ライフサイエンスコーパス: axon

1 erve conduction and metabolic support to the axon.

2 the nucleus, cytoplasm of the cell body, and axon.

3 ection likely due to coendocytosis along the axon.

4 s and sorting of these virions into neuronal axons.

5 uction velocity and metabolic support to the axons.

6 the sorting and transport of PRV virions in axons.

7 led to extensive myelination of regenerated axons.

8 naptic vesicle protein transport vesicles in axons.

9 d completely fail to remyelinate regenerated axons.

10 ows discrimination between active and silent axons.

11 trols, suggesting increased remyelination of axons.

12 oot ganglion (L-DRG) neurons with myelinated axons.

13 metabolic coupling, supports the survival of axons.

14 thereby enhancing conduction in demyelinated axons.

15 city of axotomized and spared reticulospinal axons.

16 eaching conduction failure in small diameter axons.

17 ogated deficiencies in fetal thalamocortical axons.

18 on of action potentials along the ensheathed axons.

19 plasmic localization of TDP-43 and shortened axons.

20 The WGs are postmitotic and wraps PR axons.

21 ade transport of virus particles in neuronal axons.

22 d by stimulation of midbrain dopamine neuron axons.

23 re the following: (a) Comb nerves with giant axons.

24 tin, removes minus-end-out microtubules from axons.

25 as been difficult due to size limitations of axons.

26 mechanism that controls the fate of injured axons.

27 synapse from the retina and even in retinal axons.

28 t action potential propagation in myelinated axons.

29 response to antidromic stimulation of motor axons.

30 nel clusters and the structural integrity of axons.

31 accumulates predominantly in cell bodies and axons.

32 esynaptic inhibition, are instead dynamic in axons.

33 ing recycling from endosomes, in a subset of axons.

34 etween room and physiological in the largest axons.

35 infraorbital nerve, containing about 80,000 axons.

36 demyelinated lesions with dystrophic neurons/axons.

37 he only significant load-bearing elements in axons.

38 of precise diameter determination in larger axons.

39 n interface, and the integrity of myelinated axons.

40 or of regenerative growth in NgR1-expressing axons.

41 signals along axons to the targets of those axons.

42 rial motility in zebrafish sensory and motor axons.

43 ATs, ZDHHC5 and ZDHHC8, were enriched in DRG axons.

44 are well established, it remains unclear how axons adjust strategies over time and space.

45 Peripheral sensory neurons regenerate their axon after nerve injury to enable functional recovery.

46 CK2alpha's appearance in axons after PNS nerve injury correlates with disassembly

47 ion limited regeneration of growth-competent axons after sciatic nerve and spinal cord injury.

48 Remarkably, normal optic nerve axons also show temperature dependent effects, with a fa

49 own about which PATs are present in neuronal axons, although long-distance trafficking of palmitoyl-p

50 Moreover, if each axon and dendrite strive to shorten while preserving con

51 The interface between an axon and myelin is maintained by a number of biomolecula

52 ntal framework to further explore chip-scale axon and neuron specific neural stimulation, with future

53 The squid giant axon and synapse, for example, laid the foundation for o

54 t HSV particles from neuron cell bodies into axons and along axons to axon tips in the periphery is a

55 shown to promote degeneration of optic nerve axons and apoptosis of retinal ganglion cells (RGCs), ho

56 Microtubule polarity in axons and dendrites defines the direction of intracellul

57 pam enhanced GABA-A currents on dopaminergic axons and directly inhibited release, but also likely ac

58 mice showed thinner myelin of large diameter axons and gross aberrations in myelin organization affec

59 d to axonogenesis, deficient thalamocortical axons and impaired outgrowth of thalamic axons in respon

60 then removed and stained to visualize single axons and nerve endings immunoreactive to calcitonin gen

61 The dynamic localization of HPR3 between axons and nuclei during myelination was consistent with

62 ble the robust regeneration of corticospinal axons and restore forelimb function after spinal cord in

63 ied jellyfish because of its system of giant axons and unique fast swimming/escape behaviors.

64 matic spiking, calcium signals at somata and axons, and striatal dopamine concentrations.

65 covered a narrow window (P12-P18) over which axons arborized and formed connections.

66 ve contributions from somata, dendrites, and axons are often unknown.

67 Spatial segregation of proteins to neuronal axons arises in part from local translation of mRNAs tha

68 Single axons arising from DRG were identified in the distal col

69 cells tightly associated with photoreceptor axons at stereotyped positions in both uninjured and reg

70 caffold in directing corticospinal and other axons at the junction between the striatum and globus pa

71 ells (RGCs), downregulation of Arl8B reduces axon branch density and shifts their location more proxi

72 ing that autophagy plays a prominent role in axon branch formation.

73 plays a principal role in the positioning of axon branches by spatially controlling autophagy, thus d

74 Our data suggest that Arl8B controls axon branching by controlling locally autophagy.

75 Interstitial axon branching is an essential step during the establish

76 nduction of autophagy by rapamycin increases axon branching, indicating that autophagy plays a promin

77 g ventral nerve cord produces defasciculated axon bundles that do not reach their targets.

78 are also frequently contacted by incoming IC axons, but the strength of this connection is weak.

79 s, feedback, and lateral inhibition of these axons by a large population of neurons, and the converge

80 drive dopamine release from dopamine neuron axons by activation of nicotinic acetylcholine receptors

81 cal SGs are not prevented from contacting PR axons by CG membrane.

82 e peripheral nervous system, protect injured axons by virtue of a dramatic glycolytic upregulation th

83 ateral inhibitory networks mediated by short axon cells (SACs) in the mouse olfactory bulb (OB) might

84 revealing that many afferent neurons project axon collaterals to both the lateral and medial NTS subd

85 zebrafish (bony fish) support the unbranched axon concept, with 94% of axons terminating in single gl

86 How this occurs when axons contain a plethora of proteins that can silence th

87 allows region-based quantification of total axon content in large and complex 3D structures after re

88 wever, electrical stimulation of presynaptic axons, conventionally used to evoke synaptic responses,

89 ch at the gray-white matter interface places axons crossing this region at greater risk of mechanical

90 DAI causes immediate, sporadic axon damage followed by progressive secondary axon damag

91 xon damage followed by progressive secondary axon damage.

92 although depletion of Csnk2a1 mRNA from PNS axons decreases regeneration and increases G3BP1 granule

93 NAD(+) with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not

94 glaucoma, TNF-alpha induces SARM1-dependent axon degeneration, oligodendrocyte loss, and subsequent

95 he extracellular space prior to catastrophic axon degeneration.

96 tion is a widespread mechanism of programmed axon degeneration.

97 This may be attributed to axon degeneration/neuronal death and sustained neuroinfl

98 tivation by enhancing the amplitude of giant axon depolarization.

99 retrograde signaling, a process critical for axon development and for responses to injury.

100 itive regulator of both in vitro and in vivo axon development.

101 ogies drive previously reported 2D trends in axon diameter and g-ratio.

102 This is particularly challenging when axons differ in their morphological and physiological pr

103 factory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli, whe

104 oid rupture events that lead to catastrophic axon disassembly.

105 Pathological degeneration of axons disrupts neural circuits and represents one of the

106 leads to rapid, programmed disintegration of axons distal to the site of lesion.

107 Additionally, our data showed that stretched axons do not respond to BDNF signaling, suggesting inter

108 fusion/fission defects and vacuolation, but axons do not show increased levels of H(2)O(2).

109 ression involves retinal ganglion cell (RGC) axon dysfunction that precedes frank degeneration.

110 ere they regulate dendritic spine formation, axon elongation, and pontine midline crossing in a FEZF2

111 n the establishment of neuronal polarity and axon elongation.

112 ination-related cellular processes including axon ensheathment and oligodendrocyte differentiation.

113 based on the assumption that receptor neuron axons exclusively connect to a single glomerulus without

114 demonstrate that chick dorsal root ganglion axons exhibit a tension buffering or strain-softening re

115 eatic islets are innervated by vagal sensory axons expressing Phox2b, substance P, calcitonin-gene re

116 u3f4 is normally required for SGN peripheral axon extension into the sensory domain, we used a geneti

117 Neuronal activation-mediated axon extension is dependent upon changes in the status o

118 localization of filopodial dynamics and thus axon extension.

119 t crush injury, centrally-projecting sensory axons fail to regenerate across the dorsal root entry zo

120 idity, showed a significant reduction of RGC axon fiber layer thickness, consistent with the plausibl

121 ime window for sorting into and transport in axons for further host-to-host spread.

122 Mutant axons from R-neurons fail to cross the midline, which is

123 gions can be generalized to map and quantify axons from thalamocortical, deep cerebellar, and cortica

124 demonstrated that regenerating corticospinal axons functionally integrate into spinal circuits.

125 een identified: they include two independent axon-glia interactions that converge on distinct axonal

126 is glycolytic response, paired with enhanced axon-glia metabolic coupling, supports the survival of a

127 ntaining the myelin sheath around peripheral axons (Grove et al., 2017).

128 erplay of the molecular programs that direct axon growth and cell specification, with activity-depend

129 The fundamental problem in axon growth and guidance is to understand how cytoplasmi

130 The fundamental problem in axon growth and guidance is understanding how cytoplasmi

131 tions of actin in the growth cone to produce axon growth and guidance.

132 cytoplasmic processes between NMJs to guide axon growth and NMJ reinnervation.

133 -gated calcium channels negatively regulates axon growth and regeneration of corticospinal neurons, t

134 dicate a critical role of force in promoting axon growth by facilitating microtubule (MT) polymerizat

135 ear series of impenetrable barriers, forcing axon growth cones to traverse one half of each somite as

136 We identified divergent modes of initial axon growth that prefigure disrupted differentiation of

137 early in development results in spontaneous axon growth through the injury, but this regenerative po

138 E or a conditioning injury alone, propelling axon growth well beyond the spinal injury site.

139 nules as well as increased phospho-G3BP1 and axon growth, although depletion of Csnk2a1 mRNA from PNS

140 el mechanism underlying stimulation-mediated axon growth.

141 he p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss

142 Although the basic principles of axon guidance are well established, it remains unclear h

143 uronal cdk5/p35 kinase, affects responses to axon guidance cues upstream of cdk5, specifically, to Se

144 isease (AD), as a potential key modulator of axon guidance, a neuronal process that depends on the re

145 leton dynamics and appear necessary for some axon guidance, also mediate interactions with membrane a

146 tor of neuronal migration, axonal outgrowth, axon guidance, and synaptogenesis by activating the GTPa

147 However, the inability to control axon guidance, and thus neuronal network architecture, h

148 nd included membrane receptors important for axon guidance, innate immunity, synapse development, and

149 Like axon guidance, the tuning of vascular tip cells during a

150 ment through highly constrained processes of axon guidance, which have been extensively studied.

151 F-beta and notch signaling), rap1-signaling, axon-guidance and hippo-signalling.

152 ses are unclear, but epidermal, unmyelinated axons have been shown to be the first to degenerate.

153 Adult mammalian central nervous system axons have intrinsically poor regenerative capacity, so

154 and the odorant transduction process and the axon hillock spiking mechanism of the olfactory sensory

155 ed to stable microtubules) within the distal axon, illuminating a novel mechanism underlying stimulat

156 network trained with volumes of serotonergic axons in all major brain regions can be generalized to m

157 orted recovery and regrowth of monoaminergic axons in female, but not in male mice.

158 mbined rapid in vivo labeling of single CN V axons in LgDel+/- mouse embryos, a genomically accurate

159 cal axons and impaired outgrowth of thalamic axons in response to cell-extrinsic factors.

160 ion of mRNAs that are first transported into axons in ribonucleoprotein particles (RNPs), complexes c

161 storation of Slit-N or Slit-C does not repel axons in Slit-null flies.

162 emonstrates myelination of the graft-derived axons in the corpus callosum and that their terminals fo

163 not find interneurons with locally ramifying axons in the LH [11, 12], and nearby subthalamic and tha

164 the mouse striatum and sparse noradrenergic axons in the mouse cortex in acute brain slices.

165 and, enables targeting of dense dopaminergic axons in the mouse striatum and sparse noradrenergic axo

166 n, we imaged the synaptic boutons of retinal axons in the superior colliculus.

167 action potential initiation at the mammalian axon initial segment (AIS), and modulation of AIS size b

168 SD93, but not other MaGUKs, localizes to the axon initial segment (AIS).

169 the neuronal "M-current" and cluster in the axon initial segment to regulate the firing of action po

170 eir compartment-specific requirements in the axon initial segment, in the axon shaft, at synapses or

171 rsed maladaptive shortening in the length of axon initial segments (AIS) in the mPFC of PNI mice.

172 Axon initial segments (AISs) initiate action potentials

173 d sodium channel isoform expressed in mature axon initial segments and nodes, making it critical for

174 anges in pyramidal cell dendritic spines and axon initial segments consistent with compensation for h

175 Axon injury is a hallmark of many neurodegenerative dise

176 t arises in SCs as an inherent adaptation to axon injury.

177 Structurally, geniculate axons innervated excitatory cortical targets in a prefer

178 Thalamocortical posterior nucleus (Po) axons innervating the vibrissal somatosensory (S1) and m

179 We identify layer-specific axon innervation pattern as a defining feature distingui

180 cking of palmitoyl-proteins is important for axon integrity and for axon-to-soma retrograde signaling

181 n-induced regeneration of DRG neuron central axons is abolished.

182 After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic defici

183 The regrowth of severed axons is fundamental to reestablish motor control after

184 flow through even the longest cones (0.4-mm axons) is essentially lossless.

185 While work has focused on myelin and axon loss in MS, less is known about mechanisms underlyi

186 ce in which glial cells cannot fully support axons metabolically.

187 These complex 3D axon morphologies drive previously reported 2D trends in

188 diseases, such as regression of motor neuron axons, motor neuron death, and muscle degradation and at

189 l activity-related solute homeostasis at the axon-myelin interface, and the integrity of myelinated a

190 sociated with decreased oxidative stress and axon/myelin loss.

191 phingolipid levels and is important for full axon myelination, which requires elevated levels of memb

192 ized physiological functions, such as during axon myelination.

193 In the developing nervous system, axons navigate through complex terrains that change depe

194 Spinal commissural axon navigation across the midline in the floor plate re

195 their postsynaptic partners, which requires axons not only to faithfully transfer action potentials

196 this process using live imaging of the TSM1 axon of the developing Drosophila wing.

197 Axons of dopaminergic neurons innervate the striatum whe

198 e, cytoskeletal organization has to adapt to axons of dramatically different dimensions, and to their

199 tion potential propagation by insulating the axons of neurons and by reducing membrane capacitance.

200 nificantly reduces mitochondrial motility in axons of neurons.

201 In the posterior median eyes, the axons of their first-order visual neuropils project dire

202 lative to the target neural element, whether axon or cell body.

203 critical regulators of tail regeneration and axon organization.

204 ater stages of neural development, including axon outgrowth and neuronal maturation.

205 After axon outgrowth and synapse formation, the nervous system

206 ct microbiota-dependent metabolites promoted axon outgrowth from fetal thalamic explants.

207 tinal organoid cultures without compromising axon outgrowth, addressing a major issue in the field of

208 intenance of this scaffold, and consequently axon pathfinding, is dependent on the expression of an a

209 ance, sharing common segmental organization, axon pathways, and chemical messengers.

210 Purkinje cell zones and disrupts excitatory axon patterning.

211 Ranbp1-/-, Ranbp1+/- and LgDel+/-:Raldh2+/-; axon phenotypes are seen when hindbrain patterning and C

212 Inhibitory axons preferentially innervated either L2 or L3/5 apical

213 sion mechanism, mediated largely by LP-to-A1 axons preferentially innervating specific inhibitory neu

214 mammalian peripheral auditory system through axon projections to the cochlea.

215 such behaviors [3-5], and the presence of NE axons projections in this brain nucleus [6], we assessed

216 Noninvasive measurement of axon radii could have significant impact on the understa

217 enetic stimulation of nigrostriatal dopamine axons rapidly and persistently elevated the excitability

218 not rely on hand-crafted image features for axon recognition and is robust to variations in the exte

219 V1 axons recorded in RSC were less modulated by task engage

220 lation patterns and transcriptomes, promotes axon regeneration after injury, and reverses vision loss

221 iting may provide a new option for promoting axon regeneration and functional recovery after CNS trau

222 Axon regeneration failure causes neurological deficits a

223 oRaf or optoAKT activation not only enhanced axon regeneration in both regeneration-competent and -in

224 active non-coding RNA (ncRNA) essential for axon regeneration in Caenorhabditis elegans.

225 trolling myelination after injury and during axon regeneration in the central nervous system (CNS).

226 The main limitation on axon regeneration in the peripheral nervous system (PNS)

227 had neuroprotective properties and drove CNS axon regeneration in vivo, in part via secretion of a co

228 ry strategy to promote functionally-relevant axon regeneration of adult neurons into the CNS after in

229 Ror was not required for axon regeneration or normal dendrite development, sugges

230 ynthesis and toward PL synthesis may promote axon regeneration.

231 of fatty acid synthase (Fasn) in SGC impairs axon regeneration.

232 ic kinases that regulated neuronal death and axon regeneration.

233 njury, and is cell-autonomously required for axon regeneration.

234 to a complex cellular response that includes axon regrowth and is accompanied by neurogenesis.

235 r data uncover a novel pathway that controls axon regrowth through axonal mitochondrial calcium uptak

236 netic deletion of PTEN results in robust CNS axon regrowth, while PTEN repression with short hairpin

237 lowed temporal tuning and proper guidance of axon regrowth.

238 microglia significantly improved healing and axon regrowth.

239 ors as potential regulators of developmental axon regrowth.

240 We found that peripheral axons release serine (Ser) to support the growth of exog

241 Slit2, a neural axon repellent, is expressed and released by CD34(-) OF

242 multiple key roles in neurodevelopment, from axon repulsion to dendrite elaboration.

243 Our anatomic finding that axons run in parallel to the dendrites and make multiple

244 and new sheaths were often established along axon segments previously lacking myelin.

245 irements in the axon initial segment, in the axon shaft, at synapses or in growth cones.

246 ty of lysosomes and autophagosomes along the axon shaft.

247 ear (LOC) efferent fibres re-form functional axon-somatic connections with aged IHCs, but this was se

248 Axons span extreme distances and are subject to signific

249 at in the absence of Dcc, some ganglion cell axons stalled at the optic disc, whereas others perforat

250 acer labeling of long-distance corticospinal axons suggest that recovery might be partly attributable

251 s healing process and stalls the regrowth of axons, suggesting that microglia are critical for orches

252 Hgf/Met signaling is sufficient to redirect axon targeting and disrupt the topographic map.

253 dynamics of Hgf/Met signaling to coordinate axon targeting with the developmental progression of the

254 ion of guidance factors to shape topographic axon targeting.

255 inct neuronal morphologies with a variety of axon terminal arborizations subserving their functions.

256 etina, with significantly less dendritic and axon terminal labeling in TRPM1 knockout compared to wil

257 onstrates that both kinases are contained in axon terminals and dendritic spines adjacent to the syna

258 inct clusters of acetylcholine receptors and axon terminals exhibited numerous terminal varicosities.

259 c activation of VTA glutamate cell bodies or axon terminals in NAc was sufficient to support reinforc

260 ly, silencing VTA dopamine neurons, or their axon terminals in the BA during the footshock, reduced t

261 tant characteristic of dopamine release from axon terminals in the striatum is that it is rapidly mod

262 receives S1 inputs, and activation of the S1 axon terminals increases the response to noxious stimuli

263 LRRTM4 is enriched at GABAergic synapses on axon terminals of rod bipolar cells (RBCs).

264 abeled projection neurons from (outputs) and axon terminals to (inputs) the ACC of adult rhesus monke

265 Neuronal axons terminate as synaptic boutons that form stable yet

266 ort the unbranched axon concept, with 94% of axons terminating in single glomeruli.

267 umerous ectopic Na(+) channel clusters along axons that are devoid of myelin segments.

268 ndant space-filling cytoskeletal polymers in axons that are transported along microtubule tracks.

269 Importantly, these rami carry axons that branch to iWAT, as well as axons that travel

270 te the potential mechanical vulnerability of axons that span the gray-white tissue interface.

271 carry axons that branch to iWAT, as well as axons that travel further to innervate the skin and vasc

272 ced plasticity leads to the sprouting of new axons, the formation of new synapses and the remapping o

273 on cell bodies into axons and along axons to axon tips in the periphery is an important component of

274 m the various cytoskeletal components of the axon to show that the recently discovered membrane-assoc

275 from neuron cell bodies into axons and along axons to axon tips in the periphery is an important comp

276 essing cortical neurons by exposure of their axons to light on the contralateral side.

277 s, and increased the ability of regenerating axons to penetrate the inhibitory spinal cord glial scar

278 gy by retrogradely propagating signals along axons to the targets of those axons.

279 Action potentials propagate through long axons to their postsynaptic partners, which requires axo

280 tetanus neurotoxin (TeNT) in the ipsilateral axon, to prevent Hebbian stabilization.

281 eins is important for axon integrity and for axon-to-soma retrograde signaling, a process critical fo

282 quired for Gp130/JAK/STAT3, but not DLK/JNK, axon-to-soma signaling.

283 ivation of different axonal mRNAs as severed axons transition from injury to regenerative growth.

284 rkably, one source of Netrin -1 is forebrain axons traversing the midbrain, and this is required for

285 for netrin-1-dependent filopodial responses, axon turning and branching, and fiber tract formation.

286 Following acute neural injury, severed axons undergo programmed Wallerian degeneration over sev

287 t nodes of Ranvier, a hallmark of myelinated axons, underlies effective saltatory conduction.

288 process of autonomous distal degeneration of axons upon injury.

289 trograde transport on the organelles and the axon was unknown.

290 Enhanced growth in stretched axons was also accompanied by endoplasmic reticulum (ER)

291 Spatial integration of V1 axons was remarkably similar across areas and significan

292 Selective stimulation of cholinergic axons was sufficient to induce LTP, which was prevented

293 Within single axons, we find that the variation in diameter and conduc

294 ng age-related loss of retinal ganglion cell axons, we showed a significant decline in GCL thickness,

295 New branch additions in the ipsi axon were exclusively increased by contralateral eye sti

296 erence (RNAi) was performed and dendrites or axons were removed using laser microsurgery.

297 timing is predicted to diverge between these axons when extrinsic conditions change.

298 ion, the migrating SG contact the nascent PR axon, which in turn release FGF to induce SGs' different

299 integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin's endoplasmic reticulum

300 e it is necessary at the myelin membrane for axon wrapping.