Activation of lamina I spinal cord neurons that express the substance P receptor in visceral nociception and hyperalgesia

Honoré, Prisca; Kamp, Elizabeth H.; Rogers, Scott D.; Gebhart, G.F.; Mantyh, Patrick W.

doi:10.1054/jpai.2002.27001

Cited by 42 publications

(33 citation statements)

References 39 publications

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“…This is consistent with descriptions of dermatomes in rodents, showing perineal labeling or activation of lumbosacral neurons, while nerves innervating plantar skin of the hindpaw projected primarily to L4 and L5 spinal segments (48,53). However, colonic application of irritants, such as zymosan, leads to a significant activation of spinal neurons in adjacent segments, including L4 and L5, thus providing a neuroanatomic basis for the observed hypersensitivity in both hindpaws during an inflammatory state (16). Similarly, electrophysiological experiments showed an increased size of the cutaneous receptive field after colonic administration of acetic acid (41), a finding consistent with data showing lower sensory thresholds and larger areas of pain referral in patients with functional bowel disorders (31,34).…”

Section: Discussionsupporting

confidence: 89%

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

Bielefeldt¹,

Lamb²,

Gebhart³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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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: 89%

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

Bielefeldt¹,

Lamb²,

Gebhart³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Treatment with the NK 1 antagonist SR140333B reduced the febrile response induced by zymosan, suggesting that this neuropeptide participates in this response. In models of acute visceral inflammation and nociception induced by zymosan, the internalization of NK 1 receptors has been observed in neurons in lamina I and sympathetic preganglionic neurons, indicating that the release of substance P and activation of NK 1 receptors are induced by this stimulus [39,40]. These results support the hypothesis that zymosan induces substance P release from neurons.…”

Section: Discussionsupporting

confidence: 73%

Central mediators of the zymosan-induced febrile response

Bastos-Pereira

Fraga

Dreifuss

et al. 2017

Journal of Basic and Clinical Physiology and Pharmacology

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Background: Zymosan is a fungal cell wall protein-carbohydrate complex that is known to activate inflammatory pathways through the Toll-like receptors and is commonly used to induce fever. Nevertheless, the central mediators that are involved in the zymosan-induced febrile response are only partially known. Methods:The present study evaluated the participation of prostaglandins, substance P, endothelin-1 (ET-1), and endogenous opioids (eOPs) in the zymosan-induced febrile response by using inhibitors and antagonists in male Wistar rats. Results: Both nonselective (indomethacin) and selective (celecoxib) cyclooxygenase inhibitors reduced the febrile response induced by an intraperitoneal (i.p.) injection of zymosan. Indomethacin also blocked the increase in the prostaglandin E 2 levels in the cerebrospinal fluid. An intracerebroventricular injection of the neurokinin-1, ET B , and μ-opioid receptor antagonists also reduced the febrile response induced by the i.p. injected zymosan. Moreover, the μ-opioid receptor antagonist CTAP also reduced the febrile response induced by intra-articular injection of zymosan.Conclusions: These results demonstrate that prostaglandins, substance P, ET-1, and eOPs are central mediators of the zymosan-induced febrile response.

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“…In pilot studies it was found that zymosan had inconsistent access to the gut tissue, presumably because of the mucous barrier, and this was rectified by administration of 3 ml of 30% alcohol. Ethanol solution was followed by 1 ml saline, again to rinse the colon, and 25 mg of zymosan in 1 ml saline (Sigma Chemical Company, Oakville, ON, Canada) to induce an inflammatory response (see also Coutinho et al, 1996;Honore et al, 2002). One control group consisted of naïve rats receiving only intracolonic saline and another control group received 3 ml of 30% ethanol followed by 1 ml saline.…”

Section: Induction Of Inflammationmentioning

confidence: 99%

“…As internalization of the NK-1r in the spinal cord has been interpreted as an inducer of neuronal activation (Honore et al, 1999(Honore et al, , 2002, we used NK-1r internalization as a marker of activation of peptidergic nociceptive primary sensory fibers, as well as an indirect way of inferring whether substance P could have been released from peripheral terminals of these fibers in the gut. This conjecture is based on Dale's (1935) principle that the same transmitter should be released from all terminals of a given neuron.…”

mentioning

confidence: 99%

Sensory neuron and substance P involvement in symptoms of a zymosan-induced rat model of acute bowel inflammation

et al. 2007

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Activation of lamina I spinal cord neurons that express the substance P receptor in visceral nociception and hyperalgesia

Cited by 42 publications

References 39 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

Central mediators of the zymosan-induced febrile response

Sensory neuron and substance P involvement in symptoms of a zymosan-induced rat model of acute bowel inflammation

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