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 These findings provide evidence for lesser corticospinal and larger reticulospinal influences to sp

4 ortical and reticulospinal circuits, whereas corticospinal and motoneuronal adaptations are not domin

5 e for the radial fiber scaffold in directing corticospinal and other axons at the junction between th

6 vidence in animals and humans indicates that corticospinal and reticulospinal pathways differentially

7 We showed that imbalanced corticospinal and reticulospinal tract contributions are

8 Damage to the corticospinal and reticulospinal tract has been associat

9 rst time, of imbalanced contributions of the corticospinal and reticulospinal tract to control a spas

10 ntracortical inhibition but did not modulate corticospinal and sensory cortex excitability or sensori

11 r, NT3 induced neuroplasticity of the spared corticospinal and serotonergic pathways.

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

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

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

15 e exhibited a significant 2-3-fold increased corticospinal axon density in the cervical cord below th

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

17 Moreover, Chase significantly increased corticospinal axon growth and the number of synapses for

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

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

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

21 er reinnervation by sprouting contralesional corticospinal axons after unilateral photothrombotic str

22 Rat corticospinal axons also regenerate into human donor gra

23 lls (NPCs) enable the robust regeneration of corticospinal axons and restore forelimb function after

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

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

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

27 d by cortical and subcortical stimulation of corticospinal axons before and after 20 min of TESS (30

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

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

30 recording, we demonstrated that regenerating corticospinal axons functionally integrate into spinal c

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

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

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

34 ng and neurotracer labeling of long-distance corticospinal axons suggest that recovery might be partl

35 Corticospinal axons traced from biotin-dextran-amine inj

36 ed potentials evoked by direct activation of corticospinal axons using lateromedial (LM) stimulation,

37 ed potentials evoked by direct activation of corticospinal axons using LM stimulation] and changes in

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

39 re consistent with progressive dying back of corticospinal axons, which is characteristic of the dise

40 indlimb cortex, associated with sprouting of corticospinal axons.

41 ury and tracing of dorsal column sensory and corticospinal axons; clearing and staining of unsectione

42 Training-related corticospinal cells also express increased excitability

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

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

45 reventing such activity-dependent shaping of corticospinal circuits limits motor recovery after spina

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

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

48 Neuronal phase may therefore impact corticospinal communication.SIGNIFICANCE STATEMENT Brain

49 e benefits are conserved despite appreciable corticospinal conduction delays.

50 Elevated TSC correlated moderately with corticospinal conduction failure assessed with transcran

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

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

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

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

55 rain which induces force enhancements with a corticospinal contribution.

56 The formation of corticospinal (CS) circuits, which are essential for vol

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

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

59 these extra inputs combined with the loss of corticospinal drive contribute to the pronounced weaknes

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

61 o biceps but not triceps brachii and loss of corticospinal drive to triceps brachii in humans with te

62 Corticospinal drive to upper and lower limb muscle shows

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

64 riers with and without mirror movements, but corticospinal effects and decreased peripheral DCC mRNA

65 e spared primary afferents and somatosensory corticospinal efferents sprouted in an overlapping regio

66 Plastic changes in corticospinal excitability (CSE) and motor function can

67 HSF and measured behavioral performance and corticospinal excitability (CSE) using transcranial magn

68 el-free learning task induced an increase in corticospinal excitability and a reduction in the amplit

69 MS in healthy humans of both sexes to assess corticospinal excitability and GABA-A-receptor mediated

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

71 We measured corticospinal excitability at rest with transcranial mag

72 ballistic motor task induced an increase in corticospinal excitability but did not change motor cort

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

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

75 Thus, our findings show that modulation of corticospinal excitability during observed object liftin

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

77 ships between beta event characteristics and corticospinal excitability in healthy adults.

78 eta-tACS confirm a non-selective increase in corticospinal excitability in subjects at rest; an incre

79 re, hypothesized that the plastic changes in corticospinal excitability induced by TBS are the result

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

81 strate that this weight-driven modulation of corticospinal excitability is easily suppressed by the o

82 ic stimulation studies have highlighted that corticospinal excitability is increased during observati

83 s motor system in a weight-specific fashion: Corticospinal excitability is larger when observing lift

84 (MEPs), we have previously demonstrated that corticospinal excitability is modulated by both amplitud

85 We compare the effects on corticospinal excitability of repeatedly delivering peri

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

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

88 Probing corticospinal excitability via transcranial magnetic sti

89 Corticospinal excitability was measured with motor-evoke

90 of the pinch-grip movement, the increase of corticospinal excitability was only observed for the pri

91 more, during the heavy intensity trial only, corticospinal excitability was reduced at the cortical (

92 However, the influence of these events on corticospinal excitability, a mechanism through which th

93 anial magnetic stimulation (TMS) measures of corticospinal excitability, GABA(A) (short-interval intr

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

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

96 dogenous beta oscillatory events shape human corticospinal excitability.

97 imilarly captured natural variation in human corticospinal excitability.

98 human motor cortex indicating a reduction of corticospinal excitability.

99 bcortical networks contributed to changes in corticospinal excitability.

100 on, particularly when attempting to modulate corticospinal excitability.

101 anced task level and associated increases in corticospinal excitability.

102 ound in tracts of the ventral stream and the corticospinal fasciculus, depicting a gradual reorganisa

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

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

105 generation, compensatory sprouting of spared corticospinal fibers is associated with recovery of skil

106 a growth-promoting environment for sprouting corticospinal fibers originating from the contralesional

107 o 'Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord in

108 ect subcortical/spinal (0-5 and 6-15 Hz) and corticospinal inputs (6-15 and 16-40 Hz).

109 s compared with controls, suggesting reduced corticospinal inputs to elbow extensors.

110 e high frequency band (16-40 Hz), reflecting corticospinal inputs.

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

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

113 Corticospinal motor neurons (CSMN) and callosal projecti

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

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

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

117 ctivated in the target area of reinnervating corticospinal motor neurons; and a late phase during whi

118 10 sessions of exercise combined with paired corticospinal-motor neuronal stimulation (PCMS) or sham-

119 tion over the primary motor cortex arrive at corticospinal-motor neuronal synapses of upper- or lower

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

121 corticospinal tract formation and subsequent corticospinal neuron apoptosis.

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

123 Corticospinal neurons (CSNs) represent the direct cortic

124 eceptor for the repellent Sema6D molecule in corticospinal neurons (CSNs).

125 Absence of corticospinal neurons also limited presymptomatic hyper-

126 s and premature death, but genetically lacks corticospinal neurons and other subcerebral projection n

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

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

129 Increased alpha2delta2 expression in corticospinal neurons contributed to loss of corticospin

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

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

132 Corticospinal neurons exhibited heterogeneous correlatio

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

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

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

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

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

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

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

140 Therefore, uninjured corticospinal neurons substantiate remarkable motor cort

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

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

143 athway, as chemogenetic silencing of injured corticospinal neurons transiently abrogated recovery.

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

145 Here, we demonstrate that inputs to corticospinal neurons which coincide with windows of hig

146 te the output timing from layer 5 (including corticospinal neurons) following extracellular stimulati

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

148 ly regulates axon growth and regeneration of corticospinal neurons, the cells that originate the cort

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

150 dependent of RND3 and ARHGAP35 expression in corticospinal neurons, where they regulate dendritic spi

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

152 a reduction in PlexA1 protein expression in corticospinal neurons.

153 the reinnervation process by contralesional corticospinal neurons.

154 rs a unique composition of ancestral primate corticospinal organization combined with skilled hand us

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

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

157 Corticospinal output is modulated in a task-dependent ma

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

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

160 Thus, very little LPMCv corticospinal output reaches the cervical enlargement.

161 To estimate changes in the corticospinal output, we used the size of motor evoked p

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

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

164 physiology, we provide evidence for a direct corticospinal pathway from the primary somatosensory cor

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

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

167 uch recovery relies on reorganization of the corticospinal pathway, as chemogenetic silencing of inju

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

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

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

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

172 vioural determinants leading to long lasting corticospinal plasticity and motor expertise remain unex

173 e enhances motor skill learning and promotes corticospinal plasticity.

174 ed to study the terminal organization of the corticospinal projection (CSP) from the ventral (v) and

175 are specifically activated in the denervated corticospinal projection fields in this early phase.

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

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

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

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

180 level and via corticofugal tracts, including corticospinal projections providing direct monosynaptic

181 arm cycling induces short-term plasticity in corticospinal projections to the trunk muscle in healthy

182 Corticospinal pyramidal neurons, a cell type implicated

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

184 Corticospinal regeneration requires grafts to be driven

185 mature caudalized neural grafts also support corticospinal regeneration.

186 corticospinal neurons contributed to loss of corticospinal regrowth ability during postnatal developm

187 iring of relay neurons during injury-induced corticospinal remodeling.

188 ipants with SCI with spasticity showed small corticospinal responses and maximal voluntary contractio

189 However, the amplitude of corticospinal responses elicited by transcranial magneti

190 y, rather than other pathways (including the corticospinal, rubrospinal, serotonergic, and dopaminerg

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

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

193 lso interact genetically in vivo to restrict corticospinal sprouting in mouse cervical spinal cord af

194 e through gabapentin administration promoted corticospinal structural plasticity and regeneration in

195 n primates, alongside the more sophisticated corticospinal system.

196 injury, and that larger (presumably faster) corticospinal terminals are lost, suggesting a significa

197 growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the les

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

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

200 ionship between RT and microstructure of the corticospinal tract (CST) and the optic radiation (OR),

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

202 Corticospinal tract (CST) degeneration and cortical atro

203 p, WM atrophy was accompanied by significant corticospinal tract (CST) fractional anisotropy (FA) red

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

205 The corticospinal tract (CST) is the major descending pathwa

206 form translational profiling specifically of corticospinal tract (CST) motor neurons in mice, to iden

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

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

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

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

211 timulation of the primary motor cortex (M1), corticospinal tract (CST), and reticulospinal tract (RST

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

213 CREB-mediated transcription maintain nascent corticospinal tract (CST)-relay neuron contacts.

214 en with unilateral cerebral palsy (uCP), the corticospinal tract (CST)-wiring patterns may differ (co

215 fasciculus (SLF), corpus callosum (CC), and corticospinal tract (CST).

216 ut via the somatosensory subcomponent of the corticospinal tract (S1 CST), and is critically importan

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

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

219 are the archetypal projection neurons of the corticospinal tract and corpus callosum, respectively.

220 erves or central nervous system axons of the corticospinal tract and dorsal columns, respectively.

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

222 ue properties and their variations along the corticospinal tract and optic radiation.

223 nce molecule EphA4, axonal misrouting of the corticospinal tract and spinal interneurons is manifeste

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

225 al cord target tissue of the stroke-affected corticospinal tract are mainly defined by two phases: an

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

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

228 rcuits including descending serotonergic and corticospinal tract axons and afferents from muscle and

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

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

231 Optogenetic stimulation of host corticospinal tract axons regenerating into grafts elici

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

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

234 ephalic-mesencephalic junction with abnormal corticospinal tract course.

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

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

237 n response to cortical stroke and unilateral corticospinal tract degeneration, compensatory sprouting

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

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

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

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

242 The corticospinal tract in Old World primates makes monosyna

243 Moreover, decreases in ipsi-lesional corticospinal tract integrity and increases in contra-le

244 The corticospinal tract is unique to mammals and the corpus

245 Damage to the corticospinal tract is widely studied following unilater

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

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

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

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

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

251 3% classification accuracy, using other (non-corticospinal tract) motor areas provided 87% accuracy,

252 % large hemispheric, 6.0% diencephalic, 4.3% corticospinal tract), 72.2% had spinal cord lesions (46.

253 Following damage to the corticospinal tract, both the move and hold period comma

254 CC mRNA expression, a functional ipsilateral corticospinal tract, greater "mirroring" motor represent

255 turally altered pathways, in addition to the corticospinal tract, post stroke.

256 known to strengthen following damage to the corticospinal tract, such as after stroke, partially con

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

258 disorders resulting from degeneration of the corticospinal tract.

259 spinal neurons, the cells that originate the corticospinal tract.

260 rity of the primary sensorimotor network and corticospinal tract.

261 cesses that suppress excitability within the corticospinal tract.

262 e spinal branching compared to contralateral corticospinal tract.

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

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

265 ficant bilateral clusters in the spinal cord corticospinal tracts (P < 0.01).

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

267 st a cumulative effect of lesions within the corticospinal tracts along the brain, brainstem and spin

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

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

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

271 Corticospinal tracts correlated with patients' self-rati

272 scribe the distribution of lesions along the corticospinal tracts from the cortex to the cervical spi

273 The spinal cord corticospinal tracts lesion volume fraction remained the

274 Baseline spinal cord corticospinal tracts lesion volume fraction was also ass

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

276 hypothesis could be that lesion location in corticospinal tracts plays a key role in explaining moto

277 The lesion volume fraction in the corticospinal tracts was higher in secondary and primary

278 n, brainstem and spinal cord portions of the corticospinal tracts were identified using probabilistic

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

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

281 link between lesion load and location within corticospinal tracts, and disability at baseline and 2-y

282 in motor regions (bilateral precentral gyri, corticospinal tracts, and the corpus callosum) of partic

283 Corticospinal tracts, and the thalamic radiation and cal

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

285 stroke axonal sprouting of corticobulbar and corticospinal tracts, which might have contributed to re

286 were not homogeneously distributed along the corticospinal tracts, with the highest lesion frequency

287 0001) and spinal cord (r = 0.57, P < 0.0001) corticospinal tracts.

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

289 diata, superior longitudinal fasciculus, and corticospinal tracts.

290 etries in the structural connectivity of the corticospinal tracts.

291 -based analysis confirmed the results within corticospinal tracts.

292 er and pathological involvement (2/2) of the corticospinal tracts.

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

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

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

296 so benefit from more rapid and less variable corticospinal transmission.

297 e then assessed different parts of the first corticospinal volley elicited by transcranial magnetic s

298 The first indirect (I) corticospinal volley from stimulation of the motor corte

299 by exploiting small time differences in the corticospinal volleys evoked by non-invasive stimulation

300 CMS, 180 pairs of stimuli were timed to have corticospinal volleys evoked by transcranial magnetic st