ライフサイエンスコーパス: membrane excitability

1 n secretion by linking glucose metabolism to membrane excitability.

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

3 lutamate levels and changes in MSN intrinsic membrane excitability.

4 um channels and contributes to regulation of membrane excitability.

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

6 e regulation of global synaptic strength and membrane excitability.

7 olecule that connects sleep drive to lowered membrane excitability.

8 tivities by linking cellular metabolism with membrane excitability.

9 Ion channels are key determinants of membrane excitability.

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

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

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

13 large outward conductance IKNa and arbitrate membrane excitability.

14 eurons where it regulates diverse aspects of membrane excitability.

15 ough the modulation of synaptic efficacy and membrane excitability.

16 widely used to dynamically regulate neuronal membrane excitability.

17 without significant change of the intrinsic membrane excitability.

18 n secretion by linking glucose metabolism to membrane excitability.

19 PFC pyramidal neurons, resulting in enhanced membrane excitability.

20 ent analysis applied to variables related to membrane excitability.

21 s represent an emerging strategy to regulate membrane excitability.

22 ngregate to execute a coordinated control of membrane excitability.

23 nd action potentials and regulating neuronal membrane excitability.

24 phodiesterase inhibitor increased MSN neuron membrane excitability.

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

26 thetic nervous system/hormonal regulation of membrane excitability.

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

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

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

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

31 mechanism for neurotransmitter regulation of membrane excitability.

32 tion between calcium signalling pathways and membrane excitability.

33 ate gating of potassium channels that govern membrane excitability.

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

35 subthreshold membrane potentials to control membrane excitability.

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

37 erful computational mechanism for regulating membrane excitability.

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

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

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

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

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

43 rdiac ganglia neurons and increased neuronal membrane excitability.

44 -specific changes in Purkinje cell dendritic membrane excitability.

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

46 transport, intracellular pH regulation, and membrane excitability.

47 nel expression might underlie the changes in membrane excitability.

48 ibit potassium channels and thus to increase membrane excitability.

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

50 calexcitin was highly effective in enhancing membrane excitability.

51 response that serves to normalize intrinsic membrane excitability.

52 adaptive response to increases in intrinsic membrane excitability.

53 elated to neuronal lineage and regulation of membrane excitability.

54 phosphoinositides provides local control of membrane excitability.

55 bolic sensors that couple cell energetics to membrane excitability.

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

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

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

59 auxiliary beta-subunits and thereby modulate membrane excitability.

60 he resting membrane potential and modulating membrane excitability.

61 pression and subsequent reduction in INa and membrane excitability.

62 is oocytes expressing proteins that underlie membrane excitability.

63 lates translation of this key determinant of membrane excitability.

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

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

66 he resting membrane potential and modulating membrane excitability.

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

68 neuron excitability by increasing intrinsic membrane excitability.

69 he resting membrane potential and modulating membrane excitability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 VGCC regulate membrane excitability and gene transcription along with

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

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

91 -1C provides a powerful mechanism to titrate membrane excitability and is a useful approach to define

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 2+) signal to the channel gating to regulate membrane excitability and spike firing patterns.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 5-HT increased membrane excitability at a temperature below body temper

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

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

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

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

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

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

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

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

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

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

139 Reducing membrane excitability by hyperpolarization of the restin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 In membrane excitability experiments, bath application of a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Membrane excitability in different tissues is due, in la

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Membrane excitability in the axonal growth cones of embr

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

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

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

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

195 Membrane excitability in the growth cone, which is mainl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Cardiac membrane excitability is tightly regulated by an integra

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

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

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

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

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

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

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

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

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

221 The membrane excitability of cholinergic (starburst) amacrin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 -300 microM) had two opposing effects on the membrane excitability of these cells, reflecting the act

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

249 These abnormalities in axonal membrane excitability parameters closely resembled those

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

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

252 We find that membrane excitability progressively decreases due to hyp

253 We show that membrane excitability properties have differential effec

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

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

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

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

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

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

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

261 3.4 channels effectively reduces growth cone membrane excitability, thereby limiting excessive Ca(2+)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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