Multiple Cation Channels Mediate Increases in Intracellular Calcium Induced by the Volatile Irritant, Trans-2-Pentenal in Rat Trigeminal Neurons

Inoue, Takashi; Bryant, Bruce P.

doi:10.1007/s10571-009-9428-9

Cited by 8 publications

(8 citation statements)

References 34 publications

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“…Our observations gain support from findings showing that, in rodent dorsal root ganglion neurons, the activation of TRPA1 receptors by AITC enhanced the inward currents evoked by repeated applications of AITC (36) and by the mechanical stimulation of neurites (6). The cellular mechanisms by which TRPA1 activation leads to the sensitization of CSLV fibers is unclear, but they are probably related to changes in the membrane conductance or to the resting membrane potential (19), or both. Activation of TRPA1 receptors evokes the influx of cations, such as calcium and sodium ions, which in turn can trigger the opening of voltage-gated cation channels (19) and lead to elevation of cell excitability of CSLV neurons.…”

Section: Discussionsupporting

confidence: 83%

“…The cellular mechanisms by which TRPA1 activation leads to the sensitization of CSLV fibers is unclear, but they are probably related to changes in the membrane conductance or to the resting membrane potential (19), or both. Activation of TRPA1 receptors evokes the influx of cations, such as calcium and sodium ions, which in turn can trigger the opening of voltage-gated cation channels (19) and lead to elevation of cell excitability of CSLV neurons. In addition to its abundant location on sensory neurons, TRPA1 receptors are also expressed on nonneuronal tissues including in mice and human airways (12,32).…”

Section: Discussionmentioning

confidence: 99%

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Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors

Hsu

Lin

Lee

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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-The sensitization of capsaicin-sensitive lung vagal (CSLV) afferents by inflammatory mediators is important in the development of airway hypersensitivity. Hydrogen sulfide (H 2 S) is an endogenous mediator inducing hyperalgesia through transient receptor potential ankyrin 1 (TRPA1) receptors located on nociceptors. We conducted this study to determine whether H 2S elevates the sensitivity of rat CSLV afferents. In anesthetized, artificially ventilated rats, the inhalation of aerosolized sodium hydrosulfide (NaHS, a H2S donor) caused no significant changes in the baseline activity of CSLV afferents. However, the afferent responses to right atrial injection of capsaicin or phenylbiguanide and to lung inflation were all markedly potentiated after NaHS inhalation. By contrast, the inhalation of its vehicle or NaOH (with a similar pH to NaHS) failed to enhance the afferent responses. Additionally, the potentiating effect on the afferent responses was found in rats inhaling L-cysteine (a substrate of H2S synthase) that slowly releases H2S. The potentiating effect of NaHS on the sensitivity of CSLV afferents was completely blocked by pretreatment of HC-030031 (a TRPA1 receptor antagonist) but was unaffected by its vehicle. In isolated rat CSLV neurons, the perfusion of NaHS alone did not influence the intracellular Ca 2ϩ concentration but markedly potentiated the Ca 2ϩ transients evoked by capsaicin. The NaHScaused effect was totally abolished by HC-030031 pretreatment. These results suggest that H2S induces a nonspecific sensitizing effect on CSLV fibers to both chemical and mechanical stimulation in rat lungs, which appears mediated through an action on the TRPA1 receptors expressed on the nerve endings of CSLV afferents. lung; lung vagal C fibers; afferent sensitization; H2S; TRPA1 receptors CAPSAICIN-SENSITIVE LUNG VAGAL (CSLV) afferents are nociceptive-like free nerve endings innervating all levels of the respiratory tract. CSLV afferents can detect several inhaled irritants (22, 25) and inflammatory mediators (16,25,26,39) that might in turn trigger various respiratory reflexes such as cough, mucus secretion, and bronchoconstriction (7,22). The afferents are sensitized by several mediators released because of lung inflammation (2,7,15,27), which might then exaggerate these respiratory reflexes. Therefore, the sensitization of CSLV afferents is probably involved in the pathogenesis of airway hypersensitivity in diseases such as chronic cough and asthma (7, 26, 47).Hydrogen sulfide (H 2 S), an irritant gas with the smell of rotten eggs, is emitted principally from volcanoes, hot springs, and numerous industrial sites. Lung exposure to H 2 S might lead to adverse respiratory effects, such as cough, airway irritation, airway hypersensitivity, and lung inflammation (16, 37, 41). Therefore, for the past decades, H 2 S was generally considered only an exogenous irritant. However, beginning with a report in 1996, H 2 S was suggested to act as an endogenous neuromodulator facilitating the hippocampal long-term potentiati...

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors

Hsu

Lin

Lee

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Furthermore, biological activity that is unrelated to electrophilic reactivity should be considered. For example, ( E )-2-pentenal is a strong irritant of sensory nerves, being a ligand for the TRPA1 channel [ 76 ]. Even though these volatiles are highly reactive, they do not show an indiscriminate reactivity, because steric factors are important as well; for example, the α , β -unsaturated oxo-compounds 1-penten-3-one and ( E )-2-pentenal inhibit glucose 6-phosphatase, but conjugated dienals do not [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

Chemical Compositional Changes in Over-Oxidized Fish Oils

Phung

Bannenberg²,

Vigor

et al. 2020

Foods

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A recent study has reported that the administration during gestation of a highly rancid hoki liver oil, obtained by oxidation through sustained exposure to oxygen gas and incident light for 30 days, causes newborn mortality in rats. This effect was attributed to lipid hydroperoxides formed in the omega-3 long-chain polyunsaturated fatty acid-rich oil, while other chemical changes in the damaged oil were overlooked. In the present study, the oxidation condition employed to damage the hoki liver oil was replicated, and the extreme rancidity was confirmed. A detailed analysis of temporal chemical changes resulting from the sustained oxidative challenge involved measures of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) omega-3 oil oxidative quality (peroxide value, para-anisidine value, total oxidation number, acid value, oligomers, antioxidant content, and induction time) as well as changes in fatty acid content, volatiles, isoprostanoids, and oxysterols. The chemical description was extended to refined anchovy oil, which is a more representative ingredient oil used in omega-3 finished products. The present study also analyzed the effects of a different oxidation method involving thermal exposure in the dark in contact with air, which is an oxidation condition that is more relevant to retail products. The two oils had different susceptibility to the oxidation conditions, resulting in distinct chemical oxidation signatures that were determined primarily by antioxidant protection as well as specific methodological aspects of the applied oxidative conditions. Unique isoprostanoids and oxysterols were formed in the over-oxidized fish oils, which are discussed in light of their potential biological activities.

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“…We examined bimatoprostinduced Ca 2þ response in hTRPA1-HEK and nt-TRPA1-HEK cells to conform the direct activation of TRPA1 by bimatoprost. As shown in Figure 3A, hTRPA1-HEK cells in calcium imaging assays responded robustly to bath solution application of bimatoprost (25 ng/mL), and responded again to bath solution application of 100 lM AITC, 35 a specific agonist of TRPA1, after bimatoprost washout. Furthermore, after AITC washout, hTRPA1-HEK cells responded again to bath solution application of 25 lM WIN, a synthetic and selective CB1 receptor agonist and a nonspecific agonist of TRPA1.…”

Section: Bimatoprost Induces Ca 2þ Influx In Htrpa1-hek But Not Nt-tmentioning

confidence: 89%

Bimatoprost Increases Mechanosensitivity of Trigeminal Ganglion Neurons Innervating the Inner Walls of Rat Anterior Chambers via Activation of TRPA1

Ling

Meng

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Citation: Ling Y, Hu Z, Meng Q, Fang P, Liu H. Bimatoprost increases mechanosensitivity of trigeminal ganglion neurons innervating the inner walls of rat anterior chambers via activation of TRPA1. Invest Ophthalmol Vis Sci. 2016;57:567-576. DOI:10.1167/ iovs.15-18108 PURPOSE. Our previous study found that some trigeminal ganglion (TG) nerve endings in the inner walls of rat anterior chambers were mechanosensitive, and transient receptor potential ankyrin 1 (TRPA1) was an essential mechanosensitive channel in the membrane. To address the effect of bimatoprost on the mechanosensitive TG nerve endings in the inner walls of rat anterior chambers, we investigated its effect on their cell bodies in vitro.METHODS. Rat TG neurons innervating the inner walls of the anterior chambers were labeled by anterior chamber injection of 1,1 0 -dilinoleyl-3,3,3 0 ,3 0 -tetramethylindocarbocyanine, 4-chlorobenzenesulfonate (FAST DiI). Calcium imaging and whole cell patch clamp were used on neuronal cell bodies to detect the activation effect of TRPA1 channels. Whole cell patch clamp was performed to record the currents induced by drugs and mechanical stimulation.Mechanical stimulation was applied to the neurons by buffer ejection. RESULTS. Bimatoprost mimicked the effect of TRPA1 agonists, allyl isothiocyanate (AITC), and (R)-(þ)- CONCLUSIONS.Our results indicate that bimatoprost is a novel agonist of TRPA1, and it can enhance mechanosensitivity of TG nerve endings in the inner walls of anterior eye chambers via TRPA1 activation in rats.Keywords: intraocular pressure, mechanosensitive channel, trigeminal ganglion, transient receptor potential ankyrin 1, bimatoprost L atanoprost, travoprost, and bimatoprost are three efficacious prostanoid analogs used for the treatment of glaucoma. Their effects on aqueous humor outflow are similar. Despite the well-established efficacy of these drugs on intraocular pressure (IOP), the mechanism underlying the hypotensive effect is not fully understood. Latanoprost and travoprost are prodrugs of prostaglandin (PG) FP receptor agonists. A well-studied mechanism for their enhancement of aqueous outflow is the regulation of matrix metalloproteinases and remodeling of extracellular matrix via FP receptor activation.1 However, experimental and clinical evidence suggests that bimatoprost and prostanoid FP receptor agonists stimulate different receptor populations.2-4 Studies performed on a wide array of receptors, ion channels, and transporters have demonstrated that bimatoprost does not meaningfully interact with adrenergic, cholinergic, cannabinoid, dopaminergic, or any of the known prostaglandin receptors, indicating that these receptors are not involved in the mediation of bimatoprost-induced responses.2-4 It has been shown that 17-phenyl prostaglandin F2alpha (PGF2a), an acid hydrolysis product of bimatoprost, is found in the aqueous humor after topical application of bimatoprost in humans.5 Based on the finding that 17-phenyl PGF2a is a potent FP prostanoid receptor agonist, it was proposed t...

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Multiple Cation Channels Mediate Increases in Intracellular Calcium Induced by the Volatile Irritant, Trans-2-Pentenal in Rat Trigeminal Neurons

Cited by 8 publications

References 34 publications

Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors

Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors

Chemical Compositional Changes in Over-Oxidized Fish Oils

Bimatoprost Increases Mechanosensitivity of Trigeminal Ganglion Neurons Innervating the Inner Walls of Rat Anterior Chambers via Activation of TRPA1

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