Distribution of vanilloid receptors in the rat laryngeal innervation

Koike, Shinobu; Uno, Toshiyuki; Bamba, Hitoshi; Shibata, Toshiaki; Okano, Hiroyuki; Hisa, Yasuo

doi:10.1080/00016480310000674

Cited by 23 publications

(12 citation statements)

References 10 publications

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“…Our present study confirmed these previous works and found the colocalization of nNOS with TRPV1 in the subepidermal nerve fibers and in connective tissue cells in the dermis. The colocalization of TRPV1 and nNOS was previously reported in the neurons of the intralaryngeal ganglia (Koike, 2004), suggesting an important function of both TRPV1 and nNOS involved in the sensory transmission to the spinal cord. Moreover, the colocalization in the connective tissue cells may represent a functional role in immunity and the local effects of EA.…”

Section: Discussionsupporting

confidence: 74%

TRPV1 expression in acupuncture points: Response to electroacupuncture stimulation

Abraham

Chen

2011

Journal of Chemical Neuroanatomy

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The present study was to examine the distribution of transient receptor potential vanilloid type-1 (TRPV1) receptor immunoreactivity in the acupuncture points (acupoint), and determine the influences of electroacupuncture (EA) stimulation on TRPV1 expression. EA stimulation of BL 40 was conducted in two sessions of 20 min separated by an 80 min interval in anesthetized rats. Sections of skin containing BL 40, and its non-meridian control were examined by immunolabeling with antibodies directed against TRPV1. Without EA, the number of subepidermal nerve fibers expressing TRPV1 was higher in the acupoint than in non-acupoint control skin (p<0.01). The subepidermal nerve fibers showed the co-localization of TRPV1 with peripherine, a marker for the C-fibers and A-δ fibers. The expression of TRPV1 in nerve fibers is significantly increased by EA stimulation in acupoints (p<0.01). However the upregulation in the non acupoint meridian and the non-meridian control skin were short of statistical significance. Double immunostaining of TRPV1 and neuronal nitric oxide synthase (nNOS) revealed their colocalizationin both the subepidermal nerve fibers and in the dermal connective tissue cells. These results show that a high expression of TRPV1 endowed with nNOS in subepidermal nerve fibers exist in the acupoints and the expression is increased by EA. We conclude that the higher expression of TRPV1 in the subepidermal nerve fibers and its upregulation after EA stimulation may play a key role in mediating the transduction of EA signals to the CNS, and its expression in the subepidermal connective tissue cells may play a role in conducting the local effect of the EA.

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Section: Discussionsupporting

confidence: 74%

TRPV1 expression in acupuncture points: Response to electroacupuncture stimulation

Abraham

Chen

2011

Journal of Chemical Neuroanatomy

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“…The colocalization of TRPV1 and nNOS was previously reported in the neurons [16], and TRPV1 is activated by NO through a feedback regulation mechanism between channel activation, calcium entry and NO production [45], which suggests an important function of both TRPV1 and NO involved in the sensory transmission. Previous studies from our laboratory have reported that performing EA on ST36, a vital leg acupoint, increased positive immunostaining nNOS neurons in the NTS and the GN [23].…”

Section: Discussionmentioning

confidence: 70%

Effects of electroacupuncture Zusanli (ST36) on food intake and expression of POMC and TRPV1 through afferents-medulla pathway in obese prone rats

2013

Peptides

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Objective The purpose of this study was to determine the effects of electroacupuncture (EA) ST36 on food intake and body weight in Obese Prone (OP) rats compared to obese resistant (OR) strain on a high fat diet. The influences of EA on mRNA levels of pro-opiomelanocortin (POMC), transient receptor potential vanilloid type-1 (TRPV1), and neuronal nitric oxide synthase (nNOS) were also examined in the medulla regions and ST36 skin tissue. Methods Advanced EA ST36 was conducted in two sessions of 20 min separated by an 80 min interval for 7 days. Food intake and body weight were recorded in conscious rats every day. Real time PCR was conducted in the micropunches of the medulla regions and skin tissues at the end of the treatment. Results Food intake and body weight were significantly reduced by advanced EA ST36 in OP rats, but slightly decreased in OR strain and sham-EA rats. Advanced EA ST36 produced a marked increase in POMC mRNA level in the nucleus tractus solitarius (NTS) and hypoglossal nucleus (HN) regions. TRPV1 and nNOS mRNAs were simultaneously increased in the NTS/gracile nucleus regions and in the ST36 skin regions by the EA treatment in OP rats. Conclusions We conclude that advanced EA ST36 produces an up-regulation of anorexigenic factor POMC production in the NTS/HN, which inhibits food intake and reduces body weight. EA-induced expression of TRPV1-nNOS in the ST36 and the NTS/gracile nucleus is involved in the signal transduction of EA stimuli via somatosensory afferents-medulla pathways.

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“…Electrophysiological (35,50) and immunohistochemical studies (24) have clearly indicated the presence of capsaicinsensitive afferent fibers in the larynx. These afferent fibers are thought to be nociceptive-like free nerve endings 7, and their increase in sensitivity to stimuli is analogous to primary hyperalgesia, resulting from a decrease in the threshold for pain-producing stimuli.…”

Section: Discussionmentioning

confidence: 99%

Neural and hydroxyl radical mechanisms underlying laryngeal airway hyperreactivity induced by laryngeal acid-pepsin insult in anesthetized rats

Tsai¹,

Chang²,

Ho³

et al. 2006

Journal of Applied Physiology

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Laryngopharyngeal or gastroesophageal reflux is associated with laryngeal airway hyperreactivity (LAH), but neither the cause-effect relationship nor the underlying mechanism has been elucidated. Here we established a rat model with enhanced laryngeal reflex reactivity induced by laryngeal acid-pepsin insult and investigated the neural and hydroxyl radical (*OH) mechanisms involved. The laryngeal segments of 103 anesthetized rats were functionally isolated while animals breathed spontaneously. Ammonia vapor was delivered into the laryngeal segment to measure laryngeal reflex reactivity. We found that the laryngeal pH 5-pepsin treatment doubled the reflex apneic response to ammonia, whereas laryngeal pH 7.4-pepsin, pH 2-pepsin, and pH 5-denatured pepsin treatment had no effect. Histological examination revealed limited laryngeal inflammation and epithelial damage after pH 5-pepsin treatment and more severe damage after pH 2-pepsin treatment. In rats that had received the laryngeal pH 5-pepsin treatment, the apneic response to ammonia was abolished by either denervation or perineural capsaicin treatment (PCT; a procedure that selectively blocks capsaicin-sensitive afferent fibers) of the superior laryngeal nerves, but was unaffected by perineural sham treatment. LAH was prevented by laryngeal application of either dimethylthiourea (DMTU; a *OH scavenger) or deferoxamine (DEF; an antioxidant for *OH), but was unaltered by the DMTU vehicle or iron-saturated DEF (ineffective DEF). LAH reappeared after recovery from PCT, DMTU, or DEF treatment. We conclude that 1) laryngeal insult by pepsin at a weakly acidic pH, but not at acidic pH, can produce LAH; and 2) LAH is probably mediated through sensitization of the capsaicin-sensitive laryngeal afferent fibers by a *OH mechanism.

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Distribution of vanilloid receptors in the rat laryngeal innervation

Abstract: These findings suggest that these capsaicin receptors participate in the parasympathetic innervation as well as in nociception of the rat larynx.

Cited by 23 publications

References 10 publications

TRPV1 expression in acupuncture points: Response to electroacupuncture stimulation

TRPV1 expression in acupuncture points: Response to electroacupuncture stimulation

Effects of electroacupuncture Zusanli (ST36) on food intake and expression of POMC and TRPV1 through afferents-medulla pathway in obese prone rats

Neural and hydroxyl radical mechanisms underlying laryngeal airway hyperreactivity induced by laryngeal acid-pepsin insult in anesthetized rats

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