Activation of Mechanosensitive Transient Receptor Potential/Piezo Channels in Odontoblasts Generates Action Potentials in Cocultured Isolectin B 4 –negative Medium-sized Trigeminal Ganglion Neurons

Sato, Masaki; Ogura, Kazuhiro; Kimura, Masashi; Nishi, Koichi; Ando, Masashi; Tazaki, Masakazu; Shibukawa, Yoshiyuki

doi:10.1016/j.joen.2018.02.020

Cited by 32 publications

(40 citation statements)

References 48 publications

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“…In addition, purinergic receptor (P2X3/P2Y1/P2Y12) antagonists attenuate the increase in intracellular Ca 2+ in neurons, but not in the mechanically-stimulated odontoblasts, suggesting that neuronal purinergic receptors are activated by the ATP released by the odontoblasts and its metabolite ADP [27]. Using the same odontoblast/TG neuron co-culture preparation, Sato et al showed that mechanical stimulation of odontoblast-like cells evokes inward currents in medium-sized neuron-like cells that express NF-200 immunoreactivity (a marker of myelinated neurons), but not IB4 [223]. Medium-sized TG neurons (A-δ) have been implicated in sharp pain associated with dentine hypersensitivity [20,34,38].…”

Section: Involvement Of Trp Channels In the Transduction Of Dentalmentioning

confidence: 99%

“…Medium-sized TG neurons (A-δ) have been implicated in sharp pain associated with dentine hypersensitivity [20,34,38]. Sato et al also observed that the mechanical stimulation-induced currents were attenuated by application of a cocktail of TRPV1, TRPV2, TRPV4 and TRPA1 channel antagonists, suggesting involvement of these channels in transduction of mechanical stimuli applied to the odontoblast-like cells [223]. Furthermore, application of a P2X3 antagonist attenuated the induced currents in the neuron-like cells, suggesting activation of P2X3 on the neurons by ATP released from mechanically-stimulated odontoblasts [223].…”

Section: Involvement Of Trp Channels In the Transduction Of Dentalmentioning

confidence: 99%

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The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

Hossain

Bakri

Yahya

et al. 2019

IJMS

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Dental pain is a common health problem that negatively impacts the activities of daily living. Dentine hypersensitivity and pulpitis-associated pain are among the most common types of dental pain. Patients with these conditions feel pain upon exposure of the affected tooth to various external stimuli. However, the molecular mechanisms underlying dental pain, especially the transduction of external stimuli to electrical signals in the nerve, remain unclear. Numerous ion channels and receptors localized in the dental primary afferent neurons (DPAs) and odontoblasts have been implicated in the transduction of dental pain, and functional expression of various polymodal transient receptor potential (TRP) channels has been detected in DPAs and odontoblasts. External stimuli-induced dentinal tubular fluid movement can activate TRP channels on DPAs and odontoblasts. The odontoblasts can in turn activate the DPAs by paracrine signaling through ATP and glutamate release. In pulpitis, inflammatory mediators may sensitize the DPAs. They could also induce post-translational modifications of TRP channels, increase trafficking of these channels to nerve terminals, and increase the sensitivity of these channels to stimuli. Additionally, in caries-induced pulpitis, bacterial products can directly activate TRP channels on DPAs. In this review, we provide an overview of the TRP channels expressed in the various tooth structures, and we discuss their involvement in the development of dental pain.

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Section: Involvement Of Trp Channels In the Transduction Of Dentalmentioning

confidence: 99%

Section: Involvement Of Trp Channels In the Transduction Of Dentalmentioning

confidence: 99%

The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

Hossain

Bakri

Yahya

et al. 2019

IJMS

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“…To verify the role of these low-threshold mechanoreceptors in the odontoblast cells, other studies have been performed to verify PIEZO expression in odontoblast cells. An electrophysiological study with odontoblast cells co-cultured with IB4-negative medium-sized TG neurons elucidated the role of odontoblasts as mechanosensitive transducer cells [120]. Inward currents were detected from TG neurons when mechanical stimulation was applied to neighboring odontoblast cells.…”

Section: Mechanosensitive Channels In Tooth Painmentioning

confidence: 99%

“…PIEZO2 proteins were detected selectively in odontoblastic processes that protrude into dentinal tubules. In another study, however, odontoblastic response to mechanical stimulation was inhibited by a specific antagonist of PIEZO1 [120]. These controversial results indicate the essential role of PIEZO ion channels in dental sensory systems as putative mechanosensors but also suggest that more research is needed to comprehensively understand complex dental mechanosensing systems.…”

Section: Mechanosensitive Channels In Tooth Painmentioning

confidence: 99%

Ion Channels Involved in Tooth Pain

Lee

Kim

et al. 2019

IJMS

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The tooth has an unusual sensory system that converts external stimuli predominantly into pain, yet its sensory afferents in teeth demonstrate cytochemical properties of non-nociceptive neurons. This review summarizes the recent knowledge underlying this paradoxical nociception, with a focus on the ion channels involved in tooth pain. The expression of temperature-sensitive ion channels has been extensively investigated because thermal stimulation often evokes tooth pain. However, temperature-sensitive ion channels cannot explain the sudden intense tooth pain evoked by innocuous temperatures or light air puffs, leading to the hydrodynamic theory emphasizing the microfluidic movement within the dentinal tubules for detection by mechanosensitive ion channels. Several mechanosensitive ion channels expressed in dental sensory systems have been suggested as key players in the hydrodynamic theory, and TRPM7, which is abundant in the odontoblasts, and recently discovered PIEZO receptors are promising candidates. Several ligand-gated ion channels and voltage-gated ion channels expressed in dental primary afferent neurons have been discussed in relation to their potential contribution to tooth pain. In addition, in recent years, there has been growing interest in the potential sensory role of odontoblasts; thus, the expression of ion channels in odontoblasts and their potential relation to tooth pain is also reviewed.

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“…The stimuli to the dentin surface induce [Ca 2+ ] i increases via mechanosensitive TRP channels ( Sato et al, 2015 ; Shibukawa et al, 2015 ), and Piezo channels ( Sato et al, 2018 ) in odontoblasts. The [Ca 2+ ] i increases elicit the release of ATP from pannexin-1 channels ( Sato et al, 2015 ; Shibukawa et al, 2015 ) in odontoblasts.…”

Section: Discussionmentioning

confidence: 99%

High pH-Sensitive Store-Operated Ca2+ Entry Mediated by Ca2+ Release-Activated Ca2+ Channels in Rat Odontoblasts

et al. 2018

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Odontoblasts play a crucial role in dentin formation and sensory transduction following the application of stimuli to the dentin surface. Various exogenous and endogenous stimuli elicit an increase in the intracellular free calcium concentration ([Ca2+]i) in odontoblasts, which is mediated by Ca2+ release from intracellular Ca2+ stores and/or Ca2+ influx from the extracellular medium. In a previous study, we demonstrated that the depletion of Ca2+ stores in odontoblasts activated store-operated Ca2+ entry (SOCE), a Ca2+ influx pathway. However, the precise biophysical and pharmacological properties of SOCE in odontoblasts have remained unclear. In the present study, we examined the functional expression and pharmacological properties of Ca2+ release-activated Ca2+ (CRAC) channels that mediate SOCE and evaluated the alkali sensitivity of SOCE in rat odontoblasts. In the absence of extracellular Ca2+, treatment with thapsigargin (TG), a sarco/endoplasmic reticulum Ca2+-ATPase inhibitor, induced an increase in [Ca2+]i. After [Ca2+]i returned to near-resting levels, the subsequent application of 2.5 mM extracellular Ca2+ resulted in an increase in [Ca2+]i which is a typical of SOCE activation. Additionally, application of 2-methylthioadenosine diphosphate trisodium salt (2-MeSADP), a P2Y1,12,13 receptor agonist, or carbachol (CCh), a muscarinic cholinergic receptor agonist, in the absence of extracellular Ca2+, induced a transient increase in [Ca2+]i. The subsequent addition of extracellular Ca2+ resulted in significantly higher [Ca2+]i in 2-MeSADP- or CCh-treated odontoblasts than in untreated cells. SOCE, that is activated by addition of extracellular Ca2+ in the TG pretreated odontoblasts was then suppressed by Synta66, BTP2, or lanthanum, which are CRAC channel inhibitors. Treatment with an alkaline solution enhanced SOCE, while treatment with HC030031, a TRPA1 channel antagonist, inhibited it. The amplitude of SOCE at pH 9 in the presence of HC030031 was higher than that at pH 7.4 in the absence of HC030031. These findings indicate that CRAC channel-mediated alkali-sensitive SOCE occurs in odontoblasts. SOCE is mediated by P2Y and muscarinic-cholinergic receptors, which are activated by endogenous ligands in odontoblasts.

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Activation of Mechanosensitive Transient Receptor Potential/Piezo Channels in Odontoblasts Generates Action Potentials in Cocultured Isolectin B 4 –negative Medium-sized Trigeminal Ganglion Neurons

Cited by 32 publications

References 48 publications

The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

Ion Channels Involved in Tooth Pain

High pH-Sensitive Store-Operated Ca2+ Entry Mediated by Ca2+ Release-Activated Ca2+ Channels in Rat Odontoblasts

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