Altered visceral sensation in response to somatic pain in the rat☆

Miranda, Adrian; Peles, Shachar; Rudolph, Colin; Shaker, Reza; Sengupta, Jyoti N.

doi:10.1053/j.gastro.2004.01.003

Cited by 73 publications

(76 citation statements)

References 32 publications

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“…The present results are consistent with recent reports (32,43) showing visceral hypersensitivity after repeated injections of acid into the gastrocnemius muscle in rats, associated with a sensitization of spinal neurons that receive convergent input from the colon and affected muscle. Blockade of spinal ionotropic glutamate receptors abolished this cross-sensitization in a model of acute, noninflammatory muscle, suggesting that spinal mechanisms may contribute to the coexistence of different pain disorders in patients with fibromyalgia, interstitial cystitis, or functional gastrointestinal disorders (32).…”

Section: Discussionsupporting

confidence: 94%

“…We monitored micturitions during constant infusions into the bladder, noting that peak pressures did not exceed 20 mmHg. However, pressures in the noxious range (Ͼ20 mmHg) are required to trigger clear visceromotor responses in response to colorectal distension (32,36). An alternative approach with urethral catheterization and occlusion of the urinary outflow tract cannot be performed in male mice.…”

Section: Discussionmentioning

confidence: 99%

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Convergence of sensory pathways in the development of somatic and visceral hypersensitivity

Bielefeldt¹,

Lamb²,

Gebhart³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

101

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Sensory neurons innervating different tissues converge onto second-order neurons in the spinal cord. We examined whether inflammation or transient overexpression of nerve growth factor (NGF) in one tissue triggers hypersensitivity in referral sites. Thresholds to mechanical and thermal stimulation of the hindpaw, visceromotor responses to colorectal distension, and cystometrograms were performed in appropriate controls and mice with experimentally induced cystitis, inflammation of the hindpaw or front paw, or injection of viral vectors encoding NGF or green fluorescent protein (GFP). Cystitis and NGF but not GFP overexpression in the bladder triggered bladder hyperactivity associated with mechanical and thermal hypersensitivity in cutaneous referral sites and enhanced responses to colorectal distension. Hindpaw inflammation and injection of the NGF- but not GFP-encoding viral vector or front paw inflammation induced mechanical and thermal hyperalgesia in the affected hindpaw and increased responses to colorectal distension without altering the micturition reflex. In conclusion, sensitization of sensory pathways by inflammation or NGF contributes to the development of hypersensitivity in neighboring organs and cutaneous referral sites and provides a potential mechanism underlying the coexistence of pain syndromes in patients with functional diseases.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Convergence of sensory pathways in the development of somatic and visceral hypersensitivity

Bielefeldt¹,

Lamb²,

Gebhart³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

101

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show abstract

“…However, these animals do not develop thermal hyperalgesia (Sluka et al, 2001). Instead, visceral hyperalgesia detected by electromyography occurs concurrently with somatic hyperalgesia, suggesting that somatic afferent input from the gastrocnemius muscle induces visceral hyperalgesia, possibly via viscerosomatic convergence at the level of the lower spinal cord (Miranda et al, 2004). This finding is consistent with those in fibromyalgia patients who frequently show abdominal hypersensitivity, such as irritable bowel syndrome.…”

Section: Face Validitysupporting

confidence: 80%

Animal Models of Fibromyalgia

Nagakura¹,

Ito²,

Shimizu³

2012

New Insights Into Fibromyalgia

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“…37 Similar findings of visceral hypersensitivity are observed in adult rats following recurrent neonatal somatic pain such as that induced by acid injection into a muscle or nasogastric suctioning. The adult pain hypersensitivity can be blocked by preemptive administration of glutamate receptor antagonists (given at the time of pain induction) in the case of acid injection, 38 or corticotrophin releasing factor 1 antagonist in case of nasogastric suctioning. 39 These findings and many others indicate that the changes in visceral pain responses induced during infancy can be modified by changing the neurochemical milieu during the painful experience.…”

Section: Visceral Pain During Development Alter Pain Responses In Adumentioning

confidence: 99%

Visceral Pain and Gastrointestinal Microbiome

Chichlowski

Rudolph

2015

J Neurogastroenterol Motil

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A complex set of interactions between the microbiome, gut and brain modulate responses to visceral pain. These interactions occur at the level of the gastrointestinal mucosa, and via local neural, endocrine or immune activity; as well as by the production of factors transported through the circulatory system, like bacterial metabolites or hormones. Various psychological, infectious and other stressors can disrupt this harmonious relationship and alter both the microbiome and visceral pain responses. There are critical sensitive periods that can impact visceral pain responses in adulthood. In this review we provide a brief background of the intestinal microbiome and emerging concepts of the bidirectional interactions between the microbiome, gut and brain. We also discuss recent work in animal models, and human clinical trials using prebiotics and probiotics that alter the microbiome with resultant alterations in visceral pain responses.

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Altered visceral sensation in response to somatic pain in the rat☆

Cited by 73 publications

References 32 publications

Convergence of sensory pathways in the development of somatic and visceral hypersensitivity

Convergence of sensory pathways in the development of somatic and visceral hypersensitivity

Animal Models of Fibromyalgia

Visceral Pain and Gastrointestinal Microbiome

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