ライフサイエンスコーパス: intracortical

1 nts developed new cortical lesions per year (intracortical, 1.3 +/- 1.7 vs leukocortical, 0.7 +/- 1.9

2 Here, we show that intracortical administration of NR but not NAD(+) reduce

3 ncreased postsynaptic activity of long-range intracortical afferents or scaling K(+) leak current, bu

4 These findings reveal intracortical anatomical changes in cellular layers of t

5 discharges induced in the limbic network by intracortical and brief arterial infusions of either bic

6 al circuits, they assist in consolidation of intracortical and extracortical circuits.

7 s of synapse formation, and establishment of intracortical and intercortical connections.

8 In patients, T2* in intracortical and leukocortical lesions was increased co

9 ing is associated with neural adaptations in intracortical and reticulospinal circuits, whereas corti

10 al only seizures when compared to those with intracortical and scalp seizures (50% and 25% death or s

11 l neurons are essential components of local, intracortical and subcortical circuits and are specified

12 evoked potentials (MEPs) and the activity in intracortical and subcortical pathways targeting an intr

13 Differential myelination between intracortical and subjacent white matter can be approxim

14 ses, possibly related to differences between intracortical and subjacent white matter myelination, an

15 in surgical epilepsy patients to measure the intracortical and thalamic generators of the alpha rhyth

16 How they are integrated into intracortical and thalamo-cortico-thalamic circuits is i

17 suggesting different connectivity models for intracortical and thalamocortical circuits.

18 Intracortical and WM injury are concomitant pathologic p

19 reduction in the vessel wall pulsatility of intracortical arterioles and widespread loss of perivasc

20 post-training disruption of piriform cortex intracortical association fiber synapses, hypothesized t

21 ulate incoming sensory information via their intracortical axons targeting the major thalamorecipient

22 Here we report a high-performance intracortical BCI (iBCI) for communication, which was te

23 an primates during online cursor control via intracortical BCIs in the presence of severe and abrupt

24 er, current research into the development of intracortical BMIs has focused on subjects with largely

25 ed using his own cortical signals through an intracortical brain-computer interface (iBCI).

26 n they are used in closed-loop as part of an intracortical brain-computer interface (iBCI).

27 We employed a closed-loop intracortical brain-computer interface learning paradigm

28 veraged these results to create a whole-body intracortical brain-computer interface that spreads targ

29 Hybrid kinetic and kinematic intracortical brain-computer interfaces (iBCIs) have the

30 The efficacy of wireless intracortical brain-computer interfaces (iBCIs) is limit

31 anisms of learning and its limits in a human intracortical brain-machine interface (BMI) paradigm.

32 Intracortical brain-machine interfaces (BMIs) aim to res

33 Intracortical brain-machine interfaces (BMIs) may eventu

34 High ACh levels depress intracortical but facilitate thalamocortical synapses, w

35 Moreover, elevated osteoclasts and intracortical/calvarial porosity is exacerbated by overe

36 hanced tomography we show exemplar data with intracortical capillaries uncovered at sub-micrometre le

37 onal covariance analysis revealed that these intracortical changes contributed to a gradual different

38 We found that intracortical cholinergic inputs to mouse visual cortex

39 ment takes place at both thalamocortical and intracortical circuit levels, but not at the thalamic ou

40 SPNs are an integral part of the developing intracortical circuitry and thereby can sculpt thalamoco

41 required for the developmental refinement of intracortical circuitry or whether this maturation is gu

42 orward inhibition, in concert with recurrent intracortical circuitry, produces tactile suppression.

43 and CMEPs, respectively) and the activity in intracortical circuits (suppression of voluntary electro

44 evoked potentials (MEPs) and the activity in intracortical circuits (suppression of voluntary electro

45 Because during development intracortical circuits are spontaneously active, our res

46 r PAS25 alone, MEP amplitude increased while intracortical circuits did not change.

47 bate is centered over whether feedforward or intracortical circuits generate SM, and whether this res

48 tial (MEP) amplitude, recruitment curve, and intracortical circuits including short-interval intracor

49 ural field simulations based on a scaling of intracortical circuits reproduce our empirical observati

50 We optogenetically silenced intracortical circuits to isolate thalamic inputs to lay

51 g involve adaptations in the RST, as well as intracortical circuits within M1.

52 and differential recruitment by afferent vs. intracortical circuits, dependent on cell class--suggest

53 ere no specific changes in motor thresholds, intracortical circuits, or recruitment curves.

54 interhemispheric projections between S1s and intracortical circuits, probably from somatosensory and

55 fect produced by PAS10 with little change in intracortical circuits.

56 ntaneous activity within thalamocortical and intracortical circuits.

57 defects in axonal growth and in ipsilateral intracortical-collateral formation.

58 mediated by orientation-specific changes in intracortical connections and further improvement of tha

59 were generated to provide an overview of all intracortical connections and subnetwork clusterings.

60 inputs were unaltered by DE, whereas lateral intracortical connections in L2/3 were strengthened, sug

61 Previous studies of intracortical connections in mouse visual cortex have re

62 e we show that the excitatory and inhibitory intracortical connections to a layer 2/3 neuron accord w

63 A total of 240 intracortical connections were manually reconstructed wi

64 al cortex (V1) of awake monkeys to show that intracortical connections within V1 can solve this issue

65 bition; and (4) simple spatial properties of intracortical connections.

66 ss of thalamic and a concomitant increase in intracortical connectivity.

67 rganization of thalamocortical and recurrent intracortical connectivity.

68 , with 42.9% of these seizures noted only on intracortical depth EEG and in some cases lasting for ma

69 prospective multicenter study of surface and intracortical depth electroencephalography (EEG) was per

70 nitoring, including invasive measurements of intracortical (depth) EEG (dEEG), partial pressure of ox

71 Intracortical disinhibition, but not thalamocortical dis

72 ents whose scans suffered signal loss due to intracortical electrodes.

73 well as its ease of implantation compared to intracortical electrophysiology, larger cortical coverag

74 imary visual cortex (V1) using fMRI (7T) and intracortical electrophysiology.

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

76 ls, underlying which are well-matched purely intracortical excitation and inhibition.

77 Moreover, the weight of intracortical excitation around the optimal frequency wa

78 t was slightly elongated and was expanded by intracortical excitation in an approximately proportiona

79 trengthened, resulting in a dominant role of intracortical excitation in defining the total excitator

80 mic inputs to layer 4 neurons and found that intracortical excitation linearly amplified thalamocorti

81 optimal-frequency-selective strengthening of intracortical excitation plays a dominant role in the re

82 Attenuation of ascending sensory, but not intracortical, excitation leads to axo-dendritic morphol

83 However, our understanding of intracortical excitatory and inhibitory synaptic inputs

84 Thus, intracortical excitatory circuits faithfully reinforce t

85 We found that intracortical excitatory circuits preserved the orientat

86 We silenced intracortical excitatory circuits with optogenetic activ

87 apses accompanied by a transient increase in intracortical excitatory connections.

88 ons, which also receive temporally prolonged intracortical excitatory input as well as feedforward in

89 the tuning shape of both thalamocortical and intracortical excitatory inputs to a L4 neuron became sh

90 with a reduction in the strength of lateral intracortical excitatory inputs to A1-L2/3.

91 genetically isolated the thalamocortical and intracortical excitatory inputs to individual layer 4 ne

92 thin PV interneurons to restrict the loss of intracortical excitatory synaptic input following MD in

93 inhibition was accompanied by an increase in intracortical facilitation (P < .01) and motor-evoked po

94 and adolescents is associated with increased intracortical facilitation and excessive glutamatergic a

95 Intracortical facilitation and long-term potentiation-li

96 pressed patients had significantly increased intracortical facilitation at interstimulus intervals of

97 osite was seen in women with epilepsy, where intracortical facilitation was greatest and intracortica

98 was greatest in the follicular study, where intracortical facilitation was increased (p<0.05).

99 ng-interval intracortical inhibition (LICI), intracortical facilitation, and short-latency afferent i

100 ortical inhibition, accompanied by increased intracortical facilitation, indicating cortical hyperexc

101 val intracortical inhibition and increase of intracortical facilitation, suggesting a shift toward co

102 short-interval intracortical inhibition and intracortical facilitation.

103 ativity, caused by either thalamocortical or intracortical fast AMPA-receptor excitation, leads to mo

104 lity of the corticocortical axons and normal intracortical gamma-aminobutyric acid inhibition in cont

105 Finally, we identified a possible intracortical homolog of the "object-related negativity"

106 conduit were inserted in the vicinity of an intracortical human U87MG glioblastoma xenograft, a sign

107 Cortical GM lesions were classified as intracortical (IC, only involving GM) and leucocortical

108 The intracortical implant occurred on Dec 1, 2014, and we ar

109 r microarrays that can be used as monolithic intracortical implants, fabricated from an optically tra

110 tracortical inhibition (SICI), long-interval intracortical inhibition (LICI), intracortical facilitat

111 confirmed by the reduction of long-interval intracortical inhibition (p = 0.002).

112 y and GABA-A-receptor mediated short-latency intracortical inhibition (SICI) at rest during spontaneo

113 been well demonstrated using short-interval intracortical inhibition (SICI) by transcranial magnetic

114 xamine inhibition by means of short-interval intracortical inhibition (SICI) of the contralateral pri

115 ls, input-output (IOcurve) and short-latency intracortical inhibition (SICI) recruitment curves, as w

116 After acute stroke, short-interval intracortical inhibition (SICI) was reduced over both mo

117 nial magnetic stimulation and short-interval intracortical inhibition (SICI) were recorded before and

118 racortical circuits including short-interval intracortical inhibition (SICI), long-interval intracort

119 asured the effects of a CS on short-interval intracortical inhibition (SICI).

120 hreshold, input/output curve, short interval intracortical inhibition and cortical silent period.

121 US increased GABA(A)-mediated short-interval intracortical inhibition and decreased reaction time on

122 active motor thresholds, and short-interval intracortical inhibition and facilitation.

123 onstrated by the reduction of short-interval intracortical inhibition and increase of intracortical f

124 magnitude and time course of short-interval intracortical inhibition and intracortical facilitation.

125 e demonstrate increased active long-interval intracortical inhibition and prolonged cortical silent p

126 ures probably involving GABAB (long-interval intracortical inhibition and the cortical silent period)

127 ng tasks induced a reduction in motor cortex intracortical inhibition but did not modulate corticospi

128 It is concluded that a model based on intracortical inhibition can account well for the known

129 Intracortical inhibition decreased and F-wave amplitude

130 Intracortical inhibition decreased during precision grip

131 hase of the response, as a signature of fast intracortical inhibition detectable with VSD imaging, in

132 A transporter expression, these findings put intracortical inhibition forward as an important regulat

133 essing to dynamic changes in the strength of intracortical inhibition from parvalbumin-expressing (PV

134 Since GABAA-mediated intracortical inhibition has been shown to underlie plas

135 ed cortical silent period and short-interval intracortical inhibition in both groups receiving real r

136 etween signs of spasticity and long-interval intracortical inhibition in patients with SCI.

137 Further, there was increased intracortical inhibition in primary motor cortex under h

138 on of corticospinal axons and short-interval intracortical inhibition in the first dorsal interosseou

139 Interhemispheric inhibition between S1s and intracortical inhibition in the S1 modulated the amplitu

140 red pulse paradigms: short and long interval intracortical inhibition in the same hand muscle as abov

141 The magnitude of short-interval intracortical inhibition increased in controls but not i

142 his result suggests that a potential role of intracortical inhibition is to reduce information redund

143 The essence of the model is that intracortical inhibition of a direction-selective cell i

144 excitability but did not change motor cortex intracortical inhibition or sensorimotor integration.

145 was measured with cortical silent period and intracortical inhibition paradigms.

146 n increased the amplitude of the P25/N33 and intracortical inhibition reduced the amplitude of the P2

147 There was less intracortical inhibition targeting the first dorsal inte

148 The reduction of short-interval intracortical inhibition was accompanied by an increase

149 Short-interval intracortical inhibition was decreased during voluntary

150 intracortical facilitation was greatest and intracortical inhibition was least in the luteal studies

151 Intracortical inhibition was more reduced during power g

152 Notably, intracortical inhibition was more reduced during power g

153 In secondary dystonia short interval intracortical inhibition was reduced on the affected sid

154 Mean (SD) short-interval intracortical inhibition was significantly reduced in pa

155 ched controls, whereas resting long-interval intracortical inhibition was unchanged.

156 To further examine the origin of changes in intracortical inhibition we assessed the contribution of

157 bition(,) 2.5 ms) and GABA(B) (long-interval intracortical inhibition(,) 150 ms) receptor activation

158 spinal excitability, GABA(A) (short-interval intracortical inhibition(,) 2.5 ms) and GABA(B) (long-in

159 cal silent period) and GABAA (short-interval intracortical inhibition) receptors, which are inhibitor

160 1s (interhemispheric inhibition) and within (intracortical inhibition) the iS1 at rest and during ton

161 In addition, (1) short-interval intracortical inhibition, (2) nonlinear complexity of th

162 ot occur in adolescence because of increased intracortical inhibition, a phenotype that was mimicked

163 Short-interval intracortical inhibition, a TMS-EMG measure of synaptic

164 matic reduction or absence of short interval intracortical inhibition, accompanied by increased intra

165 l excitability as assessed by short-interval intracortical inhibition, and sensorimotor interaction,

166 A startle cue decreased intracortical inhibition, but not CMEPs, during power gr

167 matic carriers, a decrease in short-interval intracortical inhibition, compared to presymptomatic car

168 Intracortical inhibition, elicited by paired stimuli, in

169 tributed this functional decline to weakened intracortical inhibition, especially GABAergic inhibitio

170 Intracortical inhibition, in the motor cortex where iMEP

171 nscranial magnetic stimulation, paired-pulse intracortical inhibition, spinal motor neuron excitabili

172 potentials were facilitated without changing intracortical inhibition, suggesting that the 5 kHz carr

173 tability variables, including short-interval intracortical inhibition, were measured in patients with

174 inhibition, as quantified by short interval intracortical inhibition.

175 d this positively correlated with changes in intracortical inhibition.

176 l-based learning tasks induced a decrease in intracortical inhibition.

177 ively, L3 neurons receive substantially more intracortical inhibition.

178 ity within cortical motor areas, and altered intracortical inhibition.

179 d this positively correlated with changes in intracortical inhibition.

180 .027) or the cortex of mice that received an intracortical injection of zymosan A (0.62 +/- 0.22 %ID/

181 rcase-reaching task and then received either intracortical injections of AAVshPTEN to delete PTEN or

182 In particular, the intracortical input became better tuned than thalamocort

183 to drive synaptic plasticity at thalamic and intracortical inputs onto L2 Pyr neurons.

184 ation and direction is thought to arise from intracortical inputs that are similarly selective(1-8).

185 shaped by a dense network of associative or intracortical inputs to piriform, which may enhance or c

186 forward (FF) processing and also strengthens intracortical inputs to primary visual cortex (V1).

187 that this form of plasticity is specific to intracortical inputs to V1 L2/3 neurons and depends on t

188 th feedforward thalamocortical and recurrent intracortical inputs, but how potential developmental ch

189 nsory cortices integrate thalamocortical and intracortical inputs.

190 tions suggests the involvement of long-range intracortical interactions in this D1 effect.

191 Intracortical interactions play a major role in all aspe

192 that Sip1 is essential for the formation of intracortical, intercortical, and cortico-subcortical co

193 e the chemotactic cytokine CXCL12 to promote intracortical interneuron migration and growth of thalam

194 ion of cortical output cells and the related intracortical interneuronal networks.

195 In patients, we measured, T2* in intracortical lesions and in the intracortical portion o

196 studies, we focused on mirror properties of intracortical LFPs recorded in the PMv and M1 hand regio

197 CBD abrogated the enhanced intracortical local field potential power, including the

198 ent-related potential (MRP), investigated as intracortical low-frequency LFP activity (<9 Hz), was mo

199 Intracortical M1 excitability was measured using paired

200 tructural magnetic resonance imaging maps of intracortical magnetization can be linked to both the be

201 uron resolution due to the scarcity of human intracortical measurements.

202 illation can be counteracted by compensatory intracortical mechanisms and that the sleep slow oscilla

203 l amplification and disamplification provide intracortical mechanisms for prioritization, Mather and

204 keys (Macaca mulatta) were implanted with an intracortical microelectrode array in the leg area of th

205 We used a chronically implanted intracortical microelectrode array to record multiunit a

206 He received two intracortical microelectrode arrays in the hand area of

207 s with amyotrophic lateral sclerosis who had intracortical microelectrode arrays placed in motor cort

208 Intracortical microelectrodes are being developed to bot

209 overed that rats with chronically indwelling intracortical microelectrodes exhibited up to an incredi

210 Intracortical microelectrodes have shown great success i

211 We implanted two 96-channel intracortical microelectrodes in the motor cortex of a 5

212 High-frequency, long-duration intracortical microstimulation (HFLD-ICMS) is increasing

213 he delivery of high-frequency, long-duration intracortical microstimulation (HFLD-ICMS) to primary mo

214 This study used intracortical microstimulation (ICMS) and electromyograp

215 ession of forelimb movement responses during intracortical microstimulation (ICMS) and movements of t

216 Intracortical microstimulation (ICMS) and recording of e

217 We addressed this knowledge gap using intracortical microstimulation (ICMS) concurrently with

218 sk-relevant sensory feedback was provided by intracortical microstimulation (ICMS) encoding egocentri

219 t mapped the M1 forelimb representation with intracortical microstimulation (ICMS) in male squirrel m

220 Consistent with this general function, intracortical microstimulation (ICMS) in the PM of suffi

221 Intracortical microstimulation (ICMS) is a powerful tool

222 Intracortical microstimulation (ICMS) of the primary som

223 Intracortical microstimulation (ICMS) of the somatosenso

224 Intracortical microstimulation (ICMS) studies have provi

225 ed circuit analysis combining layer-specific intracortical microstimulation (ICMS), CSD analysis, and

226 d smaller maps derived using high-resolution intracortical microstimulation (ICMS).

227 hing cortical areas of a "decoder" rat using intracortical microstimulation (ICMS).

228 ity coactivation by GCaMP3 were confirmed by intracortical microstimulation but were more difficult t

229 (RWA), based on its differential response to intracortical microstimulation compared with the caudal

230 We also found causal evidence that intracortical microstimulation during motor preparation

231 Here, we addressed this gap using intracortical microstimulation in a broad range of front

232 ortion of premotor and parietal cortex using intracortical microstimulation in anesthetized capuchin

233 Finally, intracortical microstimulation induces activation of onl

234 mals were randomly selected for perilesional intracortical microstimulation mapping and tissue sampli

235 inished as a result of NPT, as revealed with intracortical microstimulation mapping.

236 tact location, pressure, and timing--through intracortical microstimulation of primary somatosensory

237 to use an initially unfamiliar multichannel intracortical microstimulation signal, which provided co

238 We used paired-pulse protocols with intracortical microstimulation techniques in sedated fem

239 vement domains within M1, we used long-train intracortical microstimulation techniques to evoke movem

240 We used intracortical microstimulation to map motor cortex in tw

241 Intracortical microstimulation, Micro-PET and histologic

242 rats respond to both whisker deflection and intracortical microstimulation, suggesting that the infr

243 Using spatiotemporal patterns of intracortical microstimulation, we find that reaction ti

244 imb movements in motor cortex as assessed by intracortical microstimulation.

245 ensor to their somatosensory cortex (S1) via intracortical microstimulation.

246 or cortex of these primates using long-train intracortical microstimulation.

247 ections into the cortex, but also on dynamic intracortical modulations by specific forms of inhibitio

248 as, whose initial territory is determined by intracortical molecular determinants.

249 reflect spatial patterns of gene expression, intracortical myelin and cortical thickness, as well as

250 However, how intracortical myelin content evolves during development,

251 in-mapping technique thus seems sensitive to intracortical myelin content in normal development and a

252 e used MRI to measure cortical thickness and intracortical myelination in 297 population volunteers a

253 uctural magnetic resonance imaging marker of intracortical myelination in 68 brain regions in 248 hea

254 between prefrontal measures of morphometry, intracortical myelination, and functional connectivity w

255 es of brain organization (brain morphometry, intracortical myelination, white matter integrity, and r

256 Depth-dependent trajectories of intracortical myeloarchitectural development contribute

257 perty of a recurrent gain control fed by the intracortical network.

258 Second, intracortical networking of excitatory and inhibitory ne

259 that obtains safety information regarding an intracortical neural interface device, and investigates

260 Intracortical neural probes have been used to demonstrat

261 We studied intracortical neuronal dynamics during transitions from

262 We studied intracortical neuronal dynamics during transitions of lo

263 Here, we studied intracortical neuronal dynamics leading to propofol-indu

264 the background EEG and worse for those with intracortical only seizures when compared to those with

265 Lesions were classified as leukocortical, intracortical, or subpial.

266 , to map in vivo the spatial distribution of intracortical pathology in multiple sclerosis.

267 d cell-type-specific changes in thalamo- and intracortical pathways during learning using an automate

268 red, T2* in intracortical lesions and in the intracortical portion of leukocortical lesions visually

269 mphasizing the importance of state-dependent intracortical processing in hearing.

270 ved sensory cortices to shift between FF and intracortical processing to allow adaptation.

271 in favor of FF information at the expense of intracortical processing.

272 were strengthened, suggesting a shift toward intracortical processing.

273 Mixed-effect models of depth specific intracortical profiles demonstrated two separate process

274 Intracortical profiles were generated using magnetizatio

275 Results show that intracortical projections across the hand-face border ar

276 ns despite the presence of the more abundant intracortical projections.

277 ingle trials, demonstrating the potential of intracortical recordings for brain-computer interfaces t

278 e kinematics that were being generated using intracortical recordings from two people with tetraplegi

279 How intracortical recurrent circuits in mammalian sensory co

280 n by primary bulbar afferents, and shaped by intracortical recurrent connections, the potential for a

281 um show characteristic signatures of altered intracortical relationships compared with those at the o

282 al features of sensory processing such as an intracortical reverberation during the processing of vis

283 Intracortical seizures were accompanied by elevated hear

284 disorganization related to inhomogeneity of intracortical signal intensity.

285 em is less feedforward and more dominated by intracortical signals than previously thought, (2) inter

286 Intracortical somatosensory interfaces have now entered

287 In contrast, intracortical stimulation of L2/3 evokes strong inhibiti

288 by auditory or electrical (thalamocortical, intracortical) stimulation while randomly varying the in

289 t cortical areas are organized into distinct intracortical subnetworks.

290 types I-IV (mixed grey matter/white matter, intracortical, subpial and cortex-spanning lesions, resp

291 t unaltered inhibitory, neurotransmission at intracortical synapses in mouse models of familial hemip

292 ical synapses, whereas low levels potentiate intracortical synapses.

293 e to explore the role of thalamocortical and intracortical synaptic cooperativity (the number of coin

294 ntrinsic and synaptic mechanisms that divide intracortical synaptic excitation from L2/3 to L5B into

295 leaving meningeal Cxcl12 intact, attenuates intracortical TCA growth and disrupts tangential interne

296 psilesional thalamus, significant effect for intracortical volume (t(68) = 2.76, p = 0.008), age (t(6

297 tralesional thalamus, significant effect for intracortical volume (t(68) = 3.2, p = 0.002) and age (t

298 Clinical factors age and intracortical volume influence both ipsi- and contralesi

299 halamus volume to time since stroke, gender, intracortical volume, age, and lesion volume.

300 oration including time since stroke, gender, intracortical volume, aging, and lesion volume to better