ライフサイエンスコーパス: excitability

1 biological mechanisms underlying ventricular excitability.

2 l diseases characterized by abnormal circuit excitability.

3 Fos immunohistochemistry to examine cellular excitability.

4 pment on intercellular coupling and cellular excitability.

5 4 directly regulates post-traumatic neuronal excitability.

6 d membrane potential, thus reducing membrane excitability.

7 normal calcium-dependent cerebellar membrane excitability.

8 egulating gene networks that govern membrane excitability.

9 (v)) channel is the molecular determinant of excitability.

10 le for palmitoylation in control of neuronal excitability.

11 paminergic systems, or reduction of cortical excitability.

12 through convergent action on BLApn intrinsic excitability.

13 es in synaptic transmission and/or intrinsic excitability.

14 matergic synaptic transmission, and neuronal excitability.

15 at uses mechanical energy to affect neuronal excitability.

16 aptic plasticity and enhancement in neuronal excitability.

17 show reduced background spiking but enhanced excitability.

18 hestrate the extent and duration of neuronal excitability.

19 synaptic depression and decreased intrinsic excitability.

20 rites, to both enhance and suppress membrane excitability.

21 sion (LTD) by affecting cellular and network excitability.

22 ed A-type K(+) current, and reduced neuronal excitability.

23 er-hyperpolarization currents and changes in excitability.

24 ntral CA1 that indirectly increases neuronal excitability.

25 lyR-associated currents and enhance neuronal excitability.

26 ed for OXTR-induced augmentation of neuronal excitability.

27 nced glutamatergic transmission and neuronal excitability.

28 terventions were used to manipulate neuronal excitability.

29 a (SZ) psychosis associated with hippocampal excitability.

30 regulate information processing and network excitability.

31 onatal mice during changes in spinal network excitability.

32 e AIS channel protein Kv7.3 regulates neuron excitability.

33 lar alpha-mediated changes in focal cortical excitability.

34 ing the core synaptic machinery and membrane excitability.

35 ll volume, chloride homeostasis and neuronal excitability.

36 y without inflammation by enhancing neuronal excitability.

37 role of sensory SGCs in decreasing afferent excitability.

38 be a powerful mechanism to regulate neuronal excitability.

39 ion, which was dependent on DLK and neuronal excitability.

40 lation of synaptic transmission and neuronal excitability.

41 ellular recordings linked propensity to cell excitability.

42 e neural networks under dynamically changing excitability.

43 tic spiking and slow changes in postsynaptic excitability.

44 g membrane potential and regulating cellular excitability.

45 ent or loss of proteins can influence neuron excitability.

46 on led to a substantial decrease in neuronal excitability.

47 st-spike latencies and wideband increases in excitability.

48 manifesting as epochs of enhanced intrinsic excitability.

49 ereby represent the substrate for astroglial excitability.

50 rofoundly important for controlling neuronal excitability.

51 ignal content occurring near peaks of neural excitability.

52 e depolarization and increased smooth muscle excitability.

53 ting the motor system and affecting cortical excitability.

54 AHP) after spike bursts, regulating membrane excitability.

55 use alpha is thought to reflect focal neural excitability.

56 -protein-signaling systems that inhibit cell excitability.

57 ous neuronal states determining the system's excitability.

58 What is the impact of AIS geometry on excitability?

59 ium (Na(+)) leak currents enhance electrical excitability(1,2).

60 K(+) currents to control cellular electrical excitability(1-3).

61 l changes in models of relevance to neuronal excitability: 1) enhanced action potential repolarizatio

62 Excitability-a threshold-governed transient in transmemb

63 sociated with increased neuronal and network excitability after injury, including increased susceptib

64 eurons which coincide with windows of higher excitability also benefit from more rapid and less varia

65 The results suggest that maintenance of excitability amid parametric variation is a low-dimensio

66 ng task induced an increase in corticospinal excitability and a reduction in the amplitude of somatos

67 Abeta(42) showed enhanced neuronal intrinsic excitability and action potential firing rates.

68 chanism linking gonadal hormones to cellular excitability and anhedonia-a key feature in depressive s

69 ongoing and evoked activity through cortical excitability and argue that the co-emergence of common t

70 is over-inhibition originates from increased excitability and Ca(2+) transients in the presynaptic te

71 Heterozygous loss of DGCR8 recapitulated the excitability and calcium phenotypes and its overexpressi

72 ve channels are major regulators of neuronal excitability and cancer progression.

73 -projecting neurons also showed increases in excitability and CC input strength that was offset with

74 s at about P50, resulting in a state of hypo-excitability and cell death.

75 us remodels in preparation for delivery, the excitability and contractility of the uterine smooth mus

76 Functionally, they show reduced membrane excitability and decreased glutamatergic receptor activi

77 stimulation (TMS) to briefly alter cortical excitability and determine whether early visual areas me

78 rest in seeking food, accompanied by reduced excitability and dopamine release upon cholinergic stimu

79 ested that GlyR alpha1 subunits regulate nAc excitability and ethanol consumption.

80 onse to anxiogenic environment but had lower excitability and fewer presynaptic inputs than those of

81 ficits are linked to reductions in intrinsic excitability and firing rate of SF1 neurons.

82 itment of neuronal ensembles on the basis of excitability and functional connectivity at the time of

83 he IN nerve terminals likely augmented their excitability and GABA release, we applied a positive Kv1

84 ion ensues from homeostatic dysregulation of excitability and have tested this hypothesis by perturbi

85 s to subnucleus-specific alterations in BFCN excitability and impaired cognition.

86 d learning-related gene, Fos, also increased excitability and impaired learning.

87 mpanied by increases in near-spike-threshold excitability and input-output gain that resulted in dram

88 or understanding the foundations of cortical excitability and its monitoring in conditions like epile

89 ns involve rhythmic fluctuations of neuronal excitability and may play a crucial role in neural commu

90 hat their activation produces neuronal hyper-excitability and mechanical pain in mice.

91 of somatosensory afferent inputs on cortical excitability and neural plasticity often used transcrani

92 inflammatory signaling in modifying neuronal excitability and promoting epileptogenesis.

93 y L4 pyramidal neurons had greater intrinsic excitability and recurrent excitatory synaptic strength,

94 Fine adjustment of network excitability and regulation of synaptic strength are bot

95 provided sustained inhibition of nociceptor excitability and relief from inflammatory pain.

96 REM sleep specific suppression of net motor excitability and responsivity.

97 nandamide (AEA) signaling, controls neuronal excitability and seizure expression and regulates emotio

98 ocking TLR4 signaling augmented both network excitability and seizure susceptibility in uninjured con

99 y after brain injury reduced dentate network excitability and seizure susceptibility.

100 molecular regulators of hippocampal neuronal excitability and seizures.

101 els as regulators of hippocampal interneuron excitability and seizures.

102 condary visual cortex show reduced dendritic excitability and smaller propensity for burst firing.

103 trate that loss of SIRT1 decreases intrinsic excitability and spontaneous excitatory synaptic transmi

104 ntrast, homeostatic adaptations of intrinsic excitability and spontaneous MFR failed in hippocampal G

105 dulates NMDARs via Src to regulate beta-cell excitability and suggests NMDARs as a potential target t

106 ence of engrams, the importance of intrinsic excitability and synaptic plasticity in engrams, and the

107 tory neurons is required for normal neuronal excitability and synaptic transmission and regulates dep

108 smalemmal Best1 channels to control neuronal excitability and tactile acuity through tonic inhibition

109 rns, we systematically manipulated the local excitability and the global coupling in the virtual huma

110 tage-gated ion channels endow membranes with excitability and the means to propagate action potential

111 gated sodium (Na(V)) channels drive neuronal excitability and three subtypes - Na(V)1.7, Na(V)1.8 and

112 lt-onset mutations differentially affect the excitability and viability of Purkinje cells in vivo dur

113 euronal and cardiac action potential firing (excitability) and have major roles in human diseases suc

114 als allowed rapid Na(+)-dependent electrical excitability, and enabled the development of sophisticat

115 stasis modulates synaptic strength, membrane excitability, and firing rates, its role at the neural c

116 rse physiological events, including neuronal excitability, and have been linked to several pathologic

117 ted genes related to morphogenesis, cellular excitability, and synapse formation.

118 arge-scale, propagating patterns of cortical excitability are behaviorally relevant and may be a nece

119 and sensory-evoked potentials, intracortical excitability as assessed by short-interval intracortical

120 Diminished motor cortical excitability, as a measurement of increased resting moto

121 mbs, linked to increased sensorimotor cortex excitability, as seen in cortical myoclonus.

122 s a mathematical framework for understanding excitability, as the consequence of the properties of vo

123 LRMP and IRAG in the regulation of cellular excitability, as tools for advancing mechanistic underst

124 gs of zinc's associations with excitability, excitability-associated disorders, and myelination.

125 Noise from excessive excitability at high doses overcomes stability enhanceme

126 , which acts at postsynaptic sites to dampen excitability at short and long time scales.

127 kout (Fhf2(KO)) mice predisposes to abnormal excitability at the tissue level are not well defined.

128 ongly attenuated the difference in intrinsic excitability between wild-type (WT) and Foxp2(+/R552H) n

129 or task induced an increase in corticospinal excitability but did not change motor cortex intracortic

130 AIS normally produces a (modest) increase in excitability, but we explain how this pattern can revers

131 formation, morphology, and aberrant neuronal excitability by antibody exposure.

132 ew insights into the modulation of dendritic excitability by apical dendrite length and show that the

133 encoded by the KCNA2 gene, regulate neuronal excitability by conducting K(+) upon depolarization.

134 ling in supporting cells regulates hair cell excitability by controlling the volume of the extracellu

135 eizures, and genomic reduction of host brain excitability by deleting MapT suppressed molecular marke

136 (Na) We conclude that LITAF controls cardiac excitability by promoting degradation of NEDD4-2, which

137 Rebalancing cortical excitability by rTMS appears critical for plasticity ind

138 electrophysiological evaluation of cortical excitability by TMS.

139 is contributes to sex-specific regulation of excitability, [Ca(2+)](i), and myogenic tone in arterial

140 the inborn model, the adult-onset pattern of excitability changes believed to be pathogenic within th

141 ether, rTMS induced lasting connectivity and excitability changes from the site of stimulation, such

142 e-blink conditioning; however, corresponding excitability changes in the cerebellum in associative le

143 e backward locomotion but require additional excitability compared with forward locomotion.

144 tinct serotonin responses and have increased excitability, compared with S100a10-negative neurons.

145 associated with reduced cellular and network excitability, concurrent with an increase in the express

146 tion effects are likely to increase neuronal excitability consistent with the epileptic potential of

147 In turn, increased MN excitability contributes to restoring synaptic structure

148 Further, cellular excitability controls whether conduction across the cell

149 onic cervical SCI influenced in parallel the excitability cortical and spinal networks, having an exc

150 red behavioral performance and corticospinal excitability (CSE) using transcranial magnetic stimulati

151 s, repetitive firing parameters increase and excitability decreases with development; however, these

152 profile, with maximal firing increasing and excitability decreasing into the third postnatal week.

153 Fluctuations of cortical excitability demonstrated long-range temporal dependenci

154 dicate that the fast adaptation of intrinsic excitability depends on ongoing spiking activity but is

155 igner drugs) strategy to manipulate vHPC-NAc excitability directly in awake behaving mice.

156 with excitability, synaptic plasticity, and excitability disorders, with the CaMKII-specific peptide

157 tonic firing in Purkinje cells, but reduced excitability during evoked high frequency spiking.

158 ning and memory, such as changes in cellular excitability during memory formation.

159 ndings show that modulation of corticospinal excitability during observed object lifting is not robus

160 Reduction of mPFC neuron excitability during the first 2 postnatal weeks caused a

161 imaging findings of zinc's associations with excitability, excitability-associated disorders, and mye

162 d phase modulation of neuronal oscillations (excitability fluctuations) in auditory neurons and visua

163 Conversely, BLApn had reduced excitability following CTA.

164 Decoding network excitability from neural activity at modulator sites pre

165 stimulation (TMS) measures of corticospinal excitability, GABA(A) (short-interval intracortical inhi

166 l Ca(V)1.2 is essential for arterial myocyte excitability, gene expression and contraction.

167 ap (Dionaea muscipula) where fast electrical excitability has been described, this is most likely bas

168 t of native dopaminergic transmission on SPN excitability has not been directly demonstrated.

169 rlying OXTR-induced facilitation of neuronal excitability have not been determined.

170 Targeting circuit excitability in a focal, modular manner may prove to be

171 e recovery in rodents and increased cortical excitability in a transcranial magnetic stimulation stud

172 AChR binding across A1 layers; and (3) nAChR excitability in A1 layer (L) 5 cells.

173 MDARs in patients with depression may reduce excitability in A25, mimicking the effects of the neurot

174 nd rescue the phenotype of increased network excitability in acute hippocampal slices from the Mecp2

175 ssium current, resulting in reduced neuronal excitability in all major types of ovBNST neurons.

176 can normalize tonic inhibition and intrinsic excitability in CA1 pyramidal neurons, and rescue the ph

177 annels are critical determinants of membrane excitability in cells throughout the body, including tha

178 onstrating a causative role of visual cortex excitability in controlling visual imagery.

179 te that cerebellar Purkinje cells upregulate excitability in delay eye-blink conditioning, a form of

180 ion at specific sites alters Nav1.6-mediated excitability in dorsal root ganglion neurons.

181 l findings; additionally, we observed higher excitability in epileptogenic regions, in agreement with

182 ions in membrane potential can also modulate excitability in important ways.

183 We show a testosterone-dependent lower excitability in male versus female vHPC-NAc neurons and

184 in bacteria and control membrane electrical excitability in mammals.

185 nd to disrupt glutamatergic transmission and excitability in networks that underlie sociability and a

186 hanism to modulate Nav activity and neuronal excitability in physiological and diseased conditions.

187 performance resulting from aberrant network excitability in psychiatric and neurological diseases, s

188 tocin receptors (OXTRs) facilitates neuronal excitability in rat lateral nucleus of central amygdala

189 s to a create transient increase of neuronal excitability in response to neurotransmitters through th

190 ay exert protective effects against damaging excitability in the aftermath of TBI and that treatment

191 wo other possible manifestations of rhythmic excitability in the beta band; windows of reduced respon

192 ng shows that intrinsic plasticity regulates excitability in the long term.SIGNIFICANCE STATEMENT Pla

193 Bidirectional manipulation of neuron excitability in the mPFC during the P2-P14 period had lo

194 Reduced intrinsic excitability in UBCs was partially compensated by suppre

195 ardless of mechanism, was associated with an excitability increase.

196 Reducing excitability increased early Purkinje cell survival.

197 terictal RS are associated with lower global excitability induced by a shift in the working point of

198 hannels, uniquely able to translate membrane excitability into the cytoplasmic Ca(2+) changes that un

199 IGNIFICANCE STATEMENT Plasticity of membrane excitability ("intrinsic plasticity") has been observed

200 It is generally thought that muscle excitability is almost exclusively controlled by current

201 s and kinetics than biological systems whose excitability is apparently more robust.

202 the TLR4-dependent early increase in dentate excitability is causally associated with epileptogenesis

203 This reduced excitability is correlated with shorter apical dendrites

204 is weight-driven modulation of corticospinal excitability is easily suppressed by the observer's expe

205 These findings show that excitability is enhanced in Purkinje cells after delay e

206 studies have highlighted that corticospinal excitability is increased during observation of object l

207 in a weight-specific fashion: Corticospinal excitability is larger when observing lifts of heavy obj

208 epend on intercellular coupling and cellular excitability is not fully understood.

209 ction of GluD1(R) as a regulator of neuronal excitability is proposed to be widespread in the nervous

210 rived phase diagram, where the phenomenon of excitability is reduced to two dimensions defined as com

211 ne data show that lower resting activity and excitability levels in early visual cortex (V1-V3) predi

212 NALCN-mediated currents regulate neuronal excitability linked to respiration, locomotion and circa

213 (LTF) and long-term enhancement of neuronal excitability (LTEE), two correlates of long-term memory

214 matches in the opposing actions on dendritic excitability may relate to these compounds' cell-type an

215 xpression, notably in regulators of neuronal excitability, metabolism, and inflammatory responses, al

216 Thus, SK2 plasticity and excitability modulation are essential for specific forms

217 us to detect specific consequences of absent excitability modulation.

218 By contrast, the general intrinsic excitability, morphology and gene-profiles of the two ty

219 imanual condition as changes in corticomotor excitability, mu (9-14 Hz), and beta (15-25 Hz) oscillat

220 Homeostatic changes of intrinsic excitability occurred at a fast timescale (1-4 h) and de

221 eteromeric nAChR receptor binding, and nAChR excitability of A1 L5 cells.

222 changes in synaptic plasticity and neuronal excitability of BLA neurons in vitro in the left and rig

223 excitation/inhibition balance and increases excitability of CA3 pyramidal neurons.

224 lts suggest that differential changes in the excitability of cerebellar neurons contribute to the dis

225 GABAergic and NPY signaling to regulate the excitability of circuits in the IC and auditory thalamus

226 ABA signaling within the striatum, and hyper-excitability of cortical sensorimotor regions that might

227 axons rapidly and persistently elevated the excitability of D1 receptor-expressing SPNs (D1-SPNs).

228 release persistently enhances the intrinsic excitability of direct pathway striatal neurons.

229 mediated by diminishing the disparity in the excitability of direct- and indirect-pathway SPNs in the

230 nese concentration-dependently increased the excitability of dopamine neurons, decreased the amplitud

231 However, the intrinsic excitability of Foxp2+ cortical neurons was lower in Fox

232 injury also dampened the intrinsic membrane excitability of mature DYN neurons, and reduced their ac

233 Enhancing excitability of mediodorsal thalamus, an associative str

234 lfactory bulb (OB) transiently inhibited the excitability of mitral/tufted cells (MTCs) that relay ol

235 In the mSOD1 model of ALS, the excitability of motoneurons is poorly controlled, oscill

236 Juvenile isolation led to both reduced excitability of mPFC->pPVT neurons and increased inhibit

237 c inhibition can differentially modulate the excitability of neuron subtypes according to variation i

238 mputational simulations predict an increased excitability of neurons carrying these mutations with di

239 different neuron models predict an increased excitability of neurons carrying these mutations, which

240 t growth factor 14 (FGF14) leads to impaired excitability of neurons in clinically relevant brain are

241 r and circuit levels suggesting that reduced excitability of orexin neurons affects behavior through

242 ory dysfunction with a profound reduction of excitability of PAG neurons.

243 n PDYN neurons in the CeA of either sex, but excitability of PDYN neurons was increased in male mice

244 c interneurons (INs) and decreased intrinsic excitability of postsynaptic Purkinje neurons (PNs) resu

245 f)/J (BTBR) mice, we revealed that increased excitability of presynaptic interneurons (INs) and decre

246 ain result, at least in part, from increased excitability of primary afferents that innervate the col

247 t this arrangement can be applied to measure excitability of sciatic nerves due to a stimulation of t

248 Activation of both currents increased the excitability of secretory pituitary cells, consistent wi

249 hR in mediating the effects of oAbeta(42) on excitability of specific populations of cholinergic neur

250 mune receptor Toll-like receptor 4 (TLR4) on excitability of the hippocampal dentate gyrus and epilep

251 typically unobserved, synapses, the overall excitability of the postsynaptic neuron, and how recentl

252 scovery of their importance in regulation of excitability opens new avenues for improved therapy for

253 ACC-projecting neurons showed no changes in excitability or CC input.

254 nticipation beyond general changes in neural excitability or readiness.SIGNIFICANCE STATEMENT Probabi

255 ot modulate corticospinal and sensory cortex excitability or sensorimotor integration.

256 because they are thought to regulate neural excitability over visual areas through inhibitory contro

257 nd highest stimulus information content near excitability peaks, an effect that increases with oscill

258 that a sequential spatiotemporal pattern of excitability propagates across M1 prior to the movement

259 h simulations that these adaptive changes in excitability provide memory on timescales ranging from m

260 otor performance and decreased intrinsic UBC excitability, reducing spontaneous action potential firi

261 Lastly, our model describes how cellular excitability regulates force development.

262 erentiation and revealed changes in neuronal excitability-related genes.

263 are poorly understood and whether human SAN excitability requires voltage-gated sodium channels (Nav

264 rect (iSPN) pathways, maintain low intrinsic excitability, requiring convergent excitatory inputs to

265 MS-driven changes in connectivity and causal excitability, resting fMRI and TMS/EEG were performed be

266 Equivalent enhancement of medial geniculate excitability robustly drove auditory cortical excitation

267 eveloping spinal networks operating in a low excitability state, we found that dopamine is primarily

268 ally and transiently increased Purkinje cell excitability, stunted process extension, impaired dendri

269 a occurred without altering intrinsic muscle excitability, such that myotonia triggered by firing of

270 aneous and muscle afferent inputs on face M1 excitability suggest they play separate functional roles

271 onstrated a state of diminished corticomotor excitability, suggesting a maladaptive supraspinal pain

272 in; however, its role in regulating neuronal excitability, synaptic function and brain disorders has

273 cesses related to neurodevelopment, neuronal excitability, synaptic function and the immune system in

274 II, a Ser/Thr protein kinase associated with excitability, synaptic plasticity, and excitability diso

275 w find a role for the APP family in neuronal excitability, synaptic plasticity, and memory in adultho

276 voltage-dependent manner to control neuronal excitability, taste signaling and pathologies of depress

277 ork analysis revealed a mechanism of network excitability that regulates when a sender stimulation si

278 on and brain repair, the changes in neuronal excitability that underlie stroke recovery, and the mole

279 he network exhibits hallmarks of biochemical excitability: the annihilation of oppositely directed wa

280 uggest that APP family may regulate neuronal excitability through Kv7 channels.

281 Astrocytes maintain neuronal excitability through regulation of extracellular ion con

282 gen, and progesterone-modulate and integrate excitability throughout gestation.

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

284 he spinal locomotor network requires greater excitability to produce backward locomotion compared wit

285 evolution from a spatially limited focus of excitability to recruitment of more complex mechanisms c

286 rcuit innervation profoundly dampens circuit excitability under normal conditions.

287 rther, electrically decreasing visual cortex excitability using tDCS increases imagery strength, demo

288 system that combines regulation of neuronal excitability via glutamate receptor function and neuroin

289 ates neuronal activity: control of intrinsic excitability via the regulation of potassium channel fun

290 he heavy intensity trial only, corticospinal excitability was reduced at the cortical (P = 0.020) and

291 cDCS-mediated changes in cortical excitability were measured in vitro in mouse motor corte

292 , synaptic plasticity, and alter hippocampal excitability when occurring during postnatal periods of

293 ncreases intercellular coupling and cellular excitability, which are the main targets of pharmaceutic

294 ongoing and evoked activity through cortical excitability, which fills the long-standing gap between

295 work stability balances moderately increased excitability, which promotes accelerated unfolding of a

296 ergic transmission potently increases D1-SPN excitability with a time course that could support subse

297 ppocampal neurons to drastically shift their excitability with small changes to their sodium currents

298 emperature dependent effects, with a fall in excitability with warming.

299 mp electrophysiology revealed an increase in excitability, with a shift from phasic to tonic action p

300 that Lm128C cells exhibit elevated membrane excitability, with biophysical properties closely resemb