ライフサイエンスコーパス: cortical excitability

1 ythmic structure acts to temporally organize cortical excitability.

2 the regulation of GABAergic transmission and cortical excitability.

3 a potential mechanism for D4 in stabilizing cortical excitability.

4 rably lessens seizure severity by decreasing cortical excitability.

5 sive brain stimulation technique to modulate cortical excitability.

6 paired in subjects showing markedly enhanced cortical excitability.

7 lves similar alpha-mediated changes in focal cortical excitability.

8 role of oscillatory activity in determining cortical excitability.

9 ric disorders associated with alterations in cortical excitability.

10 ding changes of intracortical inhibition and cortical excitability.

11 been successfully applied for modulation of cortical excitability.

12 s a homeostatic synaptic factor to stabilize cortical excitability.

13 er ischemia via augmentation of perilesional cortical excitability.

14 hodology, and relatively powerful effects on cortical excitability.

15 ditory pathway, as well as in the control of cortical excitability.

16 esting cortex did not significantly modulate cortical excitability.

17 alking induced a bidirectional modulation of cortical excitability.

18 ype-dependent tonic inhibition in regulating cortical excitability.

19 arietal cortex at parameters known to reduce cortical excitability.

20 ng characteristics with PIDs and an index of cortical excitability.

21 antagonizing the effects of acetylcholine on cortical excitability.

22 antagonizing the effects of acetylcholine on cortical excitability.

23 in plays an important role in the control of cortical excitability.

24 e effect of higher per-dose pulse numbers on cortical excitability.

25 the hypothesis that the claustrum regulates cortical excitability.

26 ac effects originate from overall changes in cortical excitability.

27 dentified two sectors showing differences in cortical excitability.

28 the TMS-evoked potential (TEP), a measure of cortical excitability.

29 stimulus alpha amplitude, reflecting reduced cortical excitability.

30 Cl(-)](i) modulation with complex effects on cortical excitability.

31 power (8-13 Hz), a well-established proxy of cortical excitability.

32 and in neurological conditions that increase cortical excitability.

33 ffective doses for decreasing and increasing cortical excitability.

34 te probably indicating highest alertness and cortical excitability.

35 s is generally interpreted as an increase in cortical excitability.

36 nd anterior) characterized by differences in cortical excitability.

37 ets, consistent with an increase in auditory cortical excitability.

38 ilitation but not pulsed inhibition of motor cortical excitability.

39 of activating the motor system and affecting cortical excitability.

40 halography is a powerful tool to probe human cortical excitability.

41 rt of the volley is sensitive to superficial cortical excitability.

42 trains inserted at different phases to probe cortical excitability.

43 area does not always give the same change in cortical excitability.

44 howed equal, if not greater effects in motor-cortical excitability.

45 ear whether tACS should increase or decrease cortical excitability.

46 ures then spikes may be useful biomarkers of cortical excitability.

47 gic or dopaminergic systems, or reduction of cortical excitability.

48 applies mA currents at the scalp to modulate cortical excitability.

49 eached human cortex to impose an increase in cortical excitability.

50 (fixed latency of 167 ms) had no effects on cortical excitability.

51 opening new avenues for research into human cortical excitability.

52 ts a homeostatic role of sleep, to rebalance cortical excitability.

53 (PMEPs) to single-pulse TMS as a measure of cortical excitability.

54 as an important driving force of increasing cortical excitability.

55 luding (1) reduced D2-mediated regulation of cortical excitability, (2) reduced responsivity of corti

56 elop in the cell cortex in a process termed "cortical excitability."(3-7) In developing frog and star

57 hand, would act as a positive stimulator of cortical excitability (30% increase) to all D2-receptor

58 This is made possible in part by cortical excitability, a behavior driven by coupled posi

59 t study has identified a distinct pattern of cortical excitability across cognitive phenotypes in ALS

60 correlated with the iTBS-induced increase in cortical excitability across subjects.

61 nal factors are involved in the cyclicity of cortical excitability across the menstrual cycle.

62 There are changes in cortical excitability after stroke that may provide the

63 static increase in net synaptic strength and cortical excitability along with decreased inducibility

64 Stimulation-generated cortical excitability alterations were monitored by tran

65 ation of visual hallucinations by increasing cortical excitability and altering visual-evoked cortica

66 s used, subthreshold cathodal tACS decreased cortical excitability and anodal tACS increased excitabi

67 pha-band oscillations are thought to reflect cortical excitability and are therefore ascribed an impo

68 between ongoing and evoked activity through cortical excitability and argue that the co-emergence of

69 1) of 16 healthy subjects by probing cortico-cortical excitability and behavior.

70 owband oscillations is often correlated with cortical excitability and can relate to the timing of sp

71 ously identified through fMRI, measuring its cortical excitability and causal connectivity to downstr

72 lation (TMS) provides valuable insights into cortical excitability and connectivity but faces challen

73 tes a powerful tool to directly assess human cortical excitability and connectivity.

74 hts and subjects and provides a blueprint of cortical excitability and connectivity.

75 hese dynamic rhythms are thought to regulate cortical excitability and coordinate network interaction

76 r cortex (M1) as a probe to index changes of cortical excitability and delivered M1 tACS at 10 Hz (al

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

78 s a 'virtual-lesion' transiently suppressing cortical excitability and disrupting swallowing behaviou

79 bo) on both alpha oscillations that regulate cortical excitability and early visual-evoked P1 and N17

80 vasively measure causal and acute changes in cortical excitability and evaluated this neural response

81 ed as a delayed treatment, to safely correct cortical excitability and facilitate sensorimotor recove

82 ) to test for dose-dependent iTBS effects on cortical excitability and functional connectivity (four

83 anial magnetic stimulation (TMS) measures of cortical excitability and GABA synaptic activity in the

84 asive brain stimulation technique, modulates cortical excitability and has shown promise in improving

85 ay serve a critical role in modulating motor cortical excitability and hence represent a promising ta

86 o-occipital alpha rhythms (8-12 Hz) underlie cortical excitability and influence visual performance.

87 hibition; that is, the phasic suppression of cortical excitability and information processing once pe

88 Transcranial magnetic stimulation cortical excitability and inhibition paradigms have been

89 attributable to polarity-specific shifts in cortical excitability and instead propose a more complex

90 direct current stimulation (tDCS) modulates cortical excitability and is being used for human studie

91 cations for understanding the foundations of cortical excitability and its monitoring in conditions l

92 rive appear to mediate the increase in motor cortical excitability and largely, but not exclusively,

93 nses revealed a mismatch between measures of cortical excitability and motor output within 60 min aft

94 effects of somatosensory afferent inputs on cortical excitability and neural plasticity often used t

95 at these effects could contribute to altered cortical excitability and oscillatory activity previousl

96 sess neurophysiological changes in precuneus cortical excitability and oscillatory activity.

97 We used TMS to quantify motor cortical excitability and physiological inhibition for e

98 sity for contagious yawning is determined by cortical excitability and physiological inhibition in th

99 By contrast, TMS measures of cortical excitability and physiological inhibition were

100 otal noninvasive technique for investigating cortical excitability and plasticity across the lifespan

101 attention, and learning by slowly modulating cortical excitability and plasticity.

102 that the slow potentials reflect changes in cortical excitability and shed light on neuronal substra

103 e cardiac and respiratory cycle can modulate cortical excitability and so affect awareness.

104 upport a role for oscillations in regulating cortical excitability and suggest a plausible mechanism

105 an operant sensory discrimination increased cortical excitability and target selectivity.

106 NT Sleep is thought to globally downregulate cortical excitability and, concurrently, to upregulate s

107 e, non-invasive method of probing changes in cortical excitability and/or connectivity.

108 highest heart rate (and presumably alertness/cortical excitability) and correlates with detection per

109 ults demonstrate that the crucial factor for cortical excitability, and basic brain function in gener

110 el molecular pathway by which tDCS modulates cortical excitability, and indicate a capacity for syner

111 ent (I(M), Kv7) is an important regulator of cortical excitability, and mutations in these channels c

112 ded by few tens of milliseconds increases of cortical excitability, and that the 1- to 10-Hz rhythmic

113 While motor cortical excitability appeared insensitive to prospectiv

114 Normal menstrual cycle variations in cortical excitability are altered in a similar pattern i

115 ce that large-scale, propagating patterns of cortical excitability are behaviorally relevant and may

116 alpha-band activity, so that the changes in cortical excitability are focused over the time interval

117 Alterations in cortical excitability are implicated in the pathophysiol

118 Thus, anteroposterior differences in cortical excitability are paralleled by differences in F

119 working memory and attention, which rely on cortical excitability, are impaired during sleep depriva

120 ential advantages that arise from the use of cortical excitability as a signaling mechanism to regula

121 Rather, increased cortical excitability as depressive symptoms improve is

122 sociodemographic and clinical variables with cortical excitability as indexed by transcranial magneti

123 ) or decrease (long-term depression-like) of cortical excitability as measured by motor evoked potent

124 ses of intermittent TBS (iTBS) (1) increases cortical excitability as measured by motor-evoked potent

125 apt their functional properties to normalize cortical excitability as the disease progresses.

126 s are potential candidates for dysregulating cortical excitability as they display altered action pot

127 n dose-dependent effects at the local level (cortical excitability) as well as at a systems level (fu

128 Diminished motor cortical excitability, as a measurement of increased res

129 We demonstrated a correlation between cortical excitability, as assessed by the slope of the T

130 IL-1ra), and correlated cytokine levels with cortical excitability assessed in MS patients by means o

131 studies have identified distinct changes of cortical excitability associated with specific epilepsy

132 ed changes in the serotonergic regulation of cortical excitability at a time of extensive synaptic de

133 ) of human primary motor cortex (M1) changes cortical excitability at the site of stimulation and at

134 P component may serve as an index of current cortical excitability at the time of stimulation.

135 l magnetic stimulation as a measure of motor cortical excitability before and after each plasticity i

136 Because crossmodal phase-resetting increases cortical excitability before sensory input arrives, thes

137 Data suggest that slow rTMS reduces cortical excitability, both locally and in functionally

138 guing knee-extension exercise enhances motor cortical excitability but compromises motoneuronal excit

139 mma oscillations is not merely a function of cortical excitability, but also depends on the relative

140 human participants, we tracked instantaneous cortical excitability by inferring the magnitude of exci

141 ctive brain stimulation modality that alters cortical excitability by passing a small, constant elect

142 rred modality stimuli could "modulate" local cortical excitability by phase reset of ongoing oscillat

143 Rebalancing cortical excitability by rTMS appears critical for plast

144 III), and electrophysiological evaluation of cortical excitability by TMS.

145 esting motor thresholds-a typical measure of cortical excitability-by applying transcranial magnetic

146 ghly sensitive recurrent inhibitory circuit, cortical excitability can be modulated by one pyramidal

147 results indicate that spontaneous changes in cortical excitability can have profound consequences for

148 ave demonstrated the absence of ipsilesional cortical excitability change after diabetic strokes, sug

149 Potentiation of cortical excitability consisted of an increased firing i

150 These findings indicate that cortical excitability constitutes an important mechanism

151 In addition, the time course of cortical excitability correlates with changes in EEG syn

152 adults, and that age-related enhancement of cortical excitability correlates with degradation of tac

153 rgic enhancement both modulated pre-stimulus cortical excitability, cue- and stimulus-evoked sensory

154 s show that administration of IL-6 increases cortical excitability, culminating in epileptiform disch

155 long-term depression (LTD)-like reduction of cortical excitability (DCS-LTD), which has been tested i

156 Fluctuations of cortical excitability demonstrated long-range temporal d

157 We probed cortical excitability directly in human occipital and pa

158 ults suggest that sleep deprivation upscales cortical excitability due to enhanced glutamate-related

159 Despite highly similar effects on cortical excitability during and after stimulation, cort

160 Outcomes reveal an enhanced cortical excitability during chronic exposure to HIV-1 p

161 llations (a state characterized by increased cortical excitability during NREM sleep), affective upda

162 ironment, electrical stimulation to increase cortical excitability during training, and drugs to opti

163 er, reflect a single, general fluctuation in cortical excitability (e.g., in the alpha band).

164 Here, we propose that cortical excitability explains several important yet poo

165 induced the greatest increase on pharyngeal cortical excitability (F(1,13) = 21.244; P < 0.001).

166 Reduced cortical excitability, fast feedforward inhibition, and

167 ance (OD) shifts through biphasic changes in cortical excitability, first decreasing responsiveness t

168 l axons using LM stimulation] and changes in cortical excitability following iTBS, confirming previou

169 AP-LM latencies featured larger increases in cortical excitability following iTBS.

170 We evaluated cortical excitability following single-pulse TMS, and co

171 ests that strong static magnets can modulate cortical excitability for a limited period of time.

172 prospective loss, temporal features of motor cortical excitability for prospective gains were modulat

173 Here, we assessed cortical excitability from scalp electroencephalography

174 Specifically, trial-to-trial fluctuations in cortical excitability have been linked to fluctuations i

175 tagonism does not lead directly to increased cortical excitability hours later and thus might not be

176 n cause transient or long-lasting changes in cortical excitability; however, variable results across

177 ke, we showed that inhibition of LPA-related cortical excitability improved stroke outcome.

178 nd electroencephalographic (EEG) measures of cortical excitability in 18 healthy young adults in a ra

179 of a focal intracerebral hemorrhage (ICH) on cortical excitability in a remote, functionally connecte

180 ved stroke recovery in rodents and increased cortical excitability in a transcranial magnetic stimula

181 ect upper motor neuron damage and to explore cortical excitability in amyotrophic lateral sclerosis,

182 lement of the underlying modulation of local cortical excitability in both cases.

183 has been previously shown to modulate visual cortical excitability in both healthy individuals and av

184 overlapping functions have been ascribed to cortical excitability in cell division: control of cell

185 These results suggest an increased cortical excitability in female mice that may be indepen

186 elective alpha5-GABAAR antagonist, increases cortical excitability in healthy human subjects, as indi

187 e brain stimulation technique that can alter cortical excitability in human subjects for hours beyond

188 asive technique to induce offline changes in cortical excitability in human volunteers.

189 succession, is a useful tool to investigate cortical excitability in humans.

190 ness of these intrinsic measures to quantify cortical excitability in humans.

191 functions by modulating neuroplasticity and cortical excitability in nonsmoking subjects.

192 ggests that distinct frequencies may reflect cortical excitability in occipital versus posterior pari

193 ether, these results suggest that changes in cortical excitability in opposite directions lead to cor

194 me success in demonstrating abnormalities of cortical excitability in patients with FNS, particularly

195 within the SMA are inversely correlated with cortical excitability in primary motor cortex and are pr

196 lor synesthesia is characterized by enhanced cortical excitability in primary visual cortex and the r

197 e combined TMS-EEG to examine alterations in cortical excitability in response to pain.

198 study provides further evidence of enhanced cortical excitability in subjects with photosensitivity,

199 ed animals, VTA stimulation did not increase cortical excitability in the cocaine group.

200 electrocorticography demonstrates increased cortical excitability in the glioma-infiltrated brain.

201 the present study was to investigate in vivo cortical excitability in the human brain.

202 While vibration had little effect on cortical excitability in WC, it strongly reduced SICI in

203 determine menstrual cycle-related changes in cortical excitability in women with and without catameni

204 ains may not be sufficient to modulate local cortical excitability indexed by typical TEP amplitude m

205 ts indicate that spontaneous fluctuations in cortical excitability, indicated by patterns of prestimu

206 Spontaneous fluctuations in cortical excitability influence sensory processing and b

207 ta suggest a neurophysiological mechanism of cortical excitability involved in controlling the streng

208 We recently showed that diminished motor cortical excitability is associated with high levels of

209 Cortical excitability is best known for promoting cell p

210 other disorders where regional depression of cortical excitability is desirable.

211 Abnormal cortical excitability is evident in various movement dis

212 -7) In developing frog and starfish embryos, cortical excitability is generated through coupled posit

213 has recently become apparent, however, that cortical excitability is involved in the response of the

214 of cognition involves a circadian impact on cortical excitability is unknown.

215 edict its detection, further suggesting that cortical excitability level may mediate target detection

216 tory GABAergic neural populations in scaling cortical excitability levels, as reflected in TEP wavefo

217 , FN stimulation, which can otherwise modify cortical excitability, may alter the development of PIDs

218 udied how TRPV1 genetic polymorphisms affect cortical excitability measured with transcranial magneti

219 on vs overnight sufficient sleep affects (a) cortical excitability, measured by transcranial magnetic

220 thod of analysis shows that changes in motor cortical excitability mediating the initiation of moveme

221 -invasive brain stimulation to enhance motor cortical excitability, motoneuronal output and, ultimate

222 Because of its potential to modulate cortical excitability noninvasively, tDCS has been teste

223 ion significantly correlated with changes in cortical excitability observed following iTBS: subjects

224 rect current stimulation (tDCS) can increase cortical excitability of a targeted brain area.

225 the overall reported sensory sensitivity and cortical excitability of individuals.

226 We studied whether the different cortical excitability of these two regions reflected dif

227 findings support the idea that tACS affects cortical excitability only during online application, at

228 how MRS-assessed measures of GABA relate to cortical excitability or GABAergic synaptic activity.

229 TBS on EBCC were not due to changes in motor cortical excitability or sensory disturbance caused by c

230 c stimulation, known to transiently suppress cortical excitability, over the right dorsolateral prefr

231 , hereafter D/+) produces a similar compound cortical excitability phenotype.

232 Differences in the state of cortical excitability predicted perceptual outcomes (pho

233 We sought to characterize the cortical excitability profile of a developmental form of

234 onditions characterized by aberrant regional cortical excitability referable to mGluR5-mTOR signaling

235 uggests that this involves the regulation of cortical excitability (reflected in prestimulus alpha os

236 ioral implications of age-related changes of cortical excitability remain elusive.

237 ophysiological results showed that precuneus cortical excitability remained unchanged after 24 weeks

238 xons and their terminals) mediate changes in cortical excitability remains unaddressed.

239 pecific role of microglia in disease-related cortical excitability remains unknown.

240 coil orientations and in different states of cortical excitability (rest vs muscular contraction).

241 ired motoneuronal excitability but not motor cortical excitability, resulting in an overall depressio

242 This phenomenon, termed cortical excitability, results from coupled positive and

243 Our MMP assay shows that the depressed cortical excitability seen in the contralateral SI corte

244 alpha rhythm may serve as a general index of cortical excitability.SIGNIFICANCE STATEMENT Alpha-band

245 subthreshold tACS will increase or decrease cortical excitability.SIGNIFICANCE STATEMENT Transcrania

246 n (TMS) requires real-time identification of cortical excitability states.

247 essed the role of the Rho GAP RGA-3/4 in the cortical excitability that accompanies cytokinesis in bo

248 The depression in cortical excitability that accompanies spreading acidifi

249 Data reveal robust circadian dynamics of cortical excitability that are strongest in those indivi

250 to an overall influence of L6CT feedback on cortical excitability that could have profound implicati

251 ons, could induce the increased sensorimotor cortical excitability that eventually causes cortical my

252 netic stimulation (rTMS), induces changes in cortical excitability that last beyond stimulation.

253 m ( approximately 23 ms) intervals increased cortical excitability that lasted for up to 45 min, wher

254 tempt by A1 to sustain an operative level of cortical excitability that may involve homeostatic mecha

255 ic stimulation designed to induce changes of cortical excitability that outlast the period of TBS app

256 -, phase- and frequency-dependent effects on cortical excitability, the offline effects (i.e. after-e

257 clerosis (ALS) is characterised by increased cortical excitability, thought to reflect pathological c

258 f fast-spiking GABAergic cells that regulate cortical excitability through direct innervations onto t

259 nduced cortical hyperexcitability, restoring cortical excitability to control levels.

260 first evidence that TRPV1 channels regulate cortical excitability to paired-pulse stimulation in hum

261 To link the age-related increase of cortical excitability to perceptual changes, we measured

262 how that observers can intentionally control cortical excitability to strategically bias evidence acc

263 r neuron disease behavior scale (MiND-B) and cortical excitability using transcranial magnetic stimul

264 Cortical excitability variables, including short-interva

265 ely to be mediated by increased perilesional cortical excitability via chronic activation of the dent

266 measures design, monitoring changes in motor-cortical excitability via transcranial magnetic stimulat

267 Cortical excitability was assessed by measuring the soma

268 Starting one week after treatment, cortical excitability was assessed ex vivo.

269 Cortical excitability was assessed using motor threshold

270 Cortical excitability was assessed with motor threshold

271 The net effect on cortical excitability was evaluated by measuring the eff

272 Conversely, depression of cortical excitability was evidenced by an augmented firi

273 In controls, cortical excitability was greatest in the follicular stu

274 That local visual cortical excitability was unchanged across drug conditio

275 Similar nonuniform cDCS aftereffects on cortical excitability were also found in human neocortex

276 PAS-induced changes in cortical excitability were assessed using motor-evoked p

277 cDCS-mediated changes in cortical excitability were measured in vitro in mouse mo

278 State-dependent changes in cortical excitability were traced by simultaneously reco

279 ctivation specifically reduces visual motion cortical excitability, whereas other visual cortical reg

280 ked the effects elicited by the paw pinch on cortical excitability, whereas systemic administration o

281 ality in ongoing and evoked activity through cortical excitability, which fills the long-standing gap

282 ow-up was associated with a normalization of cortical excitability, which in turn suggests an alterat

283 Prolonged wakefulness alters cortical excitability, which is essential for proper bra

284 a further increase of the cerebello-thalamo-cortical excitability, which is maintained after theta-b

285 e measurement of movement-related changes in cortical excitability, which may be used to resolve ambi

286 so thought to be accompanied by increases in cortical excitability, which may differentially alter se

287 itude subthreshold E-fields able to increase cortical excitability with minimal sensation.

288 have been no previous studies investigating cortical excitability with particular regard to intracor

289 Reducing cortical excitability with the metabotropic glutamate re

290 Here we measured motor cortical excitability with transcranial magnetic stimula

291 t 2.0 and 3.5 kHz resulted in an increase in cortical excitability, with Experiments 2 and 3 providin

292 d that correlated with an increment in motor cortical excitability within the affected hemisphere, ex

293 er infusion (responders) exhibited increased cortical excitability within this antidepressant respons