markedly increased indices of sympathetic activity (Boisse et al., 2009; Sharma et al., 2009), suggesting that the effects of GI inflammation on sympathetic nerve dysfunction may persist in the absence of active disease. Intracellular electrophysiological recordings in vitro from the cell bodies of prevertebral ganglion neurons of guinea-pigs with TNBS-induced ileitis confirm the hyperactivity of postganglionic sympathetic neurons in response to GI inflammation (Dong et al., 2008). Despite hyperactivity of the SNS during IBD, NA levels in both the inflamed and uninflamed colonic mucosa are lower in patients with Crohn's disease (CD) than those serving as controls (Magro et al., 2002).
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2014, Seminars in ImmunologyCitation Excerpt :A similar increase in excitability has also been observed in postganglionic sympathetic neurons of the celiac ganglion during the trinitrobenzene sulfonic acid (TNBS) model of acute ileitis in guinea-pigs. TNBS-induced ileitis decreased the threshold for action potential generation, increased the proportion of spontaneously active postganglionic sympathetic neurons and enhanced the number of stimulus-evoked action potentials [80]. Although GI inflammation enhances SNS excitability, patients with ulcerative colitis exhibit reduced GI catecholamine levels compared to healthy controls [81].
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