ライフサイエンスコーパス: cortical excitability

1 trains inserted at different phases to probe cortical excitability.

2 s a homeostatic synaptic factor to stabilize cortical excitability.

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

4 er ischemia via augmentation of perilesional cortical excitability.

5 hodology, and relatively powerful effects on cortical excitability.

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

7 esting cortex did not significantly modulate cortical excitability.

8 alking induced a bidirectional modulation of cortical excitability.

9 ear whether tACS should increase or decrease cortical excitability.

10 ype-dependent tonic inhibition in regulating cortical excitability.

11 arietal cortex at parameters known to reduce cortical excitability.

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

13 antagonizing the effects of acetylcholine on cortical excitability.

14 antagonizing the effects of acetylcholine on cortical excitability.

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

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

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

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

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

20 opening new avenues for research into human cortical excitability.

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

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

23 as an important driving force of increasing cortical excitability.

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

25 ythmic structure acts to temporally organize cortical excitability.

26 the regulation of GABAergic transmission and cortical excitability.

27 a potential mechanism for D4 in stabilizing cortical excitability.

28 rably lessens seizure severity by decreasing cortical excitability.

29 sive brain stimulation technique to modulate cortical excitability.

30 paired in subjects showing markedly enhanced cortical excitability.

31 role of oscillatory activity in determining cortical excitability.

32 ric disorders associated with alterations in cortical excitability.

33 ding changes of intracortical inhibition and cortical excitability.

34 been successfully applied for modulation of cortical excitability.

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

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

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

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

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

40 Stimulation-generated cortical excitability alterations were monitored by tran

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

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

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

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

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

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

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

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

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

50 Transcranial magnetic stimulation cortical excitability and inhibition paradigms have been

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Alterations in cortical excitability are implicated in the pathophysiol

68 Rather, increased cortical excitability as depressive symptoms improve is

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Potentiation of cortical excitability consisted of an increased firing i

87 These findings indicate that cortical excitability constitutes an important mechanism

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

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

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

91 We probed cortical excitability directly in human occipital and pa

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

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

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

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

96 Reduced cortical excitability, fast feedforward inhibition, and

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

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

99 Here, we assessed cortical excitability from scalp electroencephalography

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Abnormal cortical excitability is evident in various movement dis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 The depression in cortical excitability that accompanies spreading acidifi

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

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

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

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

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

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

149 Cortical excitability variables, including short-interva

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

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

152 Cortical excitability was assessed by measuring the soma

153 Cortical excitability was assessed using motor threshold

154 Cortical excitability was assessed with motor threshold

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

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

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

158 That local visual cortical excitability was unchanged across drug conditio

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

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

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

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

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

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

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

166 Reducing cortical excitability with the metabotropic glutamate re

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

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