ライフサイエンスコーパス: callosal

1 ings of deficits in bimanual coordination in callosal absence, but using significantly improved measu

2 s difference is mechanistically explained by callosal activation of fast-spiking parvalbumin-expressi

3 several days before eye-opening, retinal and callosal activities drive massive apoptosis of GABAergic

4 rozygous Nfib-deficient animals also exhibit callosal agenesis and delayed lung maturation, indicatin

5 nique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar

6 (genetic and environmental) determining both callosal agenesis and its autistic features, and what ar

7 ised structural abnormalities, in particular callosal agenesis and pontine hypoplasia, delayed myelin

8 stinguish autistic behaviour associated with callosal agenesis from autism more generally.

9 l and cognitive impairments in subjects with callosal agenesis may overlap with the profile of autism

10 provide potential avenues for therapies for callosal agenesis or related neurodevelopmental disorder

11 directly compared a group of 26 adults with callosal agenesis to a group of 28 adults with a diagnos

12 enetic features of syndromes associated with callosal agenesis, and provides a genetic and developmen

13 erited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined i

14 In addition to the five principal features (callosal agenesis, cataracts, hypopigmentation, cardiomy

15 igence quotient and autism symptomatology in callosal agenesis, nor evidence that the presence of any

16 ns and single gene mutations associated with callosal agenesis.

17 deposts and Slit2 upregulation, resulting in callosal agenesis.

18 odevelopmental disorders are associated with callosal agenesis.

19 lity, neocortical abnormalities, and partial callosal agenesis.

20 lectual disability and frequently displaying callosal agenesis.

21 enic mice, we first assessed hippocampal and callosal anatomy in PSAPP (PS1xAPP) mice, another transg

22 frontal cortex infiltrated juxtaposed corpus callosal and cortical tissue.

23 ound to repel cortical axons into developing callosal and corticospinal pathways.

24 tor cortex of rodents occurs largely through callosal and frontal cortical association projections di

25 to investigate the anatomical development of callosal and frontal premotor projection neurons (CPN an

26 nces between these neurons with simultaneous callosal and frontal projections during development.

27 al projection neurons maintains simultaneous callosal and frontal projections in adult mice, suggesti

28 the percentage of neurons with simultaneous callosal and frontal projections, and an isolated popula

29 According to current views, callosal and non-callosal fates are determined early aft

30 ed higher mean fractional anisotropy (FA) in callosal and projection fibers (IC and corona radiata) r

31 Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-depen

32 pread abnormal diffusivity properties in the callosal and temporal lobe WM regions in individuals wit

33 ical disability in MS, and that low anterior callosal and thalamic FA have specific importance to cog

34 To assess the diagnostic performance of the callosal angle (CA) and Evans index (EI) measures and to

35 Thus, our results demonstrate that callosal as well as extracallosal anatomical connections

36 terior commissure was absent, and the corpus callosal as well as hippocampal commissural axons failed

37 Cortical pathology, callosal atrophy and axonal loss are substrates of progr

38 nal propagation and anatomical properties of callosal auditory fibers as measured with diffusion-weig

39 AC were negatively related to the volume of callosal auditory fibers.

40 Functional analysis of callosal axon conduction showed a significant improvemen

41 gen receptor beta ligand treatment to affect callosal axon demyelination and stimulate endogenous mye

42 ional functions for the sling independent of callosal axon guidance.

43 The midline glia structures important for callosal axon midline crossing appear normal in the tran

44 ost cells emitting guidance cues to instruct callosal axon navigation.

45 The meninges produce BMP7, an inhibitor of callosal axon outgrowth.

46 Callosal axon pathology progressively worsened with age

47 er positioning of migrating neurons, and the callosal axon projections important for communication be

48 understudied areas of development including callosal axon refinement.

49 decline was accompanied by brain atrophy and callosal axonal loss.

50 with the change in conductive properties of callosal axons along the anterior-posterior axis.

51 IE2(+) callosal axons also failed to cross the midline to form

52 Although callosal axons approach the midline, they fail to cross

53 mate homeostasis at a time when unmyelinated callosal axons are engaging in glutamatergic signaling w

54 ory lesion in the rat frontoparietal cortex, callosal axons become dystrophic and die back.

55 m, Slit2 expressed by the glial wedge guides callosal axons before they cross the midline, as they ap

56 pathological and functional abnormalities of callosal axons despite the presence of inflammation.

57 usly obtained by extrapolating the length of callosal axons from that of the monkey, proportionally t

58 In Neurod2/6 double-mutant mice, callosal axons lack expression of the cell adhesion mole

59 py studies revealed a marked degeneration of callosal axons long before the onset of motor symptoms.

60 Callosal axons release glutamate by vesicular fusion, wh

61 Crossing of the midline by callosal axons relies on a proper midline environment th

62 ng these results, increased vulnerability of callosal axons was documented in the brains of HD patien

63 oping chick spinal commissural axons and rat callosal axons) findings demonstrate that knockdown of K

64 a large fraction of CUX1(+) neurons project callosal axons, we speculate that microglia deficiency m

65 ry bulb and a failure of midline crossing of callosal axons.

66 neurons and turns on before outgrowth of the callosal axons.

67 ted step that occurs during remyelination of callosal axons.

68 istic extracortical features, such as corpus callosal, basal ganglia, and cerebellar abnormalities.

69 confirmed within the corticospinal tract and callosal body, and linked strongly to clinical upper mot

70 n fractional anisotropy in the left cingulum-callosal bundle.

71 fusion tract tracing (DTT) reconstruction of callosal bundles from different areas.

72 ed in a manner consistent with cell-specific callosal changes and support a shift in the overall stat

73 sensitive to both disruptions in myelin and callosal circuitry.

74 Furthermore, callosal compound action potential recordings from analo

75 re oligodendrocytes correlated with improved callosal conduction and refractoriness.

76 ribution of axon diameter, so as to estimate callosal conduction delays from different areas.

77 As in monkeys, in humans the shortest callosal conduction delays were those of motor, somatose

78 as a prerequisite for the computation of the callosal conduction distances and delays in humans, whic

79 It is generally thought that callosal connections (CCs) in primary visual cortices se

80 ith the nonparetic limb are mediated through callosal connections and the contralesional sensorimotor

81 ion, without segregating into ODCs, and that callosal connections are not patchy.

82 laces, we studied the topography of emerging callosal connections at and immediately after P6.

83 us, the development of the normal pattern of callosal connections depends on dorsal column input and

84 Similarly, we found that callosal connections in albino rats are not patchy but i

85 Our findings provide insight on the role of callosal connections in generating binocular cells.

86 strated surprisingly normal distributions of callosal connections in the nondeprived right hemisphere

87 n these findings and the known physiology of callosal connections in the visual system, we developed

88 er, in rodents the overall pattern of visual callosal connections is adult-like by postnatal day 12 (

89 y site prompted us to examine whether corpus callosal connections may play a role in this transhemisp

90 The main callosal connections of M1 and the caudal portion of PMD

91 The callosal connections of motor and premotor fields in the

92 this question, we examined the cortical and callosal connections of the primary somatosensory area (

93 Dc) were with homotopic sites, and the major callosal connections of the rostral portion of PMD (PMDr

94 l striate cortex, and the overall pattern of callosal connections revealed following multiple tracer

95 , LC offspring had a broader distribution of callosal connections than HC offspring and a significant

96 We hypothesized that the inability of callosal connections to relay ipsilateral eye input to l

97 In BEP7 ferrets we found that the pattern of callosal connections was highly anomalous and the sizes

98 Callosal connections were mostly with the region of the

99 including direct subcortical connections and callosal connections with the contralateral hemisphere.

100 role in the development of interhemispheric callosal connections, but little is known about the role

101 ain features, including changes in raphe and callosal connections, sensory processing, and myelin she

102 ition, M1 forelimb representation had sparse callosal connections, whereas M1 trunk and face represen

103 ns, as well as the premotor areas, had dense callosal connections.

104 onnectivity is mirrored in the contralateral callosal connections.

105 wo-stage pathway involving interhemispheric (callosal) connections between information processing lev

106 extract measures of structural and effective callosal connectivity between different somatosensory co

107 method to map the functional organization of callosal connectivity by combining in vivo 3D random-acc

108 Callosal connectivity tended to be strongest in the homo

109 The callosal connectivity, although homotopic, consists main

110 on to the thalamus and other ipsilateral and callosal corticocortical connections.

111 cal, periventricular subcortical lesions and callosal demyelination in relapsing-remitting experiment

112 We mapped callosal development and explored sex differences in a l

113 This defect in callosal development correlates with the expression of t

114 ouse OPC differentiation in vitro and during callosal development in vivo.

115 Even so, existing studies of callosal development tend to use parcellation schemes th

116 t1/2 double mutants display malformations in callosal development, and in corticothalamic and thalamo

117 opmental regulation of normal brain size and callosal development.

118 circuit dysfunction (n = 22), and those with callosal disconnection (n = 7).

119 circuit dysfunction (n = 22), and those with callosal disconnection (n = 7).

120 In many cases of callosal dysgenesis in both human patients and mouse mod

121 unctional astroglial migration underlies the callosal dysgenesis in conditional Fgfr1 knockout mice,

122 We propose that anomalous brain circuitry of callosal dysgenesis is determined by long-distance plast

123 n this puzzle, we investigated patients with callosal dysgenesis using structural and functional neur

124 data showed that CFC mediated the effect of callosal FA on BPA.

125 allosum (DTI), individuals with low anterior callosal FA were found to exhibit greater activity in a

126 erformance for individuals with low anterior callosal FA, greater RIPFC activity during verbal encodi

127 rformance for individuals with high anterior callosal FA.

128 (RIPFC) relative to those with high anterior callosal FA.

129 are critical downstream targets of Satb2 in callosal fate specification.

130 According to current views, callosal and non-callosal fates are determined early after a neuron's bir

131 ed the properties of the estimated occipital-callosal fiber tracts by combining them with functional

132 present and function in developing forebrain callosal fibers based on both spatial and temporal expre

133 eas in rats bilaterally enucleated at birth, callosal fibers connect topographically mismatched, mirr

134 nt) hand correlated with higher integrity of callosal fibers connecting occipital cortices, whereas l

135 raded left posterior cingulate and posterior callosal fibers in chronic alcoholics, which is consiste

136 ecifically with the fractional anisotropy of callosal fibers interconnecting SII.

137 We segmented the callosal fibers into regions based on their likely corti

138 pinal tracts, and the thalamic radiation and callosal fibers involving motor function, improved after

139 sivity perpendicular to the main axis of the callosal fibers that connect the temporal lobes.

140 tion primarily occurs in SII, is mediated by callosal fibers that interconnect homologous SII areas,

141 l axons were examined with DiI labeling, few callosal fibers were found to traverse the midline in bo

142 ve transhemispheric propagation along corpus callosal fibers.

143 de well with the projection direction of the callosal fibers.

144 ental abnormalities and accelerated aging in callosal fibers.

145 the corpus callosum: the genu, splenium and callosal fibres connecting the motor cortices.

146 cting the SMA with the striatum; and (5) SMA callosal fibres.

147 heterozygosity and Yap deletion both restore callosal formation in Nf2 mutants.

148 Corpus callosal fractional anisotropy led to the lowest sample

149 by abnormal interhemispheric processing and callosal functioning, but there have been no studies on

150 s each correlated with older age and smaller callosal genu (anterior) areas.

151 tter radial diffusivity predominantly in the callosal genu and body (both p < 0.003).

152 tter integrity, but it is less marked in the callosal genu and body in the offspring.

153 Callosal genu and body microstructure but not macrostruc

154 ty of major white matter tracts, such as the callosal genu and splenium, cingulum, optic radiations,

155 ignificantly associated with lower FA in the callosal genu, thalamus, right posterior cingulum, and f

156 Alternating phases of callosal growth and shrinkage may reflect a permanent ad

157 Thus, more detailed mapping of callosal growth processes is desirable to create a norma

158 ted interest in the mechanisms that regulate callosal growth.

159 Total brain, corpus callosal, hippocampal, thalamic and basal ganglia volume

160 The additional anomalies were as follows: callosal hypoplasia in 3 children, abnormalities of gyra

161 with additional cerebral anomalies including callosal hypoplasia or agenesis, abnormal basal ganglia

162 The principal functional unit of callosal influence comprises a facilitatory centre and a

163 areas 17 and 18 receive selective excitatory callosal input on both ongoing and evoked activity.

164 Callosal inputs also elicit more spikes in type A neuron

165 Repeatedly stimulating callosal inputs evokes progressively smaller excitatory

166 In contrast, alcoholics who have compromised callosal integrity showed less bilateral processing adva

167 the contralateral thalamus may modulate the callosal interactions that are presumed to play a role i

168 ly, it was thought a total absence of corpus callosal interhemispheric connective tissues in the BTBR

169 onto-occipital fasciculus, internal capsule, callosal isthmus, and the corona radiata (p=0.04 for FIQ

170 brain and have referenced these maps against callosal landmarks.

171 e matter volume (P<.001), a 6.9% increase in callosal length (P =.002), a 15.3% reduction in callosal

172 Study of patients with callosal lesions can provide insight into the mediation

173 We found that the patterns of callosal linkages in rats enucleated at P12, P8, and P6

174 r the development of retinotopically matched callosal linkages.

175 Callosal malformations are among the most common congeni

176 the cues that determine the mirror-symmetric callosal map exert only a weak control on the topography

177 t support the idea that retinal input guides callosal map formation by primarily promoting the large-

178 bserved that the normal, nonmirror-symmetric callosal map, as well as the anomalous, mirror-symmetric

179 whether retinal input guides development of callosal maps by promoting either the corrective pruning

180 Callosal maps were revealed by placing small injections

181 leukoencephalopathy and juxtacortical and/or callosal microhemorrhages were brain imaging features in

182 Degradation of the callosal microstructure was consistently associated with

183 rface-based mesh-modeling methods to analyze callosal morphology at extremely high spatial resolution

184 ivity of the reconstructed corticospinal and callosal motor fibres compared with controls, without ch

185 Increased callosal myelination and mature oligodendrocytes correla

186 The differences in callosal myelination suggested by these results may refl

187 Finally, we hypothesize that intrinsic and callosal networks processing different orientations and

188 Satb2) is required for proper development of callosal neuron identity and represses expression of gen

189 in regulating transcriptional mechanisms of callosal neuron specification.

190 on, multiple EphA receptors are expressed in callosal neurons and ephrin-A5 stimulates neurite outgro

191 lin sheaths along single axons of excitatory callosal neurons and inhibitory parvalbumin-expressing i

192 generation of either corticofugal neurons or callosal neurons below the cortex is sufficient to recru

193 bustly to Sema3A than those from presumptive callosal neurons expressing Satb2.

194 nd ephrin-A5 stimulates neurite outgrowth of callosal neurons in vitro.

195 The misspecified callosal neurons largely fail to form the corpus callosu

196 Ski-deficient callosal neurons lose their identity and ectopically exp

197 ctive for corticospinal neurons, but affects callosal neurons within the motor cortex in motor neuron

198 ection in a subset of early born, deep layer callosal neurons.

199 ural stem cell pool and the specification of callosal neurons.

200 o significant effect on the number of visual callosal neurons.

201 d for transcriptional repression of Ctip2 in callosal neurons.

202 a significantly higher percentage of labeled callosal neurons.

203 ispensable for axonal outgrowth of layer 2/3 callosal neurons.

204 ns, and to repress subcerebral characters in callosal neurons.

205 demonstrate a novel paradigm of cortical and callosal neuropathology in a mouse model of MS, perpetua

206 bstantially reduced compared with endogenous callosal OPCs 1 week after lesion and was lost on differ

207 f two anatomically distinguishable pathways, callosal or intracortical.

208 combined to examine the relationship between callosal organization and cortical activity across hemis

209 ovel evidence that individual differences in callosal organization are related to the extent of nondo

210 e of ocular dominance columns (ODCs), and of callosal patches in register with ipsilateral ODCs in th

211 Wnt3 expression in the cingulate callosal pathfinding axons is developmentally regulated

212 y the induction of expression of Wnt3 by the callosal pathfinding neurons, which antagonize the inhib

213 loser to the spike-firing threshold than the callosal pathway.

214 ental disorder affecting thalamostriatal and callosal pathways, also present in the affected grandmot

215 ient involving the geniculo-cortical and the callosal pathways.

216 ght exist between developing ipsilateral and callosal pathways.

217 he extent to which development of the visual callosal pattern depends on retinal influences, and expl

218 tion at P20 had no significant effect on the callosal pattern, but it still caused a reduction in the

219 We studied the mature callosal patterns in normal ferrets and in ferrets bilat

220 Callosal patterns were revealed in tangential sections f

221 which the eyes influence the development of callosal patterns, but not the size of visual cortex, en

222 ate the existence and extent of cortical and callosal plasticity in these subjects.

223 , demonstrating the plasticity and bona fide callosal potential of L4 neurons.

224 ment of retrograde labeling of NeuN-positive callosal projecting neurons and reduction in the labelli

225 d stripping of synaptic proteins in cortical callosal projecting neurons.

226 ay a critical role in the acquisition of the callosal projection fate in layer 5.

227 regulates a decision between subcortical vs. callosal projection neuron fates.

228 vidual neurons adopt either a subcortical or callosal projection neuron identity at early times durin

229 Callosal projection neurons (CPN) are a diverse populati

230 Corticospinal motor neurons (CSMN) and callosal projection neurons (CPN) are the archetypal pro

231 Callosal projection neurons (CPN) connect the cerebral h

232 dendritic complexity of Mecp2-null cortical callosal projection neurons (CPN), and that NF-kappaB si

233 e molecular development and heterogeneity of callosal projection neurons (CPN), cortical commissural

234 send projections away from the cerebrum, and callosal projection neurons (CPN), which send projection

235 ubpopulations within the broad population of callosal projection neurons (CPN), whose axons connect t

236 vo lineage reprogramming of layer 2/3 (L2/3) callosal projection neurons (CPNs) into induced corticof

237 populations of cortical projection neurons: callosal projection neurons and corticotectal projection

238 ex can be classified into two major classes: callosal projection neurons and long-range subcortical n

239 Fezf2(-/-) neurons adopt the fate of callosal projection neurons as assessed by their axonal

240 projection neurons and their replacement by callosal projection neurons cause distinctly abnormal la

241 anglion neurons, retinal ganglion cells, and callosal projection neurons during axon growth.

242 sion of exogenous Tubb2b-E421K in developing callosal projection neurons is sufficient to perturb hom

243 ther of CDO (Boc), is expressed in local and callosal projection neurons of layer II/III that synapse

244 ons in layer 5A and corticocortical neurons (callosal projection neurons similar to corticostriatal n

245 ularly subcategorize distinct populations of callosal projection neurons, often located in distinct s

246 n the early specification of subcerebral and callosal projection neurons, progressively increases aft

247 re expressed in lower cortical layers and in callosal projection neurons.

248 s in YFP(J16) mice cortex were identified as callosal projection neurons.

249 Using this approach on the developing callosal projection of the mouse cerebral cortex, we map

250 ions --> FS-PARV --> CCort) or facilitation (callosal projections --> CCol) of projecting neurons in

251 uits underlying either callosal suppression (callosal projections --> FS-PARV --> CCort) or facilitat

252 n in vitro, whereas Hsc70 activity supported callosal projections and radial neuronal migration in th

253 ciations between the structural integrity of callosal projections and the magnitude of the motor defi

254 Callosal projections are thought to play a critical role

255 the neuronal microcircuits recruited by the callosal projections are unknown.

256 er, retina input specifies the topography of callosal projections by postnatal day (P)6.

257 te that during periods of acoustic exposure, callosal projections emanating from core auditory areas

258 d circuit mapping (CRACM), to map long-range callosal projections from layer (L) 2/3 of the somatosen

259 eafness, there was a significant decrease in callosal projections from the contralateral PAF.

260 In normal rats callosal projections in striate cortex connect retinotop

261 We found that callosal projections suppress the activity of CCort pyra

262 bility of the DTI-FT measurements, occipital-callosal projections were estimated from each subject's

263 mutual repression to produce subcortical or callosal projections.

264 We find that callosal-recipient spines are more likely to cluster wit

265 t spines are more likely to cluster with non-callosal-recipient spines with similar orientation prefe

266 are distributed homogeneously throughout the callosal region in V1.

267 opy (FA) and higher mean diffusivity (MD) in callosal regions and fibre bundles coursing through the

268 The callosal regions were differentially affected by alcohol

269 re area occupied by myelinated axons in both callosal regions.

270 Neither M1 inactivation nor callosal section changed contralateral response threshol

271 ximately 2 SD FA and MD abnormalities in the callosal sectors and fibres, abnormalities that were mor

272 ange, areas of restricted diffusion, diffuse callosal signal change, and atrophy and hyperintensity o

273 wer FA in the right posterior cingulum, left callosal splenium, right inferior fronto-occipital fasci

274 Two patients with anterior callosal strokes bisected lines to the left of midline w

275 sociation between antisocial personality and callosal structural abnormalities.

276 he effects of age and sex, whereas posterior callosal structure was associated with facilitation proc

277 ndicate the following dissociation: anterior callosal structure was associated with inhibitory proces

278 differs across individuals as a function of callosal structure, supporting a role for the corpus cal

279 the smaller area of each of the fiber-based callosal subdivisions.

280 Here the size of callosal subregions and area occupied by myelin were exa

281 The absolute size of callosal subregions differed between preterm and full-te

282 unknown cortical circuits underlying either callosal suppression (callosal projections --> FS-PARV -

283 actors contribute to a maximally potentiated callosal synapse.

284 but the rules that govern the arrangement of callosal synapses on the dendrites of their target neuro

285 intact barrel cortex selectively strengthens callosal synapses to layer 5 neurons in the deprived cor

286 firmed by direct anatomical visualization of callosal synaptic connections using post hoc expansion m

287 grity, particularly in the fronto-limbic and callosal systems.

288 losal length (P =.002), a 15.3% reduction in callosal thickness (P =.04), and increased functional in

289 The temporally distinct changes in callosal thickness are likely to be a consequence of var

290 Except for the rostrum in females, callosal thickness increased across the whole surface, w

291 rkable self-organization of corticofugal and callosal tracts with a functional output, providing new

292 left temporo-parietal areas and in posterior callosal tracts.

293 recording period indicating that the corpus callosal transection did not hinder these remote propaga

294 A separate group of animals underwent corpus callosal transection prior to electrocorticography (ECoG

295 is effect was not found in animals with both callosal transections and unilateral lesions.

296 ions, or unilateral lesions, with or without callosal transections.

297 nsiderable delay, these progenitors generate callosal upper-layer neurons and glia.

298 arriers, presence of decreased white matter, callosal volume, and/or increased ventricle size was ass

299 nctate microhemorrhages in juxtacortical and callosal white matter (in seven of 11 patients).

300 ontrols showed a 22.6% increase in estimated callosal white matter volume (P<.001), a 6.9% increase i

301 ymmetry and the connecting, interhemispheric callosal white matter was also investigated; minicolumn

302 g suggest that microstructural properties of callosal white matter, which includes myelination and ax