ASIC3, a sensor of acidic and primary inflammatory pain Export

@article{citeulike:3440794, abstract = {Acid-sensing ion channels (ASICs) are cationic channels activated by extracellular acidosis that are expressed in both central and peripheral nervous systems. Although peripheral ASICs seem to be natural sensors of acidic pain (e.g., in inflammation, ischaemia, lesions or tumours), a direct demonstration is still lacking. We show that 60\% of rat cutaneous sensory neurons express ASIC3-like currents. Native as well as recombinant ASIC3 respond synergistically to three different inflammatory signals that are slight acidifications (pH 7.0), hypertonicity and arachidonic acid (AA). Moderate pH, alone or in combination with hypertonicity and AA, increases nociceptors excitability and produces pain suppressed by the toxin APETx2, a specific blocker of ASIC3. Both APETx2 and the in vivo knockdown of ASIC3 with a specific siRNA also have potent analgesic effects against primary inflammation-induced hyperalgesia in rat. Peripheral ASIC3 channels are thus essential sensors of acidic pain and integrators of molecular signals produced during inflammation where they contribute to primary hyperalgesia.}, author = {Deval, Emmanuel and No\"{e}l, Jacques and Lay, Nad\`{e}ge and Alloui, Abdelkrim and Diochot, Sylvie and Friend, Val\'{e}rie and Jodar, Martine and Lazdunski, Michel and Lingueglia, Eric}, citeulike-article-id = {3440794}, citeulike-linkout-0 = {http://www.nature.com/emboj/journal/vaop/ncurrent/abs/emboj2008213a.html}, day = {16}, journal = {EMBO Journal}, keywords = {acidic\_pain, asic3, inflammatroy\_pain}, month = {October}, posted-at = {2008-10-22 17:10:31}, priority = {3}, title = {ASIC3, a sensor of acidic and primary inflammatory pain}, url = {http://www.nature.com/emboj/journal/vaop/ncurrent/abs/emboj2008213a.html}, year = {2008} }

TY - JOUR ID - citeulike:3440794 L3 - citeulike-article-id:3440794 N2 - Acid-sensing ion channels (ASICs) are cationic channels activated by extracellular acidosis that are expressed in both central and peripheral nervous systems. Although peripheral ASICs seem to be natural sensors of acidic pain (e.g., in inflammation, ischaemia, lesions or tumours), a direct demonstration is still lacking. We show that 60% of rat cutaneous sensory neurons express ASIC3-like currents. Native as well as recombinant ASIC3 respond synergistically to three different inflammatory signals that are slight acidifications (pH 7.0), hypertonicity and arachidonic acid (AA). Moderate pH, alone or in combination with hypertonicity and AA, increases nociceptors excitability and produces pain suppressed by the toxin APETx2, a specific blocker of ASIC3. Both APETx2 and the in vivo knockdown of ASIC3 with a specific siRNA also have potent analgesic effects against primary inflammation-induced hyperalgesia in rat. Peripheral ASIC3 channels are thus essential sensors of acidic pain and integrators of molecular signals produced during inflammation where they contribute to primary hyperalgesia. JF - EMBO Journal TI - ASIC3, a sensor of acidic and primary inflammatory pain KW - acidic_pain KW - asic3 KW - inflammatroy_pain AU - Deval, Emmanuel AU - Noël, Jacques AU - Lay, Nadège AU - Alloui, Abdelkrim AU - Diochot, Sylvie AU - Friend, Valérie AU - Jodar, Martine AU - Lazdunski, Michel AU - Lingueglia, Eric PY - 2008/10/16/ UR - http://www.nature.com/emboj/journal/vaop/ncurrent/abs/emboj2008213a.html ER -