ライフサイエンスコーパス: ASIC

1 ASIC currents triggered by pH 5 disappeared in the VLM n

2 ASIC proteins can form both homotrimeric and heterotrime

3 ASIC subunits contain intracellular N and C termini, two

4 ASIC-3(+/+) FLS showed enhanced cell death when exposed

5 ASICs (acid-sensing ion channels) are proton-gated chann

6 ASICs are formed as homotrimers or heterotrimers of seve

7 ASICs are involved in fear and anxiety, learning, neurod

8 ASICs are localized to cell bodies and dendrites, includ

9 ASICs have been implicated in several neuronal disorders

10 ASICs represent a widespread communication system with u

11 Acid-sensing ion channel-1 (ASIC-1) is a proton-gated ion channel implicated in noci

12 ional homomeric Acid-sensing ion channel-1a (ASIC-1as) that can be activated by protons (coreleased w

13 on nociceptors, acid-sensing ion channel 3 (ASIC-3) is activated by decreases in pH and plays a sign

14 ate that acid-sensing ion channel subtype 3 (ASIC(3)) in thin-fibre muscle afferents contributes to t

15 ions of ASIC1 alone or combined with other 4 ASIC genes are significantly correlated with poor patien

16 We also found that accelerating ASIC desensitization by anion substitution can induce de

17 ecently showed that decreases in pH activate ASIC-3 located on fibroblast-like synoviocytes (FLS), wh

18 found in the inflammatory soup that activate ASICs.

19 t pH 6.7, which is acidic enough to activate ASICs in vivo.

20 The protons activated ASICs in lateral amygdala pyramidal neurons, generating

21 FPI induces cerebral acidosis that activates ASIC channels and contributes to secondary injury in TBI

22 modulate synaptic transmission by activating ASIC-1as at the calyx of Held-MNTB synapse.SIGNIFICANCE

23 In addition, ASIC(3)-like current responses to pH 6.7 are observed in

24 However, not all ASICs are proton-sensitive: ASIC2a is activated by acid,

25 of ligands that modulate the function of all ASICs as well as activate ASIC3 at physiological pH.

26 Although ASICs are also expressed by immune cells, this expressio

27 ated the pressor response to lactic acid, an ASIC agonist, but did not attenuate the pressor response

28 channels, and captures the open state of an ASIC.

29 90% (9/10) of the labelled neurons showed an ASIC-like response to pH 7.0, suggesting that ASIC curre

30 ation and pain parameters in ASIC-3(-/-) and ASIC-3(+/+) mice were assessed.

31 r of sucrose has been discussed from ASV and ASIC parameters, as these parameters, which are sensitiv

32 r of sucrose has been discussed from ASV and ASIC parameters.

33 ENaC and ASIC function is regulated by several serine proteases.

34 ease because of inhibitory actions on Kv and ASIC channels, respectively.

35 which included an antimicrobial peptide and ASIC channel.

36 nt with differential expression of TRPV1 and ASIC channels.

37 They also indicate that protons and ASICs are a neurotransmitter/receptor pair critical for

38 Moreover, both protons and ASICs were required for synaptic plasticity in lateral a

39 vator of ASICs is extracellular protons, and ASICs have been demonstrated to play a significant role

40 nsmembrane helices in both P2X receptors and ASICs, and the method will allow precise optical control

41 majority of current responses to pH 6.7 are ASIC(3)-like in DRG neurons with nerve endings in the hi

42 neurons innervating the hindlimb muscles are ASIC(3)-like.

43 ammalian neuronal DEG/ENaC channels known as ASICs (acid-sensing ion channels) mediate sensory percep

44 hat femoral artery occlusion mainly augments ASIC(3) expression within DRG neurons projecting C-fibre

45 lar domain that are highly conserved between ASIC isoforms.

46 eptide psalmotoxin, which profoundly blocked ASIC currents in the hippocampal neurons, had no effect

47 blocked ASICs, whereas the high dose blocked ASICs and impulse conduction in muscle afferents.

48 used in our experiments selectively blocked ASICs, whereas the high dose blocked ASICs and impulse c

49 e in NP cells which is inhibited by blocking ASIC-3 activity, suggesting that this may be a useful th

50 tes carotid body chemoreceptors through both ASIC and TASK channels.

51 n the lung and airways, which activated both ASICs and TRPV1 expressed in these sensory nerves.

52 amplitude of DRG neuron response induced by ASIC(3) stimulation is larger in occluded rats than that

53 the involvement of acid-sensing ion channel (ASIC) -3 in the response.

54 Acid-sensing ion channel (ASIC) 1a and ASIC2a are acid-sensing ion channels in cen

55 by blockade of the acid sensing ion channel (ASIC) 3.

56 lular pH, leads to acid-sensing ion channel (ASIC) activation and reflexively increases mean arterial

57 s inhibited by the acid-sensing ion channel (ASIC) blocker amiloride, absent in Na+-free bathing solu

58 Other types of acid-sensing ion channel (ASIC) channels were intact to sevanol application, excep

59 ive members of the acid-sensing ion channel (ASIC) family.

60 8 gene (Gpr68) and acid-sensing ion channel (ASIC) genes Asic1, Asic2, and Asic4 in anterior pituitar

61 at a member of the acid-sensing ion channel (ASIC) subfamily of the DEG/ENaC superfamily is an import

62 Acid-sensing ion channel (ASIC) subunits associate to form homomeric or heteromeri

63 ixture of ENaC and acid-sensing ion channel (ASIC) subunits.

64 proton-activated acid-sensing ion channels (ASIC).

65 Acid-sensing ion channels (ASICs) act as neurotransmitter receptors by responding t

66 Neuronal acid-sensing ion channels (ASICs) act as sensors for extracellular protons, but the

67 homology between acid-sensing ion channels (ASICs) and epithelial sodium channel (ENaCs), these chan

68 Acid-sensing ion channels (ASICs) are a class of trimeric cation-selective ion chan

69 The acid-sensing ion channels (ASICs) are a family of ion channels expressed throughout

70 Acid-sensing ion channels (ASICs) are a group of trimeric cation permeable channels

71 Acid sensing ion channels (ASICs) are cation-selective membrane channels activated

72 Acid-sensing ion channels (ASICs) are cation-selective proton-gated channels expres

73 Acid-sensing ion channels (ASICs) are expressed in skeletal muscle afferents, in wh

74 Acid-sensing ion channels (ASICs) are highly expressed in muscle afferents where th

75 Acid-sensing ion channels (ASICs) are neuronal Na(+)-selective channels that are tr

76 Acid-sensing ion channels (ASICs) are neuronal non-voltage-gated cation channels th

77 Acid-sensing ion channels (ASICs) are neuronal proton-gated cation channels associa

78 Acid-sensing ion channels (ASICs) are neuronal receptors for extracellular protons.

79 Acid-sensing ion channels (ASICs) are neuronal sodium-selective channels activated

80 Acid-sensing ion channels (ASICs) are neuronal, voltage-independent Na(+) channels

81 Acid-sensing ion channels (ASICs) are proton-activated channels expressed in neuron

82 Acid-sensing ion channels (ASICs) are proton-activated Na(+) channels expressed in

83 The acid-sensing ion channels (ASICs) are proton-gated cation channels activated when e

84 Acid-sensing ion channels (ASICs) are proton-gated cation channels that contribute

85 Acid-sensing ion channels (ASICs) are proton-gated cation channels that play import

86 Acid-sensing ion channels (ASICs) are proton-gated cation-selective channels expres

87 Acid-sensing ion channels (ASICs) are proton-gated members of the epithelial sodium

88 Acid-sensing ion channels (ASICs) are proton-gated Na(+) channels that are expresse

89 The acid-sensing ion channels (ASICs) are proton-gated, voltage-insensitive cation chan

90 Acid-sensing ion channels (ASICs) are sodium channels gated by extracellular proton

91 Acid-sensing ion channels (ASICs) are trimeric cation channels that undergo activat

92 Acid-sensing ion channels (ASICs) are trimeric cation-selective ion channels activa

93 Acid-sensing ion channels (ASICs) are trimeric cation-selective proton-gated ion ch

94 Acid-sensing ion channels (ASICs) are voltage-independent Na(+) channels activated

95 Acid-sensing ion channels (ASICs) are voltage-independent, amiloride-sensitive chan

96 Acid-sensing ion channels (ASICs) are widely expressed proton-gated Na(+) channels

97 ation depended on acid-sensing ion channels (ASICs) because treatment of sensory afferents in vitro w

98 Acid-sensing ion channels (ASICs) constitute a family of neuron-specific voltage-in

99 atory conditions, acid-sensing ion channels (ASICs) contribute to the pathology of MS.

100 via activation of acid-sensing ion channels (ASICs) could have therapeutic application in a host of n

101 vel and conserved acid-sensing ion channels (ASICs) DEL-7 and DEL-3 as NSM-enriched channels required

102 Acid-sensing ion channels (ASICs) detect extracellular protons produced during infl

103 Acid-sensing ion channels (ASICs) form both homotrimeric and heterotrimeric ion cha

104 he exact roles of acid-sensing ion channels (ASICs) in synaptic plasticity remain elusive.

105 The role of acid-sensing ion channels (ASICs) in the ventrolateral medulla (VLM) remains uncert

106 PV1) channels and acid-sensing ion channels (ASICs) is that their ion conduction pores dilate upon pr

107 Acid-sensing ion channels (ASICs) mediate chemosensitivity in nociceptive terminals

108 The acid-sensing ion channels (ASICs) open in response to extracellular acidic pH, and

109 Acid-sensing ion channels (ASICs) regulate synaptic activities and play important r

110 inhibit a set of acid-sensing ion channels (ASICs) to relieve pain.

111 Recently, acid-sensing ion channels (ASICs) were shown to act as neurotransmitter-gated ion c

112 pharmacology with acid-sensing ion channels (ASICs), a small family of excitatory neurotransmitter re

113 Acid-sensing ion channels (ASICs), expressed in thin muscle afferents, sense the de

114 s for protons are acid-sensing ion channels (ASICs), Na(+)- and Ca(2+)-permeable channels that are ac

115 ctive agonist for acid-sensing ion channels (ASICs), showing equal or greater efficacy compared with

116 osis can activate acid sensing ion channels (ASICs), we also studied ASIC1a(-/-) mice and found reduc

117 n and close human acid-sensing ion channels (ASICs), which are also trimers but are unrelated in sequ

118 lular protons and acid-sensing ion channels (ASICs).

119 sodium influx by acid-sensing ion channels (ASICs).

120 (Pyk2, ErbB1/2), pH-sensitive ion channels (ASICs, TASK, ROMK), and the bicarbonate-stimulated adeny

121 t other neurotransmitter-gated ion channels, ASICs show no desensitization during high-frequency stim

122 (an antagonist of acid-sensing ion channels, ASICs) and AMG8910 (a selective antagonist of the transi

123 tly the first crystal structure of a chicken ASIC was obtained.

124 out application specific integrated circuit (ASIC).

125 activation that is relevant to the classical ASIC currents, as previously described.

126 arent specific isentropic compressibilities, ASIC, were calculated from measured density, rho and spe

127 Consequently, ASICs are emerging as disease-modifying targets in MS.

128 Four genes encode six different ASIC subunits, however it is not yet clear which of the

129 ercentage of muscle afferents that displayed ASIC-like currents, the current amplitudes, and the pH d

130 f the physiologic consequences of disrupting ASIC genes in mice suggested that ASIC channels might mo

131 4-AP has differential actions on distinct ASICs, strongly inhibiting ASIC1a channels expressed in

132 tected by distinct mechanosensitive DEG/ENaC/ASIC channels, which trigger distinct cellular outputs l

133 sitive pathway requires a conserved DEG/ENaC/ASIC mechanoreceptor complex in the FLP neuron pair.

134 The most potent endogenous ASIC modulator known to date is the opioid neuropeptide

135 d in occluded rats, probably due to enhanced ASIC(3) expression in muscle sensory neurons.

136 ns as a neurotransmitter, and they establish ASICs as the postsynaptic receptor.

137 st 5 years several examples of proton-evoked ASIC excitatory postsynaptic currents have emerged.

138 We have examined ASICs from the ascidian Ciona intestinalis, a simple cho

139 n, whereas excitable secretory cells express ASIC genes and proteins.

140 Finally, ASIC-like currents were absent from triple-null mice lac

141 and show that protons are not essential for ASIC function.

142 ence of these currents in knock-out mice for ASIC-1a subunit (ASIC1a(-/-)) suggest that homomeric ASI

143 n the structure and on the pharmacophore for ASIC channel inhibition by mambalgins that could have th

144 is no known selective in vivo antagonist for ASICs.

145 Naked mole-rats, despite having functional ASICs, are insensitive to acid as a noxious stimulus and

146 During HFS, the lack of functional ASICs in synaptic transmission results in an enhanced sh

147 subunit (ASIC1a(-/-)) suggest that homomeric ASIC-1as are mediating these currents in MNTB neurons.

148 ignificant characteristic of these homomeric ASIC-1as is their permeability to Ca(2+) Activation of A

149 ocked to model structures of homomeric human ASIC-1 to generate potential interaction sites and predi

150 upon this work, homology models of the human ASICs were constructed and evaluated.

151 Together the data identify ASIC as a highly conserved channel distinctive of chorda

152 Therefore, we tested if ASICs within muscle afferents are altered in heart failu

153 We therefore imaged ASICs labeled with green and red fluorescent proteins on

154 P150 in association with protein kinase A in ASIC function.

155 presence of IL-1beta, which was abolished in ASIC-3(-/-) FLS.

156 Acidic pH resulted in an increase in ASIC-3 expression.

157 Inflammation and pain parameters in ASIC-3(-/-) and ASIC-3(+/+) mice were assessed.

158 Ca(2+) plays an important modulatory role in ASIC gating, competing with the ligand (H(+)) for its bi

159 This was supported by studies in ASIC-null mice: acid-evoked currents from ASIC3(-/-) car

160 necessity for the desensitization process in ASICs.

161 10-fold sodium/potassium selectivity in ASICs has long been attributed to a central constriction

162 thelial Na(+) (Deg/ENaC) channels, including ASIC and BLINaC.

163 conditions, these three opioids can increase ASIC channel activity, possibly giving rise to opioid-in

164 nder ischaemic conditions, and (3) increased ASIC(3) expression is largely observed in thin C-fibres

165 in A, an inhibitor of calcineurin, increased ASIC currents in Chinese hamster ovary cells and in cort

166 s up-regulated in chronic pain and increases ASIC-mediated neuronal death during acidosis.

167 in slices, a pH drop from 7.4 to 7.0 induced ASIC-like inward currents (blocked by 100 muM amiloride)

168 hodopsin-3 (Arch), proton transients induced ASIC currents in both neurons and HEK293T cells co-expre

169 ls to psalmotoxin-1, which potently inhibits ASIC-1 and not other members of the family.

170 ASIC3 antagonist APETx2 reversibly inhibits ASIC-like currents in naked mole-rat dorsal root ganglia

171 ctivated proton pump recruited a slow inward ASIC current, which required molecular proximity of the

172 in extracellular pH induces transient inward ASIC currents (IASICs) in postsynaptic MNTB neurons from

173 ave revealed that postsynaptically localized ASICs contribute to the excitatory postsynaptic current

174 We conclude that ASIC2a and -3 are the major ASIC subunits in cardiac dorsal root ganglia neurons and

175 Mammalian ASIC channels of the DEG/ENaC superfamily are gated by e

176 , endomorphin-1 (E-1) and -2 (E-2), modulate ASIC currents and the lactic acid-mediated pressor refle

177 ogenous neuropeptides that potently modulate ASICs.

178 a novel role for endomorphins in modulating ASIC function to effect lactic acid-mediated reflex incr

179 The results of anion substitution on native ASIC channels in hippocampal neurons mirrored those in h

180 1a homomers, ASIC1a/2a heteromers and native ASICs from sensory neurons to 1 ms acidification stimuli

181 idic transients, both recombinant and native ASICs show extremely rapid deactivation in outside-out p

182 and ASIC1a/2a heteromers, as well as native ASICs of sensory neurons, to follow trains of such brief

183 f these interactions are critical for normal ASIC function.

184 These results thus define the NSAID/ASIC interaction and pave the way for small-molecule dru

185 rize acid-induced current with activation of ASIC(3) in dorsal root ganglion (DRG) neurons of control

186 s their permeability to Ca(2+) Activation of ASIC-1a in MNTB neurons by exogenous H(+) induces an inc

187 For example, the amplitude of ASIC currents increases whereas desensitization decrease

188 m and application of amiloride, a blocker of ASIC channels, whereas the non-desensitizing current was

189 the development of new optimized blockers of ASIC channels.

190 has a profound effect on the contribution of ASIC and TRPV1 channels, therefore, altering the neurona

191 Inhibition or deletion of ASIC-1a leads to enhanced short-term depression, demonst

192 The rate of desensitization of ASIC-like currents activated by less acidic solutions (p

193 as an important site for the development of ASIC-targeting therapeutics.

194 ial firing was shaped by the distribution of ASIC and TRPV1 channels.

195 ndependent mechanisms mediate the effects of ASIC in vivo.

196 emistry was employed to examine existence of ASIC(3) expression in DRG neurons of thin-fibre afferent

197 Importantly, inhibition of ASIC-3 prevented the acidic pH induced proinflammatory a

198 We examined the modulation of ASIC currents by endomorphins in sensory neurons from ra

199 he other hand, the biophysical properties of ASIC-like currents were significantly different in a sub

200 Activation of ASICs in the medulla also triggered neuronal excitation.

201 medulla including the VLM, and activation of ASICs in the VLM contributes to central chemoreception.

202 studies define mechanisms for activation of ASICs, illuminate the basis for dynamic ion selectivity

203 The principal activator of ASICs is extracellular protons, and ASICs have been demo

204 ortical neurons, suggesting that activity of ASICs is inhibited by calcineurin-dependent dephosphoryl

205 e, a licensed and clinically safe blocker of ASICs, was equally neuroprotective in nerve explants and

206 es with that by amiloride, a pore blocker of ASICs.

207 lead compound for high-affinity blockers of ASICs.

208 A trimeric composition of ASICs has been suggested by crystallization.

209 IC subunits contribute to the composition of ASICs in cardiac afferents.

210 nduced a shift in the subunit composition of ASICs within muscle afferents, which significantly alter

211 Surprisingly, the deactivation of ASICs was steeply dependent on the pH, spanning nearly t

212 at diminazene accelerates desensitization of ASICs, which was, however, not explained mechanistically

213 ole protons play in mediating the effects of ASICs remains elusive.

214 y dipeptide in the structure and function of ASICs.

215 Functions of ASICs in mammals include nociception, mechanosensation,

216 t effects on the properties and functions of ASICs.

217 Despite the importance of ASICs in physiology, we know little about the mechanism

218 The molecular basis of NSAID inhibition of ASICs has remained unknown, hindering the exploration of

219 e aceturate is a small-molecule inhibitor of ASICs with a reported apparent affinity in the low micro

220 Anion modulation of ASICs provides new insight into channel gating and may p

221 The wide and varied expression patterns of ASICs, BK, and related K(+) channels suggest broad oppor

222 c developmental changes in the properties of ASICs in mouse cortical neurons.

223 t in understanding the in vivo regulation of ASICs, especially by endogenous neuropeptides that poten

224 results will help us understand the role of ASICs in exercise physiology and provide a molecular tar

225 ay help in understanding the precise role of ASICs in physiological and pathological conditions at di

226 nd to characterize function and structure of ASICs.

227 ests that activation of ASIC1a, a subtype of ASICs that is widely distributed in the brain, is necess

228 he mechanism and site of action of BigDyn on ASICs could thus enable the rational design of compounds

229 precise optical control of P2X receptors or ASICs in intact tissues.

230 Other ASIC channels also inhibited BK, although acidosis-depen

231 onal, proton-sensitive heteromers with other ASIC subunits.

232 d inactivation curves of ASIC3 but not other ASICs overlap in the presence of GMQ at pH 7.4, thereby

233 ity that GMQ may alter the function of other ASICs besides ASIC3.

234 us that was specific for ASIC1a versus other ASICs and for alpha-actinin-1 and -4.

235 ontributions of ASIC1a and ASIC2a to overall ASIC-mediated responses undergo distinct developmental c

236 Furthermore, the activation of postsynaptic ASIC-1as during high-frequency stimulation (HFS) of the

237 tter-gated ion channels because postsynaptic ASICs can be activated by the transient acidification of

238 ver, evidence for activation of postsynaptic ASICs during neurotransmission has not been established.

239 ypothesis is that activation of postsynaptic ASICs promotes depolarization, thereby augmenting N-meth

240 n acidic solutions significantly potentiated ASIC currents when compared to acidic solutions alone.

241 nhibit with the same pharmacological profile ASIC channels to exert strong analgesic effects in vivo.

242 likely to occur at the cleft and may provide ASICs with the ability to shape activity in response to

243 bstitution of this Trp in mouse ENaC and rat ASIC subunits decrease channel activity.

244 rements from a probe station and the readout ASIC was obtained.

245 A binding to AKAPs by Ht-31 peptide reduces ASIC currents in cortical neurons and Chinese hamster ov

246 Ibuprofen inhibits several ASIC subtypes, but certain ibuprofen derivatives show so

247 Despite enhanced disease severity, ASIC-3(-/-) mice did not develop mechanical hypersensiti

248 d that the ascidian genome contains a single ASIC gene that gives rise to two splice forms analogous

249 ated with application of rAPETx2, a specific ASIC(3) antagonist.

250 rents from wild-type (C57BL/6J) and specific ASIC(-/-) mice.

251 Surprisingly, ASIC-3(-/-) mice with CAIA demonstrated significantly in

252 Sustained ASIC current potentiation was also observed in neurons p

253 Additionally, the potentiation of sustained ASIC currents was greater in DRG neurons isolated from r

254 (oxycodone) would also potentiate sustained ASIC currents, which arise from ASIC3 channel isoforms.

255 Endomorphins potentiated sustained ASIC currents in both groups of dorsal root ganglion neu

256 wever, we previously reported that sustained ASIC currents in dorsal root ganglion (DRG) neurons were

257 ns resulted in potentiation of the sustained ASIC currents.

258 y, both domain-swapped and nondomain-swapped ASIC M2 conformations need to be considered.

259 ous animals have been identified that target ASICs with high specificity and potency.

260 ng therapies for drug addiction by targeting ASIC-dependent neurotransmission.

261 e snail species to identify toxins targeting ASICs.

262 We found that ASIC deactivation is extremely fast and, in contrast to

263 We found that ASIC-like currents in wild-type muscle afferents display

264 Therefore, we tested the hypothesis that ASIC channels might inhibit K(+) channel function by coe

265 ings are consistent with the hypothesis that ASIC-3 plays a protective role in the inflammatory arthr

266 microscopy and co-immunoprecipitation, that ASIC and ENaC subunits are capable of forming cross-clad

267 These data imply that ASIC down-regulation by calcineurin could play an import

268 hese observations raise the possibility that ASIC channels function as coincidence detectors for extr

269 l analysis of dye-filled neurons showed that ASIC-dependent chemosensitive cells (cells responding to

270 disrupting ASIC genes in mice suggested that ASIC channels might modulate neuronal function by mechan

271 SIC-like response to pH 7.0, suggesting that ASIC currents contribute to control of breathing.

272 The results provide the first evidence that ASICs may contribute to chemotransduction of low pH by c

273 nd further mutagenesis provide evidence that ASICs show such steeply agonist-dependent deactivation b

274 We find that ASICs deactivate surprisingly fast in response to such b

275 Here we test the hypothesis that ASICs are expressed in NTS neurons and contribute to int

276 Collectively, our data suggest that ASICs are highly expressed in the medulla including the

277 The ASIC-like current properties of the cardiac dorsal root

278 minazene and its binding site on ASIC1a, the ASIC subunit with the greatest importance in the central

279 To dissect the ASIC composition in muscle afferents, we used whole-cell

280 main is likely to remain constant during the ASIC gating cycle, whereas they may undergo relative mov

281 Further, the enhancement of the ASIC currents was resistant to pertussis toxin treatment

282 ant for the function of other members of the ASIC family.

283 ts, however it is not yet clear which of the ASIC subunits contribute to the composition of ASICs in

284 (Asic1a(-/-)) or by local treatment with the ASIC inhibitor, psalmotoxin.

285 These ASIC-1as contribute to the generation of postsynaptic cu

286 In contrast, these ASIC antagonists had only modest effects on the reflex i

287 ng and inactivating current mediated through ASICs, and a slow sustaining current via activation of T

288 Thus, ASICs have become bona fide neurotransmitter-gated ion c

289 ), and MMP-13 in joint tissue as compared to ASIC-3(+/+) mice.

290 ent proton-transporting optogenetic tools to ASICs to create two-component optogenetic constructs (TC

291 effect of all three opioids on the transient ASIC peak current was mixed (increase, decrease, no effe

292 The two ASIC subunits co-localized in medualla neurons.

293 Furthermore, pH reduction triggered typical ASIC-type currents in the medulla, including the VLM.

294 llular protons, but the mechanism underlying ASIC activation remains largely unknown.

295 Whereas ASICs are gated by protons and show a relatively low deg

296 he purpose of this study was to test whether ASIC-3-deficient mice with arthritis have altered inflam

297 e the conformational changes associated with ASIC activation and desensitization.

298 Moreover, the percentage of DRG neurons with ASIC(3)-like currents is greater after arterial occlusio

299 receptors that form a molecular complex with ASICs; the receptor on sensory neurons appears to be P2X

300 Within ASIC channel's large extracellular domain, we identified