ライフサイエンスコーパス: membrane excitability

1 -128 in regulating gene networks that govern membrane excitability.

2 the dendrites, to both enhance and suppress membrane excitability.

3 odulin, have an important role in regulating membrane excitability.

4 ium currents and a key regulator of neuronal membrane excitability.

5 neuron excitability by increasing intrinsic membrane excitability.

6 he resting membrane potential and modulating membrane excitability.

7 n secretion by linking glucose metabolism to membrane excitability.

8 s comprising the core synaptic machinery and membrane excitability.

9 es of ion channels that increase or decrease membrane excitability.

10 lutamate levels and changes in MSN intrinsic membrane excitability.

11 um channels and contributes to regulation of membrane excitability.

12 tage and play a critical role in controlling membrane excitability.

13 e regulation of global synaptic strength and membrane excitability.

14 olecule that connects sleep drive to lowered membrane excitability.

15 Ion channels are key determinants of membrane excitability.

16 m (Kir) channels is important for regulating membrane excitability.

17 for cell structure, but may directly impact membrane excitability.

18 des a direct link between actin dynamics and membrane excitability.

19 eurons where it regulates diverse aspects of membrane excitability.

20 ough the modulation of synaptic efficacy and membrane excitability.

21 widely used to dynamically regulate neuronal membrane excitability.

22 without significant change of the intrinsic membrane excitability.

23 n secretion by linking glucose metabolism to membrane excitability.

24 PFC pyramidal neurons, resulting in enhanced membrane excitability.

25 ent analysis applied to variables related to membrane excitability.

26 s represent an emerging strategy to regulate membrane excitability.

27 ngregate to execute a coordinated control of membrane excitability.

28 nd action potentials and regulating neuronal membrane excitability.

29 phodiesterase inhibitor increased MSN neuron membrane excitability.

30 ex to modulate beta-adrenergic regulation of membrane excitability.

31 thetic nervous system/hormonal regulation of membrane excitability.

32 um (K(ATP)) channel links cell metabolism to membrane excitability.

33 n of INa is, by itself, sufficient to reduce membrane excitability.

34 ion in muscle cells and neurones to regulate membrane excitability.

35 mechanism for neurotransmitter regulation of membrane excitability.

36 tion between calcium signalling pathways and membrane excitability.

37 action potential latency, and a decrease in membrane excitability.

38 ate gating of potassium channels that govern membrane excitability.

39 a new role for dimeric tubulin in regulating membrane excitability.

40 subthreshold membrane potentials to control membrane excitability.

41 ouple the metabolic status of cells with the membrane excitability.

42 erful computational mechanism for regulating membrane excitability.

43 may be a general mechanism for regulation of membrane excitability.

44 ssium channels (SK) has a profound effect on membrane excitability.

45 ead to an understanding of the regulation of membrane excitability.

46 elationship between intracellular Ca(2+) and membrane excitability.

47 analysis of these currents and their role in membrane excitability.

48 s an increased K+ conductance that modulates membrane excitability.

49 rdiac ganglia neurons and increased neuronal membrane excitability.

50 -specific changes in Purkinje cell dendritic membrane excitability.

51 ike current, in learning-specific changes in membrane excitability.

52 transport, intracellular pH regulation, and membrane excitability.

53 bolic sensors that couple cell energetics to membrane excitability.

54 nel expression might underlie the changes in membrane excitability.

55 ibit potassium channels and thus to increase membrane excitability.

56 K+ channels (GIRK) which, in turn, influence membrane excitability.

57 and Cl(-)-permeable GABAA receptor-dependent membrane excitability.

58 calexcitin was highly effective in enhancing membrane excitability.

59 ization (AHP) after spike bursts, regulating membrane excitability.

60 LTP but also from cell-autonomous changes in membrane excitability.

61 tivities by linking cellular metabolism with membrane excitability.

62 large outward conductance IKNa and arbitrate membrane excitability.

63 response that serves to normalize intrinsic membrane excitability.

64 adaptive response to increases in intrinsic membrane excitability.

65 elated to neuronal lineage and regulation of membrane excitability.

66 epolarized membrane potential, thus reducing membrane excitability.

67 phosphoinositides provides local control of membrane excitability.

68 o local regulation of Kv2.1 function and AIS membrane excitability.

69 ied by abnormal calcium-dependent cerebellar membrane excitability.

70 ather than changes in AMPA-type receptors or membrane excitability.

71 auxiliary beta-subunits and thereby modulate membrane excitability.

72 he resting membrane potential and modulating membrane excitability.

73 pression and subsequent reduction in INa and membrane excitability.

74 is oocytes expressing proteins that underlie membrane excitability.

75 lates translation of this key determinant of membrane excitability.

76 uding the globally abundant diatoms, exhibit membrane excitability [8-10].

77 ient K(+) current that dynamically regulates membrane excitability, action potential firing propertie

78 of conditioning and Purkinje cell dendritic membrane excitability after initial acquisition of the c

79 , the Hodgkin-Huxley formulation of neuronal membrane excitability and a biophysical model of metabol

80 ught to play an important role in regulating membrane excitability and action potential firing patter

81 ate that MNCs from HF rats exhibit increased membrane excitability and an enhanced input-output funct

82 , we identified two specific phenotypes: (1) membrane excitability and AP-evoked Ca(2+) entry were im

83 Ca(2+)-activated ion channels shape membrane excitability and Ca(2+) dynamics in response to

84 effector that participates in the control of membrane excitability and Ca(2+) signaling events in bet

85 upted K(ATP) channel-dependent adjustment of membrane excitability and calcium handling, compromising

86 (+) channels (Nav) are essential for myocyte membrane excitability and cardiac function.

87 e mechanism for plasticity in the control of membrane excitability and cardiac rhythm.

88 oltage-dependent potassium channels regulate membrane excitability and cell-cell communication in the

89 nels link intracellular energy metabolism to membrane excitability and contractility.

90 Hair cell calcium channels regulate membrane excitability and control synaptic transmission.

91 Functionally, they show reduced membrane excitability and decreased glutamatergic recept

92 tors in medium spiny neurons increases their membrane excitability and decreases the complexity and l

93 , female serotonergic neurons showed blunted membrane excitability and divergent inhibitory postsynap

94 s is mainly determined by the integration of membrane excitability and excitatory/inhibitory synaptic

95 that this imbalance contributes to enhanced membrane excitability and firing activity in this neuron

96 VGCC regulate membrane excitability and gene transcription along with

97 ld-type aCC/RP2 mimic both the reductions in membrane excitability and INa.

98 tes GIRK channels, leading to suppression of membrane excitability and inhibition of AP firing.

99 -1C provides a powerful mechanism to titrate membrane excitability and is a useful approach to define

100 ical role in the down-regulation of neuronal membrane excitability and is associated with a decreased

101 t (I(M)) plays a dominant role in regulating membrane excitability and is modulated by many neurotran

102 t plays a critical role in the regulation of membrane excitability and is responsible for spike-frequ

103 ibed, but no system that directly suppresses membrane excitability and is triggered by a systemically

104 Thus, membrane excitability and K(ATP) activity, to our knowle

105 ary conservation of a role for calmodulin in membrane excitability and linked behavioral responses.

106 Reduced membrane excitability and loss of postsynaptic densities

107 dings suggest that Kv3.4 reduces growth cone membrane excitability and maintains [Ca(2+)]i at an opti

108 II-targeted proteins causing disordered cell membrane excitability and myocardial dysfunction remain

109 test this, the effects of repeated stress on membrane excitability and other membrane properties of B

110 central autonomic neurones by decreasing the membrane excitability and pharmacological responsiveness

111 saturated fatty acids (PUFAs) reduce cardiac membrane excitability and prevent cardiac arrhythmias in

112 In cardiac tissue, reduced membrane excitability and reduced gap junction coupling

113 t couple the metabolic status of a cell with membrane excitability and regulate a number of cellular

114 els couple the intracellular energy state to membrane excitability and regulate a wide array of biolo

115 ated sodium (Nav) channels are essential for membrane excitability and represent therapeutic targets

116 n of the Fitzhugh-Nagumo (FN) model of nerve membrane excitability and results from the squid giant a

117 ls) play an important role in the control of membrane excitability and rhythmic neuronal activity.

118 hysiological roles, ranging from controlling membrane excitability and secretion to mediating blood c

119 2+) signal to the channel gating to regulate membrane excitability and spike firing patterns.

120 romise the function of proteins that control membrane excitability and subcellular Ca(2+) dynamics.

121 pact of SD on several fundamental aspects of membrane excitability and synaptic physiology in hippoca

122 mechanisms are employed by neurons to alter membrane excitability and synaptic strength to adapt to

123 signaling by inflicting primary disorders of membrane excitability and synaptic transmission, whereas

124 al communication, particularly modulation of membrane excitability and synaptic transmission.

125 citatory synaptic network, greater intrinsic membrane excitability, and an increased capacity for sus

126 ately 250 genes implicated in cell adhesion, membrane excitability, and cellular signaling are differ

127 tocols may be an indirect measurement of the membrane excitability, and computational models may have

128 hat homeostasis modulates synaptic strength, membrane excitability, and firing rates, its role at the

129 he hippocampal CA3-CA1 connection, increased membrane excitability, and induced RyR2 leak.

130 age-activated Ca(2+) signaling important for membrane excitability, and mutants exhibit impaired moti

131 eural function, regulating axonal transport, membrane excitability, and organization of microtubule n

132 In contrast, baseline synaptic transmission, membrane excitability, and spike timing-dependent long-t

133 including homeostatic changes in AIS length, membrane excitability, and the localization of voltage-g

134 sential in coupling cellular metabolism with membrane excitability, and their activity can be reconst

135 Interestingly, all known forms of membrane excitability are a consequence of one unique me

136 channels with important roles in regulating membrane excitability are activated exclusively by Ca(2+

137 , other mechanisms, such as modifications in membrane excitability, are available.

138 sfunction, which ultimately leads to altered membrane excitability as manifested by episodic disease.

139 We find that mutations that decrease membrane excitability as well as those that increase exc

140 This included an overall decrease in membrane excitability, as indexed by a decrease in membr

141 5-HT increased membrane excitability at a temperature below body temper

142 irect gating occurs and significantly alters membrane excitability at concentrations < or =100 nm.

143 channels, which are important regulators of membrane excitability both in heart and brain, appear to

144 els, products of the SK1-SK3 genes, regulate membrane excitability both within and outside the nervou

145 d intracellular calcium levels and increased membrane excitability, both of which have been observed

146 eptors and how these signals impact not only membrane excitability but also gene transcription in neu

147 ptors, and how these signals impact not only membrane excitability but also gene transcription in neu

148 t dependent upon the characteristics of tuft membrane excitability, but rather stemmed from the geome

149 nnel function and is critical for control of membrane excitability, but the structural basis for this

150 tivity was not because of enhanced intrinsic membrane excitability, but was accompanied by depolarize

151 (Kv) channels are key factors in controlling membrane excitability, but whether they regulate axon gr

152 ach cell type, it is dominant in controlling membrane excitability by being the only sustained curren

153 Reducing membrane excitability by hyperpolarization of the restin

154 abolism of glucose to ATP, which then alters membrane excitability by modulating ATP-dependent channe

155 in establishing the proper level of neuronal membrane excitability by regulating functional expressio

156 We found that increasing membrane excitability by removing Shaker-like K(+) chann

157 ndings suggest a unique relationship between membrane excitability, Ca2+ signaling, and prolonged neu

158 ired for core activities of neurons, such as membrane excitability, Ca2+-triggered presynaptic releas

159 Regulation of cell membrane excitability can be achieved either by modulati

160 to mutations in the primary determinants of membrane excitability (channels).

161 compared with patients with preserved muscle membrane excitability (compound muscle action potentials

162 eurons were optically stimulated to increase membrane excitability, concomitant photostimulation of H

163 ncreasing I(Nap) is sufficient to potentiate membrane excitability consistent with a seizure phenotyp

164 The literature is conflicted as to whether membrane excitability contributes to the mechanism.

165 bbits, the conditioning-related increases in membrane excitability could be mimicked by application o

166 s is now being extended to a growing list of membrane excitability disorders of the nervous system.

167 el inhibitors to provide pharmacotherapy for membrane excitability disorders, such as myotonia, epile

168 oot ganglia (DRG) and can undergo changes in membrane excitability during chronic pain.

169 rence not only blocked the downregulation of membrane excitability during epileptiform activity, but

170 designed to establish the basis for altered membrane excitability during the inhibition of mitochond

171 Our results indicate that LN(v) membrane excitability encodes time of day via a circadia

172 In membrane excitability experiments, bath application of a

173 le (10 microM) resulted in an enhancement of membrane excitability, facilitation of the occurrence of

174 annels play critical roles in the control of membrane excitability, gene expression, and muscle contr

175 duced alterations at excitatory synapses and membrane excitability have been extensively examined, th

176 utations affecting ion channels and neuronal membrane excitability have been identified in Drosophila

177 as an internal second messenger to regulate membrane excitability; however, the effector system wher

178 ng-term hormone deficiency reduced intrinsic membrane excitability (IE) as measured by the number of

179 naptically evoked excitation, but did reduce membrane excitability in a subset of gastric-projecting

180 Analysis of membrane excitability in aCC/RP2, in either background,

181 affect Na(v)1 metabolism and alter neuronal membrane excitability in Alzheimer disease patients.

182 on 5-hydroxytryptamine4 receptors increases membrane excitability in CA1 hippocampal pyramidal cells

183 d stearic acid (SA, C18:0) did not alter the membrane excitability in CA1 neurons.

184 subunits and play major roles in regulating membrane excitability in cardiac atrial, neuronal, and n

185 ing conditions and further influence RVD and membrane excitability in cells generating action potenti

186 ation of action potentials and regulation of membrane excitability in cells such as cardiomyocytes an

187 e HCN4 channels are critical determinants of membrane excitability in cells throughout the body, incl

188 Membrane excitability in different tissues is due, in la

189 d identify potential new targets to modulate membrane excitability in disease.

190 voltage-activated K(+) (BK) channels control membrane excitability in many cell types.

191 Ca) or maxi-K) are important determinants of membrane excitability in many cell types.

192 Circadian clocks regulate membrane excitability in master pacemaker neurons to con

193 ly injury modulates synaptic integration and membrane excitability in mature spinal projection neuron

194 udy, we assessed the effects of n-3 PUFAs on membrane excitability in mouse hippocampal neurons with

195 s (GIRK or Kir3) is important for regulating membrane excitability in neuronal, cardiac and endocrine

196 sium channel, Kv1.2, is a key determinant of membrane excitability in neurons and cardiovascular tiss

197 ase (AMPK) regulates neuronal morphology and membrane excitability in neurons.

198 e tonotopic distribution of input number and membrane excitability in NM closely tracks a stimulus-de

199 e proteins may play a key role in regulating membrane excitability in normal and diseased heart.

200 pose that this modulation serves to regulate membrane excitability in PC12 cells and possibly other o

201 long-lasting, cocaine-induced plasticity of membrane excitability in PFC pyramidal neurons may contr

202 on of the native M-current and regulation of membrane excitability in rat hippocampal neurons in prim

203 tral to the homeostatic mechanism regulating membrane excitability in rat visual cortical pyramidal n

204 The rank order of peptide potency on membrane excitability in response to depolarizing curren

205 activating protein (Rho-Gap), to alter their membrane excitability in response to sleep deprivation.

206 regulatory subunit genes increases intrinsic membrane excitability in thalamic neurons by potentiatin

207 Membrane excitability in the axonal growth cones of embr

208 annel, which is potentially able to modulate membrane excitability in the brain and could respond to

209 and Kv7.3 (KCNQ3), are key determinants for membrane excitability in the brain.

210 ly, are particularly important in regulating membrane excitability in the CNS and the heart.

211 shown to suppress synaptic transmission and membrane excitability in the CNS.

212 Membrane excitability in the growth cone, which is mainl

213 spensable molecular platform that determines membrane excitability in the mouse heart and brain.

214 CaM binding regulates M-channel function and membrane excitability in the native neuronal environment

215 le for betaIV-spectrin in regulation of cell membrane excitability in the pancreatic islet, define th

216 but a progressive postsynaptic reduction of membrane excitability in the ventral MeAp.

217 We find that the daily rhythm in membrane excitability in the ventral SCN (vSCN) was enha

218 for cyclooxygenase metabolites in regulating membrane excitability in various forms of synaptic plast

219 a long-lasting increase or decrease in their membrane excitability in vivo.

220 teraction of a number of factors that modify membrane excitability, including membrane depolarization

221 s study, we propose that changes in neuronal membrane excitability induced by acetylcholine may provi

222 ion contraction coupling, such as decreasing membrane excitability, injuring sarcolemmal membranes, a

223 ong ion channels, uniquely able to translate membrane excitability into the cytoplasmic Ca(2+) change

224 roles in neurons including the regulation of membrane excitability, intracellular [Ca(2+) ] regulatio

225 ng term.SIGNIFICANCE STATEMENT Plasticity of membrane excitability ("intrinsic plasticity") has been

226 ensory thalamocortical neurons, we show that membrane excitability is a critical component of dendrit

227 finding indicates that elevated postsynaptic membrane excitability is by itself insufficient to enhan

228 ircadian defective per(0) null mutant lLN(v) membrane excitability is nearly constant in LD.

229 in constant darkness (DD), wild-type lLN(v) membrane excitability is not cyclically regulated, altho

230 Cardiac membrane excitability is tightly regulated by an integra

231 ty of Kir2.6 properties, all altering muscle membrane excitability leading to paralysis.

232 fect, along with the CREB enhancement of NAc membrane excitability, may counteract drug-induced malad

233 elate changes in [Ca2+]i with alterations in membrane excitability measured by intracellular recordin

234 s classically known to affect axon guidance, membrane excitability, neurotransmission, and synaptic v

235 of a variety of neuronal functions, such as membrane excitability, neurotransmitter release, and gen

236 ed AP threshold to underlie the reduction in membrane excitability observed because of heightened exp

237 This change in membrane excitability occurred just after eye opening (P

238 We found that NTR1 increased the membrane excitability of CA1 pyramidal neurons in hippoc

239 affect either resting membrane potential or membrane excitability of CeL neurons.

240 The membrane excitability of cholinergic (starburst) amacrin

241 re (21 day) led to sustained increase in the membrane excitability of LTB neurons such that it lasted

242 channels play essential roles in regulating membrane excitability of many diverse cell types by sele

243 Neonatal injury also dampened the intrinsic membrane excitability of mature DYN neurons, and reduced

244 opment and accompanied by an increase in the membrane excitability of medial nucleus of the trapezoid

245 Bash bursts are supported by high membrane excitability of mid-line cells and are regulate

246 lease can produce a long-lasting increase in membrane excitability of midbrain dopamine neurons.

247 together with our previous findings that the membrane excitability of NAc MSNs is decreased during co

248 tations at excitatory synapses and intrinsic membrane excitability of NAc MSNs, may provide a relativ

249 Drug-induced changes in intrinsic membrane excitability of NAc neurons are thought to be c

250 aine exposure, suggesting that the decreased membrane excitability of NAc neurons may not be a persis

251 ncontingent cocaine injection, the intrinsic membrane excitability of NAc shell (NAcSh) neurons is de

252 Specifically, the membrane excitability of NAcSh medium spiny neurons (MSN

253 pretreated rats, the reexposure elevated the membrane excitability of NAcSh MSMs beyond the normal le

254 e to cocaine after long-term withdrawal, the membrane excitability of NAcSh MSNs instantly returned t

255 ults suggest that the dynamic alterations in membrane excitability of NAcSh MSNs, together with the d

256 At 21 d of withdrawal, the membrane excitability of NAcSh MSNs, which remained low

257 (NAcSh) neurons is decreased, and decreased membrane excitability of NAcSh neurons increases the acu

258 Here, we demonstrate that the membrane excitability of NAcSh neurons is differentially

259 w TTX-R resurgent currents contribute to the membrane excitability of nociceptive DRG neurons under n

260 by adenosine and therefore maintain enhanced membrane excitability of PC12 cells during long-term hyp

261 led to striking plasticity in the intrinsic membrane excitability of projection neurons (mitral cell

262 The development of the membrane excitability of PVINs is delayed and reaches ma

263 ired for the activity-dependent reduction in membrane excitability of pyramidal neurons.

264 hesis that LTP induces a change in intrinsic membrane excitability of rat cerebellar granule cells th

265 nels play a critical role in controlling the membrane excitability of skeletal muscles.

266 Furthermore, the membrane excitability of tdT-positive FSIs in the NAc wa

267 We found lower membrane excitability of the corticocortical axons and n

268 -300 microM) had two opposing effects on the membrane excitability of these cells, reflecting the act

269 utations are predicted to increase intrinsic membrane excitability or directly enhance LVA currents.

270 These abnormalities in axonal membrane excitability parameters closely resembled those

271 he acute stage, during which impaired muscle membrane excitability probably plays a more significant

272 ng cell excitability, and (2) the changes in membrane excitability produced by MCD underlie the chang

273 We find that membrane excitability progressively decreases due to hyp

274 We show that membrane excitability properties have differential effec

275 lar energetics with K(ATP) channel-dependent membrane excitability remains elusive.

276 may contribute, such as changes in neuronal membrane excitability, removal of local inhibition, or v

277 Analysis of membrane excitability shows that these effects of MF exp

278 xaenoic acid (DHA, C22:6n-3), had effects on membrane excitability similar to those of EPA.

279 nal processes including calcium homeostasis, membrane excitability, synaptic transmission, and axon g

280 anges predicted to alter proteins regulating membrane excitability, synaptic transmission, or neurona

281 activity in axons generates aftereffects on membrane excitability that can alter the conduction velo

282 el and plays an important role in regulating membrane excitability that is underscored by ClC-1 mutat

283 3.4 channels effectively reduces growth cone membrane excitability, thereby limiting excessive Ca(2+)

284 In addition, they can adjust their membrane excitability to alter spike output.

285 a variety of cellular processes ranging from membrane excitability to cellular proliferation.

286 Through hSMP, NAc neurons adjusted their membrane excitability to functionally compensate for bas

287 annels by intracellular ligands couples cell membrane excitability to important signaling cascades an

288 sensitive K+ channels (KATP channels) adjust membrane excitability to match cellular energetic demand

289 part of a homeostatic mechanism that matches membrane excitability to synaptic depolarization in mamm

290 The ability to regulate intrinsic membrane excitability, to maintain consistency of action

291 rupt touch-evoked sensory activity or reduce membrane excitability trigger accelerated neuronal aging

292 a demonstrate that n-3 PUFAs modify neuronal membrane excitability under control and drug-stimulated

293 ptic currents were unaffected, and intrinsic membrane excitability was increased after SD.

294 erm (5 day) cocaine self-administration; the membrane excitability was increased in LTB neurons but d

295 order to study CXCR4-dependent modulation of membrane excitability, we recorded in cell-attached conf

296 otide-gated K(IR)6.0(4)/SUR(4) channels link membrane excitability with cellular metabolism is contro

297 Ca(2)(+) plays a crucial role in connecting membrane excitability with contraction in myocardium.

298 for channel/enzyme operation and integrates membrane excitability with metabolic cascades.

299 rcolemma of cardiac myocytes where they link membrane excitability with the cellular bioenergetic sta

300 es showed that Lm128C cells exhibit elevated membrane excitability, with biophysical properties close