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      Decanoic acid attenuates the excitability of nociceptive trigeminal primary and secondary neurons associated with hypoalgesia

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          Abstract

          Background

          Acute application of decanoic acid (DA) in vivo suppresses the excitability of spinal trigeminal nucleus caudalis (SpVc) wide dynamic range (WDR) neurons associated with the short-term mechanical hypoalgesia via muscarinic M 2 receptor signaling; however, the effect of DA on nociceptive trigeminal ganglion (TG) and SpVc nociceptive-specific (NS) neuronal excitability under in vivo conditions remains to be determined. The present study investigated whether this effect could be observed in naive rats.

          Results

          Extracellular single-unit recordings were made from TG and SpVc NS neurons of pentobarbital-anesthetized rats in response to orofacial noxious mechanical stimuli. DA inhibited the mean firing frequency of both TG and SpVc NS neurons, reaching a maximum inhibition of discharge frequency within 1–5 minutes and reversing after approximately 10-minutes; however, this DA-induced suppression of SpVc NS neuronal firing frequency did not occur in rats administered with methoctramine intravenously prior to stimulation.

          Conclusion

          This in vivo study indicated that firing of TG and SpVc NS neurons induced by mechanical hypoalgesia through peripheral M 2 receptors could be inhibited by acutely administered DA, implicating the potential of DA in the future treatment of trigeminal pain.

          Perspective

          This article presents that the acute DA application suppresses the excitability of TG and SpVc NS neurons associated with mechanical hypoalgesia via peripheral M 2 receptor signaling, supporting DA as a potential therapeutic agent in complementary and alternative medicine for the attenuation of nociception.

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          Most cited references 23

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          Ethical guidelines for investigations of experimental pain in conscious animals.

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            TRPA1 modulates mechanotransduction in cutaneous sensory neurons.

            Transient receptor potential ankyrin 1 (TRPA1) is expressed by nociceptive neurons of the dorsal root ganglia (DRGs) and trigeminal ganglia, but its roles in cold and mechanotransduction are controversial. To determine the contribution of TRPA1 to cold and mechanotransduction in cutaneous primary afferent terminals, we used the ex vivo skin-nerve preparation from Trpa1(+/+), Trpa1(+/-), and Trpa1(-/-) adult mouse littermates. Cutaneous fibers from TRPA1-deficient mice showed no deficits in acute cold sensitivity, but they displayed striking deficits in mechanical response properties. C-fiber nociceptors from Trpa1(-/-) mice exhibited action potential firing rates 50% lower than those in wild-type C-fibers across a wide range of force intensities. Adelta-fiber mechanonociceptors also had reduced firing, but only at high intensity forces (>100 mN). Surprisingly, the firing rates of low-threshold Abeta and D-hair mechanoreceptive fibers were also altered. TRPA1 protein and mRNA expression was assessed in DRG neurons and cutaneous innervation by using Trpa1 in situ hybridization, an antibody for TRPA1, and an antibody for placental alkaline phosphatase (PLAP) in mice in which PLAP was substituted for Trpa1. DRG neurons of all sizes expressed Trpa1 mRNA or PLAP immunoreactivity. TRPA1 or PLAP immunolabeling was detected not only on many thin-caliber axons and intraepidermal endings but also on many large-caliber axons as well as lanceolate and Meissner endings. Epidermal and hair follicle keratinocytes also express TRPA1 message and protein. We propose that TRPA1 modulates mechanotransduction via a cell-autonomous mechanism in nociceptor terminals and possibly through a modulatory role in keratinocytes, which may interact with sensory terminals to modify their mechanical firing properties.
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              Use of complementary therapies for arthritis among patients of rheumatologists.

              Use of complementary and alternative medicine (CAM) is common among persons with chronic conditions. To identify correlates of and describe patients' perspective on use of CAM for rheumatologic conditions. Telephone survey. Three university practices and three private rheumatology practices. 232 of 428 eligible consecutive patients (54%) with scheduled appointments. Patients answered questions on CAM use, functional status, pain, provider satisfaction, and health services utilization. Chart reviews provided demographic information and rheumatologic diagnoses. Bivariate analyses identified correlates of four CAM outcomes (history, magnitude, and frequency of CAM use and communication about CAM use with a physician), and multiple logistic regression identified independent correlates of regular CAM use. Approximately two thirds of the respondents (n = 146) had used CAM. Of these 146 respondents, 82 (56%) currently used CAM and 132 (90%) regularly used CAM or had done so in the past. Fifty-five respondents (24%) had used three or more types of CAM. In multivariate analyses, persons who used CAM regularly were more likely to have osteoarthritis (odds ratio, 5.6 [95% CI, 1.9 to 16.8]), severe pain (odds ratio, 2.5 [CI, 1.4 to 4.8]), and a college degree (odds ratio, 2.6 [CI, 1.3 to 5.4]) than patients who had never used CAM. Nearly half of the respondents discussed CAM use with their physicians. The most common reasons for not disclosing CAM use were that the physician had not asked about it and that the patient forgot to tell the physician; fear of disapproval was rarely cited. Discussions about CAM use between patient and physician occurred more frequently among patients with fibromyalgia and persons who regularly used CAM or used several types of CAM. Patients with rheumatologic conditions frequently use CAM. Severe pain and osteoarthritis predict regular use of CAM but do not predict a greater likelihood of discussing CAM use with physicians. Routine inquiry by physicians will probably detect CAM use.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2018
                14 November 2018
                : 11
                : 2867-2876
                Affiliations
                [1 ]Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan, m-takeda@ 123456azabu-u.ac.jp
                [2 ]Department of Emergency, Minami Touhoku Hospital, Iwanuma, Miyagi 989-2483, Japan
                Author notes
                Correspondence: Mamoru Takeda, Laboratory of Food and Physiological Sciences, Department of Life and Food Sciences, School of Life and Environmental Sciences, Azabu University, 1-17-71, Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan, Tel +81 42 769 1886, Fax +81 42 769 2212, Email m-takeda@ 123456azabu-u.ac.jp
                Article
                jpr-11-2867
                10.2147/JPR.S181032
                6241697
                © 2018 Nakajima et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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