Best1Is a Gene Regulated by Nerve Injury and Required for Ca2+-Activated Cl−Current Expression in Axotomized Sensory Neurons

Boudes, Mathieu; Sar, Chamroeun; Menigoz, Aurelie; Hilaire, Cécile; Péquignot, Marie O.; Kozlenkov, Alexei; Marmorstein, Alan D.; Carroll, Patrick; Valmier, Jean; Scamps, Frédérique

doi:10.1523/jneurosci.1312-09.2009

Cited by 36 publications

(47 citation statements)

References 45 publications

(66 reference statements)

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“…Such a lack of coupling between CaCC and VGCC in nociceptors may be required in order to avoid a self-maintaining positive feedback loop, since if Ca 2+ influx through VGCC would significantly activate CaCC (and inhibit M channels), this would then cause depolarization and Ca 2+ influx through VGCC and further amplification of the cycle. Interestingly, Tmem16a is highly expressed in the majority of small DRG neurons but not in large neurons (32); moreover, it was recently suggested that Best1 underlies CaCC in large neurons (58). Taken together, these two observations may indicate that CaCC in different types of neurons consist of distinct molecular components.…”

Section: Discussionmentioning

confidence: 95%

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

Liu¹,

Linley²,

Du³

et al. 2010

J. Clin. Invest.

259

442

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Bradykinin (BK) is an inflammatory mediator and one of the most potent endogenous pain-inducing substances. When released at sites of tissue damage or inflammation, or applied exogenously, BK produces acute spontaneous pain and causes hyperalgesia (increased sensitivity to potentially painful stimuli). The mechanisms underlying spontaneous pain induced by BK are poorly understood. Here we report that in small nociceptive neurons from rat dorsal root ganglia, BK, acting through its B 2 receptors, PLC, and release of calcium from intracellular stores, robustly inhibits M-type K + channels and opens Ca 2+ -activated Cl -channels (CaCCs) encoded by Tmem16a (also known as Ano1). Summation of these two effects accounted for the depolarization and increase in AP firing induced by BK in DRG neurons. Local injection of inhibitors of CaCC and specific M-channel openers both strongly attenuated the nociceptive effect of local injections of BK in rats. These results provide a framework for understanding spontaneous inflammatory pain and may suggest new drug targets for treatment of such pain.

show abstract

Section: Discussionmentioning

confidence: 95%

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

Liu¹,

Linley²,

Du³

et al. 2010

J. Clin. Invest.

259

442

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show abstract

“…2003; Boudes et al . 2009; Boudes & Scamps, 2012), in small neurons such coupling is rarely seen (Andre et al . 2003; Liu et al .…”

Section: Coupling Between Ano1 and Endoplasmic Reticulum; Is This A Gmentioning

confidence: 99%

Activation of Ca²⁺‐activated Cl⁻ channel ANO1 by localized Ca²⁺ signals

Jin

Shah

et al. 2014

The Journal of Physiology

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Ca2+‐activated chloride channels (CaCCs) regulate numerous physiological processes including epithelial transport, smooth muscle contraction and sensory processing. Anoctamin‐1 (ANO1, TMEM16A) is a principal CaCC subunit in many cell types, yet our understanding of the mechanisms of ANO1 activation and regulation are only beginning to emerge. Ca2+ sensitivity of ANO1 is rather low and at negative membrane potentials the channel requires several micromoles of intracellular Ca2+ for activation. However, global Ca2+ levels in cells rarely reach such levels and, therefore, there must be mechanisms that focus intracellular Ca2+ transients towards the ANO1 channels. Recent findings indeed indicate that ANO1 channels often co‐localize with sources of intracellular Ca2+ signals. Interestingly, it appears that in many cell types ANO1 is particularly tightly coupled to the Ca2+ release sites of the intracellular Ca2+ stores. Such preferential coupling may represent a general mechanism of ANO1 activation in native tissues.

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“…Best1 has been shown to be up-regulated by nerve injury and required for CaCC expression in axotomized sensory neurons. However, there is no significant difference in CaCC in sensory neurons from Best1 knockout mice compared with wildtype mice, prompting the suggestion that Best3 may have a compensatory effect (Boudes et al, 2009). In the same study, no change of mRNAs for TMEM16A and TMEM16B was found in the DRGs after axotomy.…”

Section: Sensory Neuronsmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. LXXXV: Calcium-Activated Chloride Channels

Huang¹,

Wong²,

Jan³

2011

Pharmacol Rev

159

139

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Best1Is a Gene Regulated by Nerve Injury and Required for Ca²⁺-Activated Cl⁻Current Expression in Axotomized Sensory Neurons

Cited by 36 publications

References 45 publications

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

Activation of Ca²⁺‐activated Cl⁻ channel ANO1 by localized Ca²⁺ signals

International Union of Basic and Clinical Pharmacology. LXXXV: Calcium-Activated Chloride Channels

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Best1Is a Gene Regulated by Nerve Injury and Required for Ca2+-Activated Cl−Current Expression in Axotomized Sensory Neurons

Cited by 36 publications

References 45 publications

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

Activation of Ca2+‐activated Cl− channel ANO1 by localized Ca2+ signals

International Union of Basic and Clinical Pharmacology. LXXXV: Calcium-Activated Chloride Channels

Contact Info

Product

Resources

About

Best1Is a Gene Regulated by Nerve Injury and Required for Ca²⁺-Activated Cl⁻Current Expression in Axotomized Sensory Neurons

Activation of Ca²⁺‐activated Cl⁻ channel ANO1 by localized Ca²⁺ signals