Suppression of ASIC activity by the activation of A1 adenosine receptors in rat primary sensory neurons

Wei, Shuang; Hao, Jia‐Wei; Qiao, Wen‐Long; Li, Qing; Liu, Tingting; Qiu, Chun‐Yu; Hu, Wang‐Ping

doi:10.1016/j.neuropharm.2021.108924

Cited by 3 publications

(2 citation statements)

References 56 publications

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“…The present data showed that CPA-induced inhibition of ATP currents was lack after the DRG neurons were intracellularly dialyzed with the G i/o protein inhibitor PTX, the adenylate cyclase activator forskolin, or the cAMP analog 8Br-cAMP, indicating involvement of G i/o -proteins and intracellular cAMP signaling. Our recent study has shown that CPA suppresses acid sensing ion channels via A1 adenosine receptors and intracellular G i/o -proteins and cAMP signaling cascades in rat DRG neurons [50]. Consistent with current results, previous studies have shown that ATP-induced currents are modulated by intracellular cAMP-PKA signaling [51,52].…”

Section: Discussionsupporting

confidence: 91%

A1 Adenosine Receptor Activation Inhibits P2X3 Receptor–Mediated ATP Currents in Rat Dorsal Root Ganglion Neurons

Hao

Qiao

et al. 2022

Mol Neurobiol

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Purinergic signaling is involved in multiple pain processes. P2X3 receptor is a key target in pain therapeutics, while A1 adenosine receptor signaling plays a role in analgesia. However, it remains unclear whether there is a link between them in pain. The present results showed that the A1 adenosine receptor agonist N 6 -cyclopentyladenosine (CPA) concentration-dependently suppressed P2X3 receptor-mediated and α,β-methylene-ATP (α,β-meATP)-evoked inward currents in rat dorsal root ganglion (DRG) neurons.CPA signi cantly decreased the maximal current response of α,β-meATP, as shown a downward shift of its concentration-response curve. The CPA-induced suppression was independent on the clampingvoltageof the membrane. Inhibition of ATP currents by CPA was completely prevented by the A1 adenosine receptor antagonist KW-3902, and disappeared after the intracellular dialysis of either the G i/oprotein inhibitor pertussis toxin, the adenylate cyclase activator forskolin, or the cAMP analog 8-Br-cAMP.Morover, CPA suppressed the membrane potential depolarization and action potential burst induced by α,β-meATP in DRG neurons. Finally, CPA relieved α,β-meATP-induced nociceptive behaviors in rats by activating peripheral A1 adenosine receptors in dose-dependent manner. These results indicated that CPA inhibited P2X3 receptor activity in rat primary sensory neurons by activating A1 adenosine receptors, G i/oproteins and intracellular cAMP signaling, revealing a novel peripheral mechanism underlying its analgesic effect.

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Section: Discussionsupporting

confidence: 91%

A1 Adenosine Receptor Activation Inhibits P2X3 Receptor–Mediated ATP Currents in Rat Dorsal Root Ganglion Neurons

Hao

Qiao

et al. 2022

Mol Neurobiol

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“…Nevertheless, the presence of ASIC proteins in the human petrosal ganglion neurons is reported here for the first time. In addition, there is ample functional, physiological, and pharmacological evidence for the presence of all ASIC subunits in rat and mouse spinal ganglia [38][39][40][41]. Thus, the present results suggest that the sensory neurons of the human petrosal ganglion can detect wide ranges of drops in pH, and therefore acidosis, since it expresses all ASIC subunits.…”

Section: Discussionsupporting

confidence: 52%

Acid-Sensing Ion Channels’ Immunoreactivity in Nerve Profiles and Glomus Cells of the Human Carotid Body

Martínez-Barbero,

García-Mesa,

Cobo

et al. 2023

IJMS

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The carotid body is a major peripheral chemoreceptor that senses changes in arterial blood oxygen, carbon dioxide, and pH, which is important for the regulation of breathing and cardiovascular function. The mechanisms by which the carotid body senses O2 and CO2 are well known; conversely, the mechanisms by which it senses pH variations are almost unknown. Here, we used immunohistochemistry to investigate how the human carotid body contributes to the detection of acidosis, analyzing whether it expresses acid-sensing ion channels (ASICs) and determining whether these channels are in the chemosensory glomic cells or in the afferent nerves. In ASIC1, ASIC2, and ASIC3, and to a much lesser extent ASIC4, immunoreactivity was detected in subpopulations of type I glomus cells, as well as in the nerves of the carotid body. In addition, immunoreactivity was found for all ASIC subunits in the neurons of the petrosal and superior cervical sympathetic ganglia, where afferent and efferent neurons are located, respectively, innervating the carotid body. This study reports for the first time the occurrence of ASIC proteins in the human carotid body, demonstrating that they are present in glomus chemosensory cells (ASIC1 < ASIC2 > ASIC3 > ASIC4) and nerves, presumably in both the afferent and efferent neurons supplying the organ. These results suggest that the detection of acidosis by the carotid body can be mediated via the ASIC ion channels present in the type I glomus cells or directly via sensory nerve fibers.

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Targeting sensory neuron GPCRs for peripheral neuropathic pain

Uniyal,

Tiwari,

Tsukamoto

et al. 2023

Trends in Pharmacological Sciences

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Suppression of ASIC activity by the activation of A1 adenosine receptors in rat primary sensory neurons

Cited by 3 publications

References 56 publications

A1 Adenosine Receptor Activation Inhibits P2X3 Receptor–Mediated ATP Currents in Rat Dorsal Root Ganglion Neurons

A1 Adenosine Receptor Activation Inhibits P2X3 Receptor–Mediated ATP Currents in Rat Dorsal Root Ganglion Neurons

Acid-Sensing Ion Channels’ Immunoreactivity in Nerve Profiles and Glomus Cells of the Human Carotid Body

Targeting sensory neuron GPCRs for peripheral neuropathic pain

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