Subdiaphragmatic vagal afferent innervation in activation of an opioidergic antinociceptive system in response to colorectal distension in rats

Gschossmann, Juergen M.; Mayer, Emeran A.; Miller, J. C.; Raybould, Helen E.

doi:10.1046/j.1365-2982.2002.00345.x

Cited by 36 publications

(35 citation statements)

References 30 publications

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“…However, it is possible that inflammatory changes modulated in the vagally innervated proximal colon result in changes in the enteric nervous system in the remainder of the colon (29), resulting in a reduction in acetylcholine release. This may account for the effect of vagotomy on colitis seen in this and other studies (20,26,27,30). We also demonstrate the same profile of results using the maternal deprivation model.…”

Section: Discussionsupporting

confidence: 88%

Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression

Ghia¹,

Blennerhassett²,

Collins³

2008

J. Clin. Invest.

162

156

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Clinical and experimental evidence indicates that intestinal inflammatory conditions can be exacerbated by behavioral conditions such as depression. The recent demonstration of a tonic counterinflammatory influence mediated by the vagus nerve in experimental colitis provides a potential link between behavior and gut inflammation. Here we show that experimental conditions that induced depressive-like behaviors in mice increased susceptibility to intestinal inflammation by interfering with the tonic vagal inhibition of proinflammatory macrophages and that tricyclic antidepressants restored vagal function and reduced intestinal inflammation. These results show that reserpine-induced monoamine depletion and maternal separation, 2 models for depression, produced a vulnerability to colitis by a mechanism involving parasympathetic transmission and the presence of gut macrophages. The tricyclic antidepressant desmethylimipramine protected against this vulnerability by a vagal-dependent mechanism. Together these results illustrate the critical role of the vagus in both the vulnerability to inflammation induced by depressive-like conditions and the protection afforded by tricyclic antidepressants and rationalize a clinical evaluation of both parasympathomimetics and tricyclic antidepressants in treatment of inflammatory bowel disease.

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Section: Discussionsupporting

confidence: 88%

Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression

Ghia¹,

Blennerhassett²,

Collins³

2008

J. Clin. Invest.

162

156

View full text Add to dashboard Cite

show abstract

“…Moreover, the opioid receptor antagonist naloxone did not affect the overall response or the response attenuation to CRD in C57BL/6 mice at any dose tested, further supporting that the opioid system is most likely not involved in the attenuation of the VMR seen in mice. That naloxone did not affect the VMR to CRD conflicts with results in rats, which however do not display a transient response, 17,18 but is similar to results obtained in mice. 25,26 The difference seen between rats and mice may reflect alternative linkages between stress responses and visceral pain in these two species.…”

Section: Discussionsupporting

confidence: 75%

“…It has been proposed that there is an ongoing opioid-driven tone in the gastrointestinal sensory system, as naloxone increased the VMR to CRD in both naïve and trinitro-benzenesulphonic acid-treated rats. 17,18 Therefore, in the current study, the magnitude and duration of the transient VMR was investigated in detail in order to evaluate whether endogenous opioids are involved in the attenuation of the VMR in mice. We also evaluated whether the opioid system in general is involved in the attenuation mechanism of the VMR by giving the prototypic nonspecific opioid receptor antagonist naloxone.…”

Section: Discussionmentioning

confidence: 99%

Involvement of κ‐opioid receptors in visceral nociception in mice

Larsson

Bayati

Lindström

et al. 2008

Neurogastroenterology Motil

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It has been shown that the behavioural responses to chemically evoked visceral nociception are increased in transgenic mice lacking the j-opioid receptor (KOR). The aim of the present study was to evaluate the contribution of KOR in mechanically evoked visceral pain by performing colorectal distension (CRD) and monitoring the subsequent visceromotor response (VMR) in control mice (KOR +/+ ) and in mice lacking KOR (KOR )/) ). Pseudo-affective visceral pain responses were evoked in conscious mice using increasing (10-80 mmHg) and repeated (12 · 55 mmHg) phasic CRD paradigms. The resulting VMR was determined by monitoring the electromyographic activity of the abdominal muscle. The increasing and repeated CRD paradigms, respectively, evoked similar responses in both KOR +/+ and KOR )/) mice. The selective KOR-agonists U-69593 (5 and 25 mg kg )1 , s.c.) and asimadoline (25 mg kg )1 , s.c.) significantly decreased the VMR in KOR +/+ mice, while having no effect in KOR )/) mice. In contrast, the selective l-opioid receptor agonist fentanyl significantly reduced the VMR in both types of mice and appeared more efficacious in KOR )/) mice. The opioid receptor antagonist naloxone (0.3-30 mg kg )1 s.c.) did not affect the response to CRD in C57BL/6 mice at any dose tested. In conclusion, the data confirm that the KOR agonists used in this study inhibit the VMR to CRD in mice by acting via KOR receptors. In addition, the data suggest that the endogenous opioid system is not likely to modulate the VMR to mechanically evoked visceral pain in mice.

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“…Another study showed that a slight but insignificant increase in the VMR to noxious gastric distension after chronic vagotomy (51). However, other studies have shown that vagotomy blunts the VMR to upper cervical esophageal distensions (22) and significantly enhanced the VMR to tonic CRD in conscious rats (17). In this study, we demonstrated that chronic subdiaphragmatic vagotomy decreases the threshold and enhances the VMR to all grades of CRD (470, 106, 51, and 54% increases in VMR to CRD at 20, 40, 60, and 80 mmHg, respectively).…”

Section: Discussionmentioning

confidence: 97%

Subdiaphragmatic vagal afferent nerves modulate visceral pain

Chen¹,

Wu²,

Cao³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Activation of the vagal afferents by noxious gastrointestinal stimuli suggests that vagal afferents may play a complex role in visceral pain processes. The contribution of the vagus nerve to visceral pain remains unresolved. Previous studies reported that patients following chronic vagotomy have lower pain thresholds. The patient with irritable bowel syndrome has been shown alteration of vagal function. We hypothesize that vagal afferent nerves modulate visceral pain. Visceromotor responses (VMR) to graded colorectal distension (CRD) were recorded from the abdominal muscles in conscious rats. Chronic subdiaphragmatic vagus nerve sections induced 470, 106, 51, and 54% increases in VMR to CRD at 20, 40, 60 and 80 mmHg, respectively. Similarly, at light level of anesthesia, topical application of lidocaine to the subdiaphragmatic vagus nerve in rats increased VMR to CRD. Vagal afferent neuronal responses to low or high-intensity electrical vagal stimulation (EVS) of vagal afferent A␦ or C fibers were distinguished by calculating their conduction velocity. Low-intensity EVS of A␦ fibers (40 A, 20 Hz, 0.5 ms for 30 s) reduced VMR to CRD at 40, 60, and 80 mmHg by 41, 52, and 58%, respectively. In contrast, high-intensity EVS of C fibers (400 A, 1 Hz, 0.5 ms for 30 s) had no effect on VMR to CRD. In conclusion, we demonstrated that vagal afferent nerves modulate visceral pain. Low-intensity EVS that activates vagal afferent A␦ fibers reduced visceral pain. Thus EVS may potentially have a role in the treatment of chronic visceral pain. colorectal distension; vagal afferent A␦ or C fibers; visceromotor responses ALTHOUGH IT IS GENERALLY HELD that pain arising from the viscera is mediated exclusively by spinal afferents, vagal afferents primarily convey interoceptive information that is important in regulating autonomic function but do not contribute to the perception of pain. However, there is growing evidence that the vagus nerve may play a complex role in these processes (5,32,35,46). Electrical physiological studies have demonstrated that electrical or chemical stimulation of thoracic vagal and sympathetic afferent fibers activated C1-C3 spinothalamic tract (STT) neurons, which received input from noxious mechanical stimulation of somatic fields including the neck and jaw regions (6, 7). Studies have shown that vagal afferents respond to nociceptive mechanical and chemical stimulation and this leads to brain stem representation of nociceptive signals (35,46,51). Noxious gastric distension resulted in c-Fos expression in the nucleus of the solitary tract (NTS), the location of second order neurons receiving vagal afferent input from the stomach. This increase in c-Fos response is blunted by vagotomy but persists after spinal cord transection (51). Although vagal afferents are activated by gastrointestinal noxious stimuli, the contribution of the vagus nerve to visceral pain remains unresolved. It is well known that a hot drink or a nourishing meal (stimulation of various abdominal receptors) is relaxing and helps to ca...

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Subdiaphragmatic vagal afferent innervation in activation of an opioidergic antinociceptive system in response to colorectal distension in rats

Cited by 36 publications

References 30 publications

Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression

Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression

Involvement of κ‐opioid receptors in visceral nociception in mice

Subdiaphragmatic vagal afferent nerves modulate visceral pain

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