ライフサイエンスコーパス: SK channel

1 e-related modulation of the apamin-sensitive SK channel.

2 rate set by the deactivation kinetics of the SK channel.

3 ed by Ca(2+) -dependent activation of IK and SK channels.

4 re unaffected by inhibitors of TRPV4, IK and SK channels.

5 and a decrease in the functional activity of SK channels.

6 did not affect currents through TRPV4, IK or SK channels.

7 (+) cells that were inhibited by blockers of SK channels.

8 Rac1 in synaptic compartments and modulating SK channels.

9 2+) sensing by CaM and mechanical opening of SK channels.

10 pharmacological targets of riluzole include SK channels.

11 ensory neurons possibly via Ca(2+)-activated SK channels.

12 detect binding events between the apamin and SK channels.

13 artially due to blockade of apamin-sensitive SK channels.

14 ligand to study the activation properties of SK channels.

15 a selective antagonist of calcium-activated SK channels.

16 es of the interaction between calmodulin and SK channels.

17 elevates intracellular Ca(2+) and activates SK channels.

18 hrough the endoplasmic reticulum to activate SK channels.

19 actions were also inhibited by activation of SK channels.

20 on conductance that coupled to activation of SK channels.

21 of Ca(2+)-activated small-conductance K(+) (SK) channels.

22 he small conductance, Ca(2+)-activated K(+) (SK) channels.

23 and small conductance Ca(2+)-activated K(+) (SK) channels.

24 g those associated with 'small-conductance' (SK) channels.

25 by small-conductance Ca(2+)-activated K(+) (SK) channels.

26 all conductance calcium-activated potassium (SK) channels.

27 all-conductance calcium-activated potassium (SK) channels.

28 mall-conductance Ca(2+)-activated potassium (SKs) channels.

29 rather than a specific molecular coupling to SK channels accounts for the reduced SFA of Ca(v)1.3(-/-

30 we also find that KCNQ and apamin-sensitive SK channels act synergistically to regulate firing rate

31 In contrast, SK channels activated by APs at the soma of these neuron

32 Additionally, SK channels activated by Tb(3+) demonstrate a remarkably

33 ice, we investigated the role of Ca(v)1.3 on SK channel activation and how this functional coupling a

34 n response to increases in EC calcium and IK/SK channel activation and suggest that EC Kir channels c

35 examined purinergic receptor (P2Y) mediated SK channel activation as a mechanism for purinergic rela

36 action potentials (APs), and compare this to SK channel activation at the soma.

37 As a result SK channel activation by backpropagating APs gated STDP

38 This A(1)-mediated, prolonged SK channel activation has not been described previously.

39 hen K(V)7/M channel activity is compromised, SK channel activation significantly and uniquely reduces

40 pe) Ca(2+) channels as the Ca(2+) source for SK channel activation.

41 SK-channel activation and the subsequent reduction in Ca

42 p4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.

43 An SK channel activator (SKA-31) decreased contractions dur

44 litude of mAHP of NAcS MSNs were reversed by SK channel activator 1-EBIO and mimicked by the SK chann

45 ment of the patient with chlorzoxazone, a BK/SK channel activator, partially improved motor function,

46 agment, itself a target for drugs modulating SK channel activities, plays a unique role in coupling C

47 ortantly, we demonstrate that Rac1 modulates SK channel activity and firing patterns of Purkinje cell

48 The mechanism by which p75 regulates SK channel activity appears to involve its ability to ac

49 Ca) channels and identify distinct roles for SK channel activity in regulating calcium- versus sodium

50 To determine if SK channel activity was indeed eliminated, seconds-long

51 e rescued by pharmacological augmentation of SK channel activity.

52 usive and SNX increases EPSPs independent of SK channel activity.

53 esicle release, and upregulated postsynaptic SK channel activity.

54 ponses in CA1 neurons by decreasing synaptic SK channel activity.

55 mall conductance Ca(2+)-activated potassium (SK) channel activity in Purkinje cells from p75(-/-) mic

56 ceptor potential vanilloid 4) channel and IK/SK channel agonists were highly attenuated by Kir channe

57 SK channels allow efflux of potassium ions when intracel

58 nism where M(1) receptor activation inhibits SK channels, allowing enhanced NMDAR activity and leadin

59 es that link Ca(2+) influx through NMDARs to SK channels and Ca(2+) influx through R-type Ca(2+) chan

60 vated K(+) channels (i.e., small-conductance SK channels and large-conductance BK channels).

61 enous SK currents, reducing coupling between SK channels and NMDA receptors (NMDARs) and increasing p

62 improves motor neuron function by acting on SK channels and suggest that SK channels may be importan

63 s the molecular and functional properties of SK channels and their physiological roles in central neu

64 all-conductance calcium-activated potassium (SK) channel and CB1 cannabinoid receptor activation.

65 rmediate- and small-conductance K(+) (IK and SK) channels and endothelial nitric oxide synthase (eNOS

66 of small-conductance Ca(2+)-activated K(+) (SK) channels and reveals an important role for both SK2

67 Small conductance Ca(2+)-activated K(+) (SK) channels and voltage-gated A-type Kv4 channels shape

68 ized, CF-EPSPs mainly activate T-type VGCCs, SK channels, and A-type VGKCs that limit the transient V

69 m afterhyperpolarization (mAHP), mediated by SK channels, and SK3 protein levels in the NAcS decrease

70 c signal integration, via over-activation of SK channels, and synapse plasticity, phenotypes rescued

71 cium-dependent small conductance potassium ('SK') channels, and longer-lasting and voltage-dependent

72 cium-dependent small conductance potassium ('SK') channels, and longer-lasting and voltage-dependent

73 s, small conductance Ca-activated potassium (SK) channels, and NMDA receptors.

74 rototypes for arteries with predominantly IK/SK channel- and eNOS-dependent vasodilatation, respectiv

75 and in vivo Using local applications of the SK channel antagonist apamin in vitro, we show that bloc

76 Injections of the specific SK channel antagonist apamin into PLC increased Fos expr

77 SK channels are a potential pharmacological target for m

78 ing somatic excitability in central neurons, SK channels are also expressed in the postsynaptic membr

79 ore, we also show that KCNQ channels but not SK channels are downstream effectors of serotonin modula

80 lockers, we provide evidence that functional SK channels are expressed in the somata and proximal den

81 studies demonstrate that in MNNs, NMDARs and SK channels are functionally coupled, forming a local ne

82 e receptors are Ca(2+)-impermeable, and thus SK channels are not efficiently activated by synaptic ac

83 ced the same result, suggesting that somatic SK channels are not tightly colocalized with their calci

84 Because SK channels are predominantly expressed in atrial myocyt

85 SK channels are predominantly expressed in the atria as

86 SK channels are proposed to be assembled as tetramers si

87 ith this, mRNA levels for the SK3 subunit of SK channels are significantly higher in ventral CA1 pyra

88 SK channels are stable macromolecular complexes of the i

89 We found that SK channels are tonically activated and contribute to th

90 Interestingly, SK channels are transiently activated by calcium sparks

91 SK channels are voltage independent and their gating is

92 iac small conductance Ca(2+)-activated K(+) (SK) channels are activated solely by Ca(2+), but the SK

93 nd small conductance Ca(2+) -activated K(+) (SK) channels are critical synaptic and intrinsic mechani

94 nd small conductance Ca(2+) -activated K(+) (SK) channels are critical synaptic and intrinsic mechani

95 all conductance calcium-activated potassium (SK) channels are required for the slow inhibitory compon

96 ctance calcium-activated potassium channels (SK channels) are present in spines and can be activated

97 -conductance Ca(2+)-activated K(+) channels (SK channels) are widely expressed throughout the central

98 We propose SK channels as a potential target for modulating SAN rat

99 ioning, and point toward a downregulation of SK channels as a potential underlying mechanism.

100 ramidal cell excitability and highlights BLA SK channels as promising targets for the treatment of an

101 While SK channels at the soma have long been known to contribu

102 that the conformation of the ID fragment in SK channels becomes readily identifiable in the presence

103 t under control conditions but present after SK channel block.

104 SK channel blockade abolished the mAHP and revealed an a

105 SK channel blockade caused a small depolarization in spi

106 bath application of apamin, suggesting that SK channel blockade likely increased excitability by a p

107 SK channel blockade slows repolarization and subsequent

108 SK channel blockade with apamin or UCL1684 increased the

109 hreshold depolarization was increased during SK channel blockade, indicating that depolarizing input

110 c plasticity is mimicked and occluded by the SK channel blocker apamin and is absent in Purkinje cell

111 nhibitory current by 56 +/- 12%, whereas the SK channel blocker apamin decreased the NECA-induced cur

112 Moreover, the SK channel blocker apamin enhanced the input-output func

113 channel activator 1-EBIO and mimicked by the SK channel blocker apamin.

114 d by Ca(2+)-activated slow conductance K(+) (SK) channel blocker apamin.

115 Local application of bicuculline but not the SK-channel blocker apamin attenuated the effects of LHb

116 TRPV4 and SK channel blockers also increased contractions of intac

117 These results suggest SK channel blockers as potentially interesting anti-AF d

118 applications of irreversible and reversible SK channel blockers, we provide evidence that functional

119 r study reveals a new level of regulation of SK channels by cAMP-PKA and suggests that ion channel to

120 Furthermore, LTP requires inhibition of SK channels by mGluR1, which removes a negative feedback

121 We found that SK channels can be fully activated by nanomolar concentr

122 hese findings suggest that Ca(2+) -sensitive SK channels can translate changes in cellular Ca(2+) int

123 IK/SK channels co-localized with TRPV4(EC) channels at myoe

124 chemical studies suggests that in the intact SK channel complex, the N-lobe of calmodulin provides li

125 hat small-conductance Ca(2+)-activated K(+) (SK) channels constitute a new target for treatment of at

126 ot changes in Ca(2+) -mediated activation of SK channels, contributes to exacerbated MNC activity in

127 The SK channel contribution to excitatory postsynaptic poten

128 However, the precise mechanisms by which SK-channels control the induction of synaptic plasticity

129 ated whether the Ca(2+) -sensitive nature of SK channels could explain arrhythmic SAN pacemaker activ

130 cts on neuronal excitability, with dendritic SK channels counter-intuitively promoting rather than su

131 in PAs, revealing preferential TRPV4(EC) -IK/SK channel coupling in MAs and TRPV4(EC) -eNOS coupling

132 ry arteries, which may explain TRPV4(EC) -IK/SK channel coupling in mesenteric arteries and its absen

133 er, our studies also support a blunted NMDAR-SK channel coupling in MNNs of HF rats, establishing it

134 Inhibition of SK channels decreased AP firing frequency by 66% and inc

135 Potassium currents through SK channels demonstrate inward rectification, which furt

136 We also show that SK channel dendritic distribution is dynamic and under t

137 These SK-channel-dependent deficits led to markedly increased

138 and the rectification characteristics of an SK channel determine its impact on early, plateau, and r

139 of small-conductance Ca(2+)-activated K(+) (SK) channels did not produce similar effects.

140 Blocking SK channels disrupted the one-to-one signal transmission

141 mplementary approaches, we found that native SK channel distribution in pyramidal neurons, across the

142 (V)7/M channels are operative, activation of SK channels during repetitive firing does not notably af

143 that postsynaptic activation of K(V)1.x and SK channels during spiking suppresses the subsequent eff

144 uture studies will examine the expression of SK channels during the aging process in GnRH neurons.

145 all conductance calcium-activated potassium (SK)-channel dysfunction causes hippocampal neuron hypere

146 eal a causal link for the first time between SK channel dysregulation and 5-HT neuron activity in a l

147 Opposite effects were observed using the SK channel enhancer NS309.

148 amin in vitro, we show that blocking somatic SK channels enhances action potential output, whereas bl

149 Small-conductance Ca(2+) -activated K(+) (SK) channels expressed in ventricular myocytes (VMs) are

150 Small-conductance Ca(2+) -activated K(+) (SK) channels expressed in ventricular myocytes are dorma

151 ein kinase A (PKA) levels, strongly limiting SK channel expression at the pyramidal neuron soma.

152 Our studies suggest that a reduction in SK channel expression, but not changes in Ca(2+) -mediat

153 y suggest that the calcium is present at the SK channel for a very short time after each action poten

154 We report that NMDARs and SK channels form a functional Ca(2+) -dependent negative

155 We find that native SK channels from rat hippocampal neurons reside primaril

156 dult anxiety-like behavior by downregulating SK channel function and protein expression, which leads

157 Although an increased SK channel function contributes to adaptive physiologica

158 t that a posttranslational downregulation of SK channel function in thin distal dendrites is a signif

159 GluN3A knock-out mice, cocaine did not alter SK channel function or VTA DA neuron firing.

160 scular defects in a C. elegans SMA model and SK channel function was required for this beneficial eff

161 eveal that chronic adolescent stress impairs SK channel function, which contributes to an increase in

162 onses, it remains unknown whether changes in SK channel function/expression contribute to exacerbated

163 We conclude that SK channels have demonstrable effects on SAN pacemaking

164 ese data indicate that somatic and dendritic SK channels have opposite effects on neuronal excitabili

165 ABSTRACT: Small conductance K(+) (SK) channels have been implicated as modulators of spont

166 conductance Ca(2+)-activated K(+) channels (SK channels) have been reported in excitable cells, wher

167 In CA1 pyramidal cells, SK channels in dendritic spines were shown to regulate s

168 In conclusion, upregulation of SK channels in diseased VMs is mediated by hyperadrenerg

169 ere we report that CaCCs coexist with BK and SK channels in inferior olivary (IO) neurons that send c

170 GSK1016790A (10 nm) selectively activated IK/SK channels in MAs and eNOS in PAs, revealing preferenti

171 (EC) sparklets preferentially couple with IK/SK channels in mesenteric arteries and with eNOS in pulm

172 TRPV4(EC) channels co-localize with IK/SK channels in mesenteric arteries but not in pulmonary

173 However, whether NMDARs and SK channels in MNNs are functionally coupled, and whethe

174 his work, we investigated whether NMDARs and SK channels in MNNs are functionally coupled, and whethe

175 ) influx through TRPV4 channels can activate SK channels in PDGFRalpha(+) cells and prevent bladder o

176 We conclude that SK channels in spines and dendrites of cortical pyramida

177 Here we investigate the activation of SK channels in spines and dendrites of rat cortical pyra

178 These findings indicate that activation of SK channels in spines by backpropagating APs plays a key

179 etermining the intrinsic open probability of SK channels in the absence of Ca(2+), affecting the appa

180 s differential expression with more abundant SK channels in the atria and pacemaking tissues compared

181 SK channels in the NAcS may serve as a target to treat a

182 yonic development suggests an involvement of SK channels in the regulation of developmental processes

183 However, the presence of functional SK channels in the somata and their role in controlling

184 all-conductance calcium-activated potassium (SK) channels in rat MNTB principal neurons.

185 rmediate- and small-conductance K(+) (IK and SK) channels in some vascular beds and endothelial nitri

186 all-conductance calcium-activated potassium (SK) channels in the MNTB neurons from rats of either sex

187 of Ca(2+) -activated small conductance K(+) (SK) channels in the murine SAN.

188 of small conductance Ca(2+)-activated K(+) (SK) channels in these cells is far higher ( approximatel

189 ating ion-channel activity, specifically the SK channels, in hyperexcitability defects in FXS.

190 Activation of SK channels increased mitochondrial K(+) currents, where

191 Blocking SK channels increased the amount of long-term potentiati

192 l inhibition of calcium-activated potassium (SK) channels increases the variability in their firing p

193 fication is in fact an intrinsic property of SK channels independent of intracellular blockers.

194 Blockers of TRPV4 or SK channels inhibited currents activated by GSK and incr

195 When the SK channel inhibitor AP14145 was tested in these animals

196 e a current that displayed no sensitivity to SK channel inhibitors and a decreased sensitivity to IKC

197 urrent that displayed typical sensitivity to SK channel inhibitors, while expressed IKCa channel curr

198 pecific subcellular membrane localization of SK channels is likely to represent the basis for a choli

199 gest that dysfunction of voltage-independent SK channels is the primary cause of CA3 neuronal hyperex

200 ive small-conductance Ca(2+)-activated K(+) (SK) channels is responsible for the postshock APD shorte

201 le and subcellular localization of different SK channel isoforms in lumbar spinal alpha-motoneurons (

202 We imaged SK channels labeled with fluorophore-tagged apamin and m

203 ity produces intermittent hyperactivation of SK channels, leading to arrhythmic pauses alternating wi

204 on by acting on SK channels and suggest that SK channels may be important therapeutic targets for SMA

205 all-conductance calcium-activated potassium (SK) channels mediate a potassium conductance in the brai

206 all-conductance calcium-activated potassium (SK) channels mediate medium after-hyperpolarization (AHP

207 ed a common cellular mechanism (reduction in SK channel-mediated AHP) that led to the learning-induce

208 ponse composed of a transient Ca2+-dependent SK channel-mediated hyperpolarization and a TRPC-mediate

209 The generation and magnitude of the SK channel-mediated hyperpolarization depended solely on

210 primary resonance was also influenced by the SK channel-mediated medium AHP (mAHP), because the SK bl

211 utput function, and also that a reduction in SK channel-mediated, apamin-sensitive AHP is a critical

212 Up4A induced P2Y1R-SK-channel-mediated hyperpolarization in isolated PDGFRa

213 lcium-activated small conductance potassium (SK) channel member SK3 and mitochondrial ROS.

214 This SK channel model replicates key features of I(SK) record

215 -conductance Ca(2+)-activated K(+) channels (SK channels) modulate excitability and curtail excitator

216 Bath application of a positive SK channel modulator (1-EBIO) normalized firing in ex vi

217 SK channel modulators, CyPPA and SKA-31, induced signifi

218 with fluorophore-tagged apamin and monitored SK channel nanoclustering at the single molecule level b

219 d residues in the S6 transmembrane domain of SK channels near the inner mouth of the pore that collec

220 In vivo, we demonstrate that inhibiting SK channels normalizes chronic social isolation-induced

221 nism underlies the functional recruitment of SK channels not only in cardiac disease, but also in nor

222 High K intake increased SK channel number per patch and increased the ROMK chann

223 gene is solely responsible for encoding the SK channels of inner hair cells.

224 Further, we found that the impact of SK channels on the SMT critically depended on the voltag

225 ctance calcium-activated potassium channels (SK channels) on dendritic excitability in male and femal

226 Intracellular application of selective SK-channel openers or a genetic reintroduction of an N-t

227 potential output, whereas blocking dendritic SK channels paradoxically reduces the generation of dend

228 r of spikes fired in bursts, indicating that SK channels play an important role in maintaining dopami

229 These data reveal that SK channels play crucial roles in regulating the resting

230 We conclude that although SK channels play little role in generating SFA in PVN-RV

231 all-conductance calcium-activated potassium (SK) channels play an important role in regulating neuron

232 S: Small conductance Ca(2+) -activated K(+) (SK) channels play an important role in regulating the ex

233 Small-conductance Ca(2+)-activated K(+) (SK) channels play essential roles in the regulation of c

234 We also observed that blockade of SK channels potentiated NMDAR-evoked firing, and abolish

235 reduced expression of small-conductance Kca (SK) channel protein in the BLA of socially isolated (SI)

236 Therefore, proximal SK channels provide a "second line of defense" against i

237 We speculate that SK channels provide a mechanism for rapidly sensing chan

238 aspartate receptors (NMDARs) activates spine SK channels, reducing EPSPs and the associated spine hea

239 e calcium-dependent potassium (SK) channels; SK channels regulate firing of VTA DA neurons, but this

240 all-conductance calcium-activated potassium (SK) channels regulate action potential firing and shape

241 lly-plausible, dendritic spine, we show that SK-channels regulate calmodulin activation specifically

242 indicate that a dorsal-ventral difference in SK channel regulation of NMDAR activation has a profound

243 The coactivation of GIRK and SK channels represents a novel mechanism of adenosine-me

244 ur model further predicts that inhibition of SK channels results in a depolarisation of action potent

245 through CaV(2.3) VSCCs selectively activates SK channels, revealing the presence of functional Ca mic

246 Small conductance Ca(2+)-activated K(+) (SK) channels sense intracellular Ca(2+) concentrations v

247 n to the cortical surface to block dendritic SK channels shifted the distribution of action potential

248 SK channels show a distinct subcellular localization tha

249 olarized PDGFRalpha(+) cells (the alpha1A AR-SK channel signal pathway).

250 g motor complexes (CMMCs) via the alpha1A AR-SK channel signal pathway.

251 y leads to LL HC hyperpolarization served by SK channels.SIGNIFICANCE STATEMENT The fish lateral line

252 all-conductance calcium-dependent potassium (SK) channels; SK channels regulate firing of VTA DA neur

253 n part, by loss of FMRP interaction with the SK channels (specifically the SK2 isoform), without chan

254 ns lead to the adult expression map for each SK channel subunit and how their coexpression in the sam

255 Three isoforms of SK channel subunits (SK1, SK2, and SK3) are found to be

256 The three SK channel subunits display different developmental expr

257 f heteromultimeric complexes among different SK channel subunits in atrial myocytes.

258 f heteromultimeric complexes among different SK channel subunits in native cardiac tissues.

259 e onset of expression and regions expressing SK channel subunits in the embryonic and postnatal devel

260 pecific ligands of the different isoforms of SK channel subunits may offer a unique therapeutic oppor

261 Real-time PCR measurements of SK channel subunits mRNA in supraoptic nucleus punches r

262 subcellular compartments of some neurons as SK channel subunits.

263 the past two decades, positive modulators of SK channels such as NS309 and 1-EBIO have been developed

264 gCRND8 cortex by pharmacological blockade of SK channels, suggesting a novel target for the treatment

265 els supporting faster synaptic waveforms and SK channels supporting slower synaptic waveforms.

266 Ca(v)1.3 slows down MCC firing by activating SK channels that maintain Na(V) channel availability hig

267 nd to enhance NMDAR activation by inhibiting SK channels that otherwise act to hyperpolarize postsyna

268 is associated with an enhanced activation of SK channels that strongly suppresses NMDAR activation at

269 ward currents and produce a model for BK and SK channels that we use to reproduce the outward current

270 of small conductance Ca-activated potassium (SK) channels that are found in the spine, resulting in i

271 the small-conductance Ca(2+)-activated K(+) (SK) channels that are part of a multiprotein complex con

272 m-sensitive calcium conductance coupled with SK channels, that is pharmacologically distinct from L-,

273 luding the small conductance activated K(+) (SK) channels, that maybe modulated by this signaling pat

274 2+)-activated K(+) channels, known as BK and SK channels, the physiological importance of Ca(2+)-acti

275 iate and small conductance potassium (IK and SK) channels, thereby causing hyperpolarization and endo

276 ng and the high Ca(2+) sensitivity of IK and SK channels to cause vasodilation.

277 To allow studies on the contribution of SK channels to different phases of development of single

278 RPV4 sparklet-mediated stimulation of IK and SK channels to promote vasodilation.

279 g apamin, a toxin that specifically binds to SK channels, to the tip of an AFM cantilever, we are abl

280 Understanding the mechanisms of SK channel trafficking may provide new insights into the

281 SK channel transcripts are expressed at early stages of

282 esis that post-translational modification of SK channels under conditions accompanied by enhanced adr

283 SK channels underlie important physiological functions b

284 he negative feedback loop between NMDARs and SK channels was blunted or absent in MNNs of heart failu

285 The effect of apamin on dendritic SK channels was occluded when R-type calcium channels we

286 l conductance Ca(2)(+) -activated potassium (SK) channel was developed and incorporated into a physio

287 Moreover, SK channels were activated by action potentials and affe

288 SK channels were activated by intracellular Ca(2+) spark

289 SK channels were also activated by Ca(2+) influx through

290 onic cAMP-PKA levels also controlled whether SK channels were expressed in nanodomains as single enti

291 f muscarinic receptors, TRPV4 channels or IK/SK channels were reduced, but not eliminated, by Kir cha

292 s during autonomous firing were reduced when SK channels were removed, and a nearly equal reduction i

293 ly regulated by Ca2+ -activated K+ channels (SK-channels) which are in turn inhibited by neuromodulat

294 found that in MNNs of sham rats, blockade of SK channels with apamin (200 nM) significantly increased

295 Blocking SK channels with apamin depolarized the resting membrane

296 aging, we demonstrate that the inhibition of SK channels with apamin results in a location-dependent

297 P waveform and developed a computer model of SK channels with rectification features.

298 Inhibition of SK channels with the specific blocker apamin prolonged a

299 the Ca(2+) /voltage-dependent inhibition of SK channels without changing their sensitivity to activa

300 sients activates, but higher [Ca(2+)] blocks SK channels, yielding a transient outward-like I(SK) tra