Effect of Carbon Dioxide on Calcitonin Gene‐Related Peptide Secretion From Trigeminal Neurons

Vause, Carrie V.; Bowen, Elizabeth J.; Spierings, Egilius L.H.; Durham, Paul L.

doi:10.1111/j.1526-4610.2007.00850.x

Cited by 33 publications

(39 citation statements)

References 82 publications

(167 reference statements)

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“…Vause et al (Vause C et al 2007) have recently shown that treatment of cultured trigeminal neurons with CO 2 under isohydric conditions inhibits sensory nerve activation as induced by capsaicin or KCl, and leads to a subsequent decrease in neuropeptide, i. e. CGRP, release. They proposed an involvement of inhibition of calcium channels.…”

Section: Discussionmentioning

confidence: 99%

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Trigeminal antihyperalgesic effect of intranasal carbon dioxide

et al. 2010

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Aims-Clinical studies demonstrate attenuation of trigeminal-related pain states such as migraine by intranasal CO 2 application. This study investigated the underlying mechanisms of this observation and its potential use to reverse trigeminal pain and hypersensitivity.Main methods-We used a behavioral rat model of capsaicin-induced trigeminal thermal hyperalgesia, intranasal CO2 application and several pharmacologic agents such as carbonic anhydrase, acid-sensing ion channels (ASICs), and TRPV1 blocker as well as acidic buffer solutions to investigate and mimick the underlying mechanism.Key findings-Intranasal CO 2 application produced a robust dose-dependent antihyperalgesic effect in rats that lasted at least one hour. Blockade of nasal carbonic anhydrase with a dorzolamide solution (Trusopt® ophthalmic solution) showed only a non-significant decrease of the antihyperalgesic effect of intranasal CO 2 application. Pharmacologic blockade of ASICs or TRPV 1 receptor significantly attenuated the antihyperalgesic effect of CO 2 application. The effect of intranasal CO 2 application could be mimicked by application of pH4, but not pH 5, buffer solution to the nasal mucosa. As with CO 2 application, the antihyperalgesic effect of intranasal pH4 buffer was blocked by nasal application of antagonists to ASICs and TRPV 1 receptors.Significance-Our results indicate that intranasal CO 2 application results in a subsequent attenuation of trigeminal nociception, mediated by protonic activation of TRPV 1 and ASIC channels. A potential central mechanism for this attenuation is discussed. The antihyperalgesic effects of intranasal CO 2 application might be useful for the treatment of trigeminal pain states.

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Section: Discussionmentioning

confidence: 99%

“…There is evidence that CO 2 can decrease the release of pain-related neurotransmitters from cultured sensory neurons (Vause C et al 2007). In addition, clinical observations have found intranasal CO 2 to alleviate headache by an unknown mechanism (Spierings EL 2005).…”

Section: Introductionmentioning

confidence: 99%

Trigeminal antihyperalgesic effect of intranasal carbon dioxide

et al. 2010

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“…Other animals were either left untreated or were injected with the vehicle, which was HBS at pH 7.4. The concentration of NO donor and pH were chosen since we had previously shown that they can stimulate neuropeptide release from cultured trigeminal ganglia neurons (Bellamy et al, 2006, Vause et al, 2007). The nitrite concentration of the NO-proton solution that was injected into the TMJ capsule was determined using the Griess Reagent System (Promega, Madison, WI, USA) following the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide-proton stimulation of trigeminal ganglion neurons increases mitogen-activated protein kinase and phosphatase expression in neurons and satellite glial cells

2008

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Elevated nitric oxide (NO) and proton levels in synovial fluid are implicated in joint pathology. However, signaling pathways stimulated by these molecules that mediate inflammation and pain in the temporomandibular joint (TMJ) have not been investigated. The goal of this study was to determine the effect of NO-proton stimulation of trigeminal neurons on the in vivo expression of mitogen-activated protein kinases (MAPKs) and phosphatases (MKPs) in trigeminal ganglion neurons and satellite glial cells. Low levels of the active MAPKs ERK, JNK, and p38 were localized in the cytosol of neurons and satellite glial cells in unstimulated animals. However, increased levels of active ERK and p38, but not JNK, were detected in the cytosol and nucleus of V3 neurons and satellite glial cells 15 min and 2 h following bilateral TMJ injections of a NO donor diluted in pH 5.5 medium. While ERK levels returned to near basal levels 24 h after stimulation, p38 levels remained significantly elevated. In contrast to MKP-2 and MKP-3 levels that were barely detectable in neurons or satellite glial cells, MKP-1 staining was readily observed in satellite glial cells in ganglia from unstimulated animals. However, neuronal and satellite glial cell staining for MKP-1, MKP-2, and MKP-3 were all significantly increased in response to NO-protons. Increased active ERK and p38 levels as well as elevated MKP levels were also detected in neurons and satellite glial cells located in V2 and V1 regions of the ganglion. Our data provide evidence that NO-proton stimulation of V3 neurons results in temporal and spatial changes in expression of active ERK and p38 and MKPs in all regions of the ganglion. We propose that in trigeminal ganglia these cellular events, which are involved in peripheral sensitization as well as control of inflammatory and nociceptive responses, may play a role in TMJ pathology.

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“…These effects may occur due to an increase in capillary blood flow triggered by hypercapnia, by a decreased consumption of cutaneous oxygen or by a rightward shift of the oxygen (O 2 ) dissociation curve (Bohr effect) 1 . It is known that intranasal CO 2 may inhibit trigeminal neuronal activation (in rats) and suppress in vitro calcitonin gene-related peptide (CGRP) release 2 . Based on this assumption, the efficiency of intranasal noninhaled CO 2 was investigated in the treatment of seasonal allergic rhinitis (SAR) 3 .…”

Section: Carboxytherapy Is a Technique Originated In 1930 Inmentioning

confidence: 99%

Effects of subcutaneous carbon dioxide on calcitonin gene related peptide and substance P secretion in rat skin

et al. 2014

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PURPOSE:To investigate the subcutaneous injection of carbon dioxide (CO 2 ) on neuropeptides Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP) secretion in rat skin. METHODS:Fifty-six Wistar-EPM rats were distributed in two groups: one for CGRP analysis, the other for SP analysis. Each group was subdivided into four subgroups: control (Cont), control with needle (ContNd), CO 2 injection (CO 2 Inj) and atmospheric air injection (AirInj) -with seven animals each. Sample analyses of partial skin were conducted by Western Blotting (WB). RESULTS:In SP group, there was a decrease in the amount of neuropeptides in subgroups CO 2 Inj and AirInj. Similarly, in CGRP group, there was a decrease in the amount of pro-CGRP neuropeptides (15 kDa) in subgroups CO 2 Inj and AirInj; Nevertheless, there was no decrease in the amount of CGRP (5 kDa) in any subgroups.CONCLUSION: Subcutaneous injection of CO 2 and atmospheric air decreased the amount of Substance P and pro-Calcitonin GeneRelated Peptide (15 kDa) neuropeptides in rat skin.

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Effect of Carbon Dioxide on Calcitonin Gene‐Related Peptide Secretion From Trigeminal Neurons

Cited by 33 publications

References 82 publications

Trigeminal antihyperalgesic effect of intranasal carbon dioxide

Trigeminal antihyperalgesic effect of intranasal carbon dioxide

Nitric oxide-proton stimulation of trigeminal ganglion neurons increases mitogen-activated protein kinase and phosphatase expression in neurons and satellite glial cells

Effects of subcutaneous carbon dioxide on calcitonin gene related peptide and substance P secretion in rat skin

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