ライフサイエンスコーパス: corticospinal

1 sults indicate that the relationship between corticospinal activity and movement is dynamic and that

2 s, which led to changed associations between corticospinal activity and movement.

3 he spared cortical hemisphere and its direct corticospinal and indirect corticobulbospinal connection

4 The corticospinal and rubrospinal systems function in skille

5 ependent interactions between the developing corticospinal and rubrospinal systems, two key systems f

6 bursts in M1 contribute to the maturation of corticospinal and sensorimotor networks required for the

7 We found robust sprouting of uninjured corticospinal and serotonergic fibers in a rat cervical

8 We found robust sprouting of uninjured corticospinal and serotonergic fibers in a rat hemisecti

9 hat C9orf72 promoter activity is enriched in corticospinal and spinal motor neurons as well as in oli

10 tion that the RORalpha INs are innervated by corticospinal and vestibulospinal projection neurons, ar

11 d lower regional FA in multiple commissural, corticospinal, and association tracts.

12 anterior commissure and the corticothalamic, corticospinal, and thalamocortical tracts.

13 ly axon reflexes generated by stimulation of corticospinal axon branches, which cross the midline.

14 ticospinal axons, suggesting that reciprocal corticospinal axon changes are functional.

15 onal antibody infusion resulted in increased corticospinal axon collateral branches with presynaptic

16 ERK/MAPK hyperactivation also led to reduced corticospinal axon elongation, but was associated with e

17 In murine models of SCI, we report robust corticospinal axon regeneration, functional synapse form

18 prouting that was accompanied by significant corticospinal axon withdrawal and a decrease in corticos

19 d by cortical and subcortical stimulation of corticospinal axons (MEPs and CMEPs, respectively) and t

20 Rat corticospinal axons also regenerate into human donor gra

21 in SVZ and CP gene expression, with loss of corticospinal axons and gain of corticotectal projection

22 MEPs) and subcortical (CMEPs) stimulation of corticospinal axons and short-interval intracortical inh

23 nt determinant in the organization of mature corticospinal axons and spinal motor circuits.

24 tive interactions between proprioceptive and corticospinal axons are an important determinant in the

25 Moreover, corticospinal axons can emerge from neural grafts and re

26 Rather, treatment caused corticospinal axons from the less affected hemisphere to

27 his question, we examined plastic changes in corticospinal axons in response to two complementary pro

28 cal work in primates has suggested that only corticospinal axons originating in caudal primary motor

29 fter stroke induced significant sprouting of corticospinal axons originating in the peri-infarct cort

30 re length-dependent disorders affecting long corticospinal axons, and the most common autosomal domin

31 tentials showed parallel changes to those of corticospinal axons, suggesting that reciprocal corticos

32 indlimb cortex, associated with sprouting of corticospinal axons.

33 ulted in a significant loss of contralateral corticospinal boutons from M2 compared with controls.

34 pinal cord triggered by action potentials of corticospinal cells during free behavior.

35 cortex ablating 90% of the cross-projecting corticospinal cells.

36 ough targeted ablation, a potential role for corticospinal, cerebello-rubro-spinal, and hypothalamic

37 ypothesis was based on how somatosensory and corticospinal circuits adapt to injury during developmen

38 ules, providing a logic for parallel-ordered corticospinal circuits to orchestrate multistep motor sk

39 are compatible with the hypothesis that the corticospinal circuits used to control reaching evolved

40 e trajectories of limb movements mediated by corticospinal circuits, suggesting an interaction betwee

41 limits the formation of new synapses between corticospinal collaterals and relay neurons, delays thei

42 ables prediction of the remodeling of spared corticospinal connection and spinal motor circuits after

43 he early postnatal development of functional corticospinal connections in human infants is not fully

44 he early postnatal development of functional corticospinal connections in human infants is not fully

45 ticospinal axon withdrawal and a decrease in corticospinal connections on cholinergic interneurons in

46 y and informs the target-specific control of corticospinal connections to promote functional recovery

47 t rhizotomy led to a significant increase in corticospinal connections, including those on cholinergi

48 scular coherence as indicators of functional corticospinal connectivity in healthy infants aged 1-66

49 ojection neuron generation, thereby altering corticospinal connectivity, and produced long-lasting al

50 rain which induces force enhancements with a corticospinal contribution.

51 esis of preferential rubrospinal rather than corticospinal control for early movements.

52 nal circuits could thus transform unilateral corticospinal control signals into bilateral movements.

53 les, descending motor tracts (containing the corticospinal, corticobulbar, and corticopontine tracts)

54 Here we explore the connectivity between corticospinal (CS) neurons in the motor cortex and muscl

55 ctions during the evolution of the mammalian corticospinal (CS) system.

56 These data suggest that the corticospinal drive to lower and upper limb muscles show

57 Corticospinal drive to upper and lower limb muscle shows

58 th ALSFRS-R and King's stage correlated with corticospinal DTI measures.

59 ypes of non-invasive brain stimulation alter corticospinal excitability (CSE).

60 transcranial magnetic stimulation measuring corticospinal excitability (CSE).

61 There was no change in corticospinal excitability after learning a motor skill

62 here was a substantial transient decrease in corticospinal excitability after learning a motor skill

63 in each experiment were correlated with the corticospinal excitability after learning.

64 There was a negative correlation between corticospinal excitability and RT, such that larger moto

65 hint at a top-down, cognitive enhancement of corticospinal excitability as a neural signature of plac

66 transcranial magnetic stimulation to measure corticospinal excitability at 6, 21, 36, 96, and 126 min

67 We measured corticospinal excitability at rest with transcranial mag

68 nt experiments, we abolished the decrease in corticospinal excitability by applying theta burst stimu

69 Together, these experiments suggest that corticospinal excitability changes act as a physiologica

70 Our findings suggest that changes in corticospinal excitability during gross more than fine f

71 ical SCI have an altered ability to modulate corticospinal excitability during movement preparation w

72 neural mechanisms contributing to changes in corticospinal excitability during these gripping configu

73 Our results show that corticospinal excitability is altered in the preparatory

74 We then tested whether the corticospinal excitability of the hand representation un

75 Our novel findings show that changes in corticospinal excitability present during power grip com

76 Corticospinal excitability was measured with motor-evoke

77 Corticospinal excitability was quantified using resting

78 between individual differences in intrinsic corticospinal excitability, local cortical GABA levels,

79 connectivity, cerebral blood flow (CBF), and corticospinal excitability, respectively, before and 4 w

80 bcortical networks contributed to changes in corticospinal excitability.

81 human motor cortex indicating a reduction of corticospinal excitability.

82 er primary motor cortex provided an assay of corticospinal excitability.

83 on, particularly when attempting to modulate corticospinal excitability.

84 tract (CST) containing approximately 96% of corticospinal fibers but spared approximately 3% of CST

85 We suggest that slowly conducting corticospinal fibers from old M1 generate weak late mono

86 or cortex, sprouting of spared contralateral corticospinal fibers into the affected hemicord is one m

87 Furthermore, we demonstrated that corticospinal fibers sprouting to the denervated side of

88 tract (RN/RST) compensates for developmental corticospinal injury?

89 left cervical spinal hemicord devoid of its corticospinal input revealed widespread plastic response

90 eutic intervention targeting the ipsilateral corticospinal linkage from cM1 may promote proximal, and

91 owever, the importance of alsin function for corticospinal motor neuron (CSMN) health and stability r

92 in GABAergic neurons rescued the deficits in corticospinal motor neuron development of CB1-null mice

93 of gene sets that collectively define mouse corticospinal motor neurons (CSMN).

94 e in the soma and proximal dendrites of both corticospinal motor neurons (CSMNs) and spinal motor neu

95 disease characterized by axon shortening in corticospinal motor neurons and progressive spasticity o

96 Although overt cell death of corticospinal motor neurons does not occur until disease

97 ot account for the specific vulnerability of corticospinal motor neurons in ALS.

98 ower (ventral horn) and upper motor neurons (corticospinal motor neurons in layer V), mutant profilin

99 pasticity and length-dependent axonopathy of corticospinal motor neurons.

100 y, owing to a length-dependent axonopathy of corticospinal motor neurons.

101 terized by progressive age-dependent loss of corticospinal motor tract function.

102 is effectively transmitted across recurrent corticospinal networks.

103 the consistency of the relationship between corticospinal neuron activity and movement through in vi

104 corticospinal tract formation and subsequent corticospinal neuron apoptosis.

105 ity of descending late indirect (I) waves in corticospinal neurons (4.3 ms; I-wave protocol) or at an

106 Corticospinal neurons (CSNs) represent the direct cortic

107 nct, share an intriguing cellular component: corticospinal neurons (CSP) in layer 5B.

108 ved in suppressing anatomical plasticity, in corticospinal neurons and in primary cortical neuron cul

109 patch-clamp recordings of up to four labeled corticospinal neurons and testing of 3489 potential syna

110 that a specific set of excitatory inputs to corticospinal neurons are suppressed during motor prepar

111 very after SCI and support a focus on spared corticospinal neurons as a target for therapy.

112 ity of distinct sets of excitatory inputs to corticospinal neurons during the warning period of vario

113 e, yet we know little about the way in which corticospinal neurons engage spinal interneurons.

114 lateral sclerosis (ALS), a disease in which corticospinal neurons exhibit selective vulnerability, t

115 Corticospinal neurons exhibited heterogeneous correlatio

116 contribute to the selective degeneration of corticospinal neurons in amyotrophic lateral sclerosis (

117 issociate the roles of injured and uninjured corticospinal neurons in mediating recovery, we transien

118 Second, corticospinal neurons in the same region of area 5 termi

119 Similarly, directly injured corticospinal neurons in vivo also exhibit a specific in

120 is suggests that the inhibition of inputs to corticospinal neurons is not involved in preventing the

121 e first evidence that late synaptic input to corticospinal neurons may represent a novel therapeutic

122 animals, local connectivity is biased toward corticospinal neurons projecting to the same spinal cord

123 inactivate spared dorsolaterally projecting corticospinal neurons specifically by injecting adeno-as

124 Therefore, uninjured corticospinal neurons substantiate remarkable motor cort

125 ence that a lateral region within area 5 has corticospinal neurons that are directly linked to the co

126 ion within area 5 contains a motor area with corticospinal neurons that could function as a command a

127 ilencing uninjured dorsolaterally projecting corticospinal neurons via activation of the inhibitory D

128 Ablation of the corticospinal neurons with sprouting axons abolishes the

129 O), which is upstream of alpha2-chimaerin in corticospinal neurons, exhibited similar abducens wander

130 ecting versus spared dorsolateral projecting corticospinal neurons, we established a transient silenc

131 ses, as well as spinal cord interneurons and corticospinal neurons.

132 upregulates miR-21 and downregulates PTEN in corticospinal neurons.

133 We suggest that low excitability of both corticospinal output and its facilitatory synaptic input

134 s of inhibitory and excitatory inputs to the corticospinal output cells.

135 ges are ultimately funneled through a stable corticospinal output channel or whether the corticospina

136 subcortical premotoneuronal network shaping corticospinal output during human precision grip.

137 Corticospinal output is modulated in a task-dependent ma

138 ABSTRACT: Corticospinal output is modulated in a task-dependent ma

139 corticospinal output channel or whether the corticospinal output itself is plastic.

140 rdinated balance of activity upstream of the corticospinal output neurons.

141 of the quiescent motor cortex increased the corticospinal output.

142 TS: In uninjured humans, transmission in the corticospinal pathway changes in a task-dependent manner

143 In uninjured humans, transmission in the corticospinal pathway changes in a task-dependent manner

144 ate the pivotal role of a minor dorsolateral corticospinal pathway in mediating spontaneous recovery

145 transiently silenced the minor dorsolateral corticospinal pathway spared by our injury.

146 o monitor changes in the excitability of the corticospinal pathway.

147 organization) in fiber tracts that included corticospinal pathways and the splenium and genu of the

148 iffer in the intrinsic excitability of their corticospinal pathways and, perhaps more generally, thei

149 suggest that individuals with more excitable corticospinal pathways are faster to initiate planned re

150 e, we establish that complete transection of corticospinal pathways in the pyramids impairs locomotio

151 from the MEP onset, suggesting that indirect corticospinal pathways were less likely to be involved t

152 to neural maturation, such as myelination of corticospinal pathways, neuronal pruning, and synaptogen

153 naptic signaling among functionally distinct corticospinal populations in Fischer 344 rats from postn

154 lesion) on the terminal distribution of the corticospinal projection (CSP) from intact, ipsilesional

155 To further our understanding of the corticospinal projection (CSP) from the hand/arm represe

156 abeling confirmed the former type to include corticospinal projection neurons (CSpPNs) and corticotha

157 tem cells enables robust regeneration of the corticospinal projection within and beyond spinal cord l

158 ged, in part, by the presence of ipsilateral corticospinal projections (iCSP).

159 trolling their paretic hands via ipsilateral corticospinal projections already in the preoperative si

160 r increases or decreases the excitability of corticospinal projections from M1, contingent on the int

161 upraspinal fatigue and the responsiveness of corticospinal projections to an arm muscle.

162 Elevations in the excitability of corticospinal projections to the forearm were observed f

163 acilitate, or inhibit, the responsiveness of corticospinal projections to upper limb muscles.

164 ory influence on spared ipsilesional frontal corticospinal projections, and that restoration of a fav

165 Corticospinal pyramidal neurons, a cell type implicated

166 is exerted by two sets of descending fibers, corticospinal/pyramidal and extrapyramidal.

167 ecause of our almost total dependence on the corticospinal/pyramidal system for the effectuation of m

168 ead, that an increasing preponderance of the corticospinal/pyramidal system over motor control is an

169 Corticospinal regeneration requires grafts to be driven

170 mature caudalized neural grafts also support corticospinal regeneration.

171 ntrol conditions and resulted in a 14% lower corticospinal responsiveness during this short bout (P <

172 ring maximum voluntary contraction (MVC) and corticospinal responsiveness was monitored via TMS-evoke

173 ts showed significantly less muscle-specific corticospinal sensitivity during action observation, as

174 result in spontaneous regrowth of transected corticospinal, sensory or serotonergic axons through sev

175 These results provide direct evidence of corticospinal synaptic plasticity in vivo at the level o

176 The motor cortex and the corticospinal system contribute to the control of a prec

177 response of the rubrospinal system following corticospinal system developmental injury.

178 s under activity-dependent regulation by the corticospinal system for establishing mature RST connect

179 eloping rubrospinal system competes with the corticospinal system in establishing the red nucleus mot

180 roups presented enhanced excitability of the corticospinal system in the muscle specifically involved

181 radually emerges during subsequent postnatal corticospinal system maturation; the nature of circuit d

182 cal projections at 7 weeks of age, while the corticospinal system was inactivated, and at 14 weeks, a

183 functions of the rubrospinal system and the corticospinal system, the other major system for limb co

184 In contrast to the corticospinal system, where sprouting of fibers and rear

185 y-dependent interactions with the developing corticospinal system.

186 f force could change the excitability of the corticospinal system.

187 the most efficient noninvasive facilitatory corticospinal tES known so far, which is 20 Hz transcran

188 was predicted by axial diffusivity along the corticospinal tract (beta = 4.6 x 10(3); P < .001), Symb

189 tex of neonatal mice enables regeneration of corticospinal tract (CST) axons after spinal cord injury

190 Partial injury to the corticospinal tract (CST) causes sprouting of intact axo

191 lumn SCI that bilaterally ablated the dorsal corticospinal tract (CST) containing approximately 96% o

192 tions and whether the RN/RST compensates for corticospinal tract (CST) developmental motor impairment

193 own to promote axon collateral growth in the corticospinal tract (CST) following stroke and focal TBI

194 to investigate whether an imaging measure of corticospinal tract (CST) injury in the acute phase can

195 aches, we discovered that the anatomy of the corticospinal tract (CST) is abnormal in patients with N

196 The corticospinal tract (CST) is the most important motor sy

197 Of descending pathways, the corticospinal tract (CST) is thought to be the most crit

198 iption factor Sox11 increases axon growth by corticospinal tract (CST) neurons after spinal injury.

199 ggests that these connections come only from corticospinal tract (CST) neurons in the subdivision of

200 neurons in the adult mammalian CNS, notably corticospinal tract (CST) neurons, display a much lower

201 The limited rewiring of the corticospinal tract (CST) only partially compensates the

202 is the limited regrowth of the axons in the corticospinal tract (CST) that originate in the motor co

203 g the contralateral spinal projection of the corticospinal tract (CST) to investigate the effects of

204 release of glutamate within the ipsilesional corticospinal tract (CST), and an enhanced NMDA-mediated

205 In the context of injury to the corticospinal tract (CST), brainstem-origin circuits may

206 scending motor pathway for motor skills, the corticospinal tract (CST), sprout after brain or spinal

207 The primate corticospinal tract (CST), the major descending pathway

208 spinal cord often assess regeneration of the corticospinal tract (CST).

209 tudy the primary descending motor tract, the corticospinal tract (CST).

210 identified measures of brain injury (smaller corticospinal tract [CST] injury), cortical function (gr

211 quantitation of myelin loss of fibres of the corticospinal tract and associated macrophage burden, as

212 e white matter integrity in the ipsilesional corticospinal tract and bilateral corpus callosum was in

213 te matter pathology was confirmed within the corticospinal tract and callosal body, and linked strong

214 AD or CJD cases, CHIT1 was expressed in the corticospinal tract and CHIT1 staining colocalised with

215 's stage correlated with DTI measures of the corticospinal tract and mid-callosum.

216 Tractography of the corticospinal tract and the medial lemniscus was perform

217 imaging (n = 10) evidence of disease in the corticospinal tract and white matter projections involvi

218 white matter volume change encompassing the corticospinal tract at the level of the right internal c

219 Competitive interactions are known to shape corticospinal tract axon outgrowth and withdrawal during

220 city of descending serotonergic pathways and corticospinal tract axonal regeneration.

221 n-1-null mutant (knock-out) mice, dieback of corticospinal tract axons also is reduced after SCI.

222 Adult corticospinal tract axons do not regenerate because they

223 pression of Sox11 to stimulate the growth of corticospinal tract axons in the cervical spinal cord an

224 Sprouting of spared corticospinal tract axons in the contralesional spinal c

225 include the sprouting patterns of descending corticospinal tract axons into spinal gray matter after

226 able for the robust spontaneous sprouting of corticospinal tract axons seen after pyramidotomy in pos

227 to the lesion level, and greater numbers of corticospinal tract axons sprout rostral to the lesion.

228 akness resulting from distal degeneration of corticospinal tract axons.

229 KEY POINTS: The corticospinal tract contributes to the control of finger

230 ABSTRACT: It is well accepted that the corticospinal tract contributes to the control of finger

231 otor outcome after stroke, but assessment of corticospinal tract damage alone is unlikely to be suffi

232 r are not established although the extent of corticospinal tract damage is suggested to be a contribu

233 ; however, the cases with moderate to severe corticospinal tract degeneration showed right-sided temp

234 In contrast, the cases with no or equivocal corticospinal tract degeneration were more likely to sho

235 Only one case, without corticospinal tract degeneration, was found to have a he

236 eneration; and (iii) moderate to very severe corticospinal tract degeneration.

237 currence of cases of type C pathology having corticospinal tract degeneration.

238 neuron involvement and FTD might reflect the corticospinal tract degeneration.

239 ded into three groups based on the degree of corticospinal tract degeneration: (i) no corticospinal t

240 of corticospinal tract degeneration: (i) no corticospinal tract degeneration; (ii) equivocal cortico

241 icospinal tract degeneration; (ii) equivocal corticospinal tract degeneration; and (iii) moderate to

242 iod where the functional connections between corticospinal tract fibres and spinal motoneurones under

243 period where functional connections between corticospinal tract fibres and spinal motoneurones under

244 Loss of Map2k1/2 (Mek1/2) led to deficits in corticospinal tract formation and subsequent corticospin

245 of corpus callosum, anterior commissure, and corticospinal tract formation.

246 The corticospinal tract in Old World primates makes monosyna

247 In this study we examined the role of the corticospinal tract in pathway reorganization following

248 ter in the hand knob area; the region of the corticospinal tract in the centrum semiovale, in the pos

249 Baseline impairment also correlated with corticospinal tract injury (R(2) = 0.52), though not inf

250 ructural magnetic resonance imaging measured corticospinal tract injury and infarct volume.

251 ctivity with a structural measure of injury (corticospinal tract injury) performed better than either

252 complicated HSP suggests that the "primary" corticospinal tract involvement known to occur in these

253 ninjured) monkeys, we performed a unilateral corticospinal tract lesion at the thoracic level.

254 I, we created bilaterally complete medullary corticospinal tract lesions in adult mice, eliminating a

255 Results While considering damage within a corticospinal tract mask resulted in 73% classification

256 ined by progressive neurodegeneration of the corticospinal tract motor neurons.

257 contrast, myelination of motor axons in the corticospinal tract of the spinal cord occurred normally

258 spinal cord receive the synaptic inputs from corticospinal tract or serotonergic axons, limited bouto

259 Corticospinal tract signs were frequent, including exten

260 The corticospinal tract was affected, as reflected by delaye

261 The corticospinal tract was most likely to be damaged in bot

262 However, while damage in the corticospinal tract was the best indicator of motor defi

263 cISMS with stimulation of the contralateral corticospinal tract yielded no evidence of response occl

264 y relevant white matter (corpus callosum and corticospinal tract) and deep grey matter (thalamus) str

265 3% classification accuracy, using other (non-corticospinal tract) motor areas provided 87% accuracy,

266 DTI showed displacement of the ipsilateral corticospinal tract, whereas MR spectroscopy showed abse

267 training may produce plastic changes in the corticospinal tract, which are responsible for improveme

268 , anterior thalamic radiation, cingulum, and corticospinal tract.

269 s early damage and lack of maturation of the corticospinal tract.

270 to execute the ipsilateral extension of the corticospinal tract.

271 rity of the primary sensorimotor network and corticospinal tract.

272 cesses that suppress excitability within the corticospinal tract.

273 f72 carriers with ALS or ALS-FTD, changes in corticospinal tractography measures correlated with chan

274 d tract-specific integrity of PC and lateral corticospinal tracts (CST).

275 l diffusivity and disease duration along the corticospinal tracts (r = 0.806, P < 0.01) was found.

276 essed atrophy in white matter in the cranial corticospinal tracts and grey matter in sensorimotor cor

277 es in several white matter tracts, including corticospinal tracts and optic radiations, indicating pr

278 uals had signal abnormalities in the central corticospinal tracts and spinal cord where imaging was a

279 , encompassing parts of the corpus callosum, corticospinal tracts and superior longitudinal fasciculu

280 Corticospinal tracts correlated with patients' self-rati

281 at, over time, truncated M1 could damage the corticospinal tracts of human patients.

282 y) and of the structural connectivity of the corticospinal tracts within the brainstem (by magnetic r

283 ally when the structural connectivity of the corticospinal tracts within the brainstem is asymmetric.

284 rmed the most significant alterations in the corticospinal tracts, and captured additional significan

285 ring of the outer blades, and involvement of corticospinal tracts, thalami, and spinal cord.

286 esions spread beyond precentral cortices and corticospinal tracts, to include the corpus callosum; fr

287 etries in the structural connectivity of the corticospinal tracts.

288 -based analysis confirmed the results within corticospinal tracts.

289 s its adult onset or its specificity for the corticospinal tracts.

290 hange, and atrophy and hyperintensity of the corticospinal tracts.

291 l CST misprojections, resulting in bilateral corticospinal tracts.

292 1, contributes to axonal degeneration in the corticospinal tracts.

293 ngitudinal fasciculi, uncinate fasciculi and corticospinal tracts.

294 atistics, and tractography-based analysis on corticospinal tracts.

295 Thus, deficits in corticospinal transmission after human SCI extend to the

296 mill training with an incline may facilitate corticospinal transmission and improve the control of th

297 ex after a cervical SCI that interrupts most corticospinal transmission but results in partial recove

298 erall our findings indicate that deficits in corticospinal transmission in humans with chronic incomp

299 spinal epidural recordings of the descending corticospinal volleys.

300 ic resting-state functional connectivity and corticospinal white matter microstructure.