ライフサイエンスコーパス: spinal

1 otential need to sacrifice the facial and/or spinal accessory nerves and because of a likely margin-p

2 Compared to other visceral organs, uterine spinal afferent endings displayed noticeably less morpho

3 d peptide (CGRP)-immunoreactivity of uterine spinal afferent endings supplied by thoracolumbar DRG.

4 ory innervation to the uterus is provided by spinal afferent nerves, whose cell bodies lie predominan

5 n) that underlies the gut-brain axis, is via spinal afferent neurons, with cell bodies in dorsal root

6 is, where sensation and pain are mediated by spinal afferents and fear and anxiety (the affective asp

7 ile the origin of the cell bodies of uterine spinal afferents is clear, the identity of their sensory

8 ocomotor sensitization, withdrawal and supra-spinal analgesia were facilitated, consistent with a ton

9 Spinal and bulbar muscular atrophy (SBMA) is a hereditar

10 volume and the growth rate of NF2-associated spinal and cranial meningiomas point to the differences

11 We recorded from both spinal and motor cortical cells in monkeys responding to

12 most common sites of distant metastases, and spinal bone metastasis is the most common source of neur

13 Markers of stress reactivity together with spinal/brain opioid receptor expression were also measur

14 lamina", covering the neural elements of the spinal canal during screw placement provides manual feed

15 milar for forward and backward locomotion in spinal cats.

16 ticospinal axons functionally integrate into spinal circuits.

17 Spinal commissural axon navigation across the midline in

18 Swelling of the brain or spinal cord (CNS edema) affects millions of people every

19 functional images of both brain and cervical spinal cord (CSC) simultaneously and examined their spat

20 .0001), brainstem (r = 0.45, P < 0.0001) and spinal cord (r = 0.57, P < 0.0001) corticospinal tracts.

21 Spinal cord (SC) contributions to the slower components

22 The terminal ileum and thoracic spinal cord (T(11)) were sampled for evaluating ileitis

23 transcutaneous electrical stimulation of the spinal cord (TESS) promotes functional recovery in human

24 transcutaneous electrical stimulation of the spinal cord (TESS) promotes recovery of function in huma

25 ") to evaluate tissue samples from the C2-C6 spinal cord 3 days after a C3/C4 hemi-crush injury (C3Hc

26 multiple sclerosis (MS), knowledge about how spinal cord abnormalities translate into clinical manife

27 , real-time, continuous objective measure of spinal cord activation in response to therapy via record

28 med to examine pain relief and the extent of spinal cord activation with ECAP-controlled closed-loop

29 in transmission of voluntary commands to the spinal cord after damage (e.g., after stroke or spinal c

30 The spinal cord also expresses all dopamine receptors; howev

31 embling the cerebral cortex or the hindbrain/spinal cord and assemble them with human skeletal muscle

32 jects to undergo 7 T imaging of the cervical spinal cord and brain as well as conventional 3 T brain

33 d 16.11% alpha-tubulin acetylation for mouse spinal cord and brain homogenate tissue, respectively, a

34 Scale, white matter lesion fractions in the spinal cord and brain of the 9-Hole Peg Test and cortica

35 etween the colon and central nervous system (spinal cord and brain) that underlies the gut-brain axis

36 4 inhibits immune-cell infiltration into the spinal cord and completely abrogates immune responses to

37 pression in the midbrain-hindbrain boundary, spinal cord and dorsal root ganglia.

38 We demonstrate that GBF1 is present in mouse spinal cord and muscle tissues and is particularly abund

39 re often severe and predominantly affect the spinal cord and optic nerve.

40 Conclusion Gadolinium was retained in the spinal cord and peripheral nerves in rats exposed to mul

41 ount of alpha2delta-1-GluN1 complexes in the spinal cord and the level of alpha2delta-1-bound GluN1 p

42 udies demonstrate that CS projections to the spinal cord are eliminated in an activity-dependent mann

43 ful in this perspective, but studies for the spinal cord are lacking.

44 Neurons within the spinal cord are sensitive to environmental relations and

45 ntromedial, and away from the ventrolateral, spinal cord as the frequency of fictive locomotion incre

46 ng to the existence of the BBB and the blood-spinal cord barrier have been terrible and threatening c

47 Spinal cord blood vessels of CMH-treated mice showed red

48 matosensory input is modulated in the dorsal spinal cord by a network of excitatory and inhibitory in

49 ssion through distinct pathways in different spinal cord cell types and further implicate the importa

50 p in the diagnostic algorithm is to rule out spinal cord compression before evaluating other causes o

51 The spinal cord corticospinal tracts lesion volume fraction

52 However, correlation with spinal cord cross-sectional area-a predictor of disabili

53 fraction from neuronal tissue lysates after spinal cord crush injury of mice.

54 However, Hmx functions in spinal cord development have not been analyzed.

55 ng early-stage serotonergic neurons into the spinal cord for cardiovascular functional recovery after

56 ors by protecting mitochondria and hence the spinal cord from secondary injury.

57 thesis that sensorimotor circuits within the spinal cord generate backward locomotion and adjust it t

58 generating axons to penetrate the inhibitory spinal cord glial scar.

59 viral vector induced pig model of high-grade spinal cord glioma and may potentially be used in precli

60 dy, we report the production of a high-grade spinal cord glioma model in pigs using lentiviral gene t

61 redictors of EDSS score in PMS were cervical spinal cord GM CSA and brain GM volume (R(2) = 0.44).

62 stic regression analysis identified cervical spinal cord GM CSA and T2 lesion volume as independent p

63 Cervical spinal cord GM lesions may subsequently cause GM atrophy

64 in cholesterol synthesis, was reduced in the spinal cord GM of ALS patients.

65 eostasis is adversely affected in the in the spinal cord gray matter (GM), and if so, whether it is b

66 Lesion fractions within the spinal cord grey and white matter were related to the le

67 e 9-Hole Peg Test and cortical thickness and spinal cord grey matter cross-sectional area of the Time

68 and practical tool for clinical quantitative spinal cord imaging.

69 ell-related signaling spreads to the DRG and spinal cord in females, but remains localized to the sci

70 t a single session of TESS over the cervical spinal cord in individuals with incomplete chronic cervi

71 fictive locomotion when bath-applied in the spinal cord in vitro.

72 pathways of protection in heart, brain, and spinal cord injuries.

73 5 (18.88) years) with subacute (ie, 1 month) spinal cord injury (25 patients with neuropathic pain, 1

74 ection to spinal motor neurons from ischemic spinal cord injury (ISCI).

75 Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), examination.

76 ll (NSPC) grafts can integrate into sites of spinal cord injury (SCI) and generate neuronal relays ac

77 Spinal cord injury (SCI) is a common cause of disability

78 or muscle injury, but the Acomys response to spinal cord injury (SCI) is unknown.

79 munity long after SCI.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) significantly disrupts immunity

80 In spinal cord injury (SCI), the initial damage leads to a

81 of a million individuals in the US live with spinal cord injury (SCI).

82 promotes recovery of function in humans with spinal cord injury (SCI).

83 promotes functional recovery in humans with spinal cord injury (SCI).

84 ical deficits and long-term disability after spinal cord injury (SCI).

85 spinothalamic tract function-at 1 month post-spinal cord injury is associated with the emergence and

86 growth and functional recovery in vivo in a spinal cord injury model through a unique mechanism of a

87 Spinal cord injury remains a scientific and therapeutic

88 PCMS without exercise in 13 individuals with spinal cord injury with similar characteristics.

89 al axons and restore forelimb function after spinal cord injury(1); however, the molecular mechanisms

90 nal cord after damage (e.g., after stroke or spinal cord injury), possibly assisting recovery of func

91 rly complete recovery of neonatal mice after spinal cord injury, and suggest strategies that could be

92 er, patients with impaired voiding following spinal cord injury, patients undergoing nonurologic surg

93 As rats are used extensively to model spinal cord injury, we asked if the S1 CST response is c

94 w flexor and extensor muscles after cervical spinal cord injury.

95 igration and functional repair in vivo after spinal cord injury.

96 different degrees of paralysis and levels of spinal cord injury.

97 owth-competent axons after sciatic nerve and spinal cord injury.

98 for cardiovascular functional recovery after spinal cord injury.

99 te whether ED peptide has similar effects in spinal cord injury.

100 SNs) are interconnected across the brain and spinal cord is unclear.

101 h antigen-presenting cells (APCs) within the spinal cord leptomeninges in experimental autoimmune enc

102 Despite the prevalence of cervical spinal cord lesions and atrophy, brain pathology seems m

103 d male sex, younger age, and the presence of spinal cord lesions as independent factors that increase

104 e sclerosis showed a greater predominance of spinal cord lesions nearer the outer subpial surface com

105 oglia treated with peptidase inhibitors into spinal cord lesions of adult mice, and found that both t

106 Cervical spinal cord lesions were mapped voxel-wise as a function

107 f presynaptic and postsynaptic NMDARs at the spinal cord level and that presynaptic NMDARs play a pro

108 a signaling in nociceptive modulation at the spinal cord level.

109 1b synthesis attenuates nerve injury-induced spinal cord microglia activation and pain hypersensitivi

110 Spinal cord microglia contribute to nerve injury-induced

111 a cross talk is necessary for eliciting this spinal cord microglia phenotype and also for conferring

112 w that it is possible to consistently elicit spinal cord microglia via systemic delivery of inflammog

113 tical for nerve injury-induced activation of spinal cord microglia, but the responsible endogenous TL

114 Moreover, by quantitative immunostaining of spinal cord MNs, we found corresponding protein level ch

115 Conclusion Cervical spinal cord MRI involvement has a central role in explai

116 tudy evaluated three-dimensional T1-weighted spinal cord MRI scans in seropositive participants with

117 cytochrome c activities, leading to reduced spinal cord neuronal cell apoptosis and smaller lesion a

118 nd prevents degeneration of cultured primary spinal cord neurons derived from SMA mice.

119 cuits restoring locomotion in mice following spinal cord neurostimulation.

120 ast-enhancing focal lesions in the brain and spinal cord observed on MRI.

121 opathology in the developing mouse brain and spinal cord of both sexes.

122 Ectopic CSF-cNs in the spinal cord of C57Bl/6N mice emerge during whole period

123 erlie the ectopic position of CSF-cNs in the spinal cord of C57Bl/6N mice.

124 ein 43 (TDP-43) are evident in the brain and spinal cord of patients that present across a spectrum o

125 es do not cause loss of motor neurons in the spinal cord or denervation at the neuromuscular junction

126 uromuscular junction, peripheral nerves, the spinal cord or the brain and discuss the autoimmune mech

127 extrahypothalamic brain areas and the lumbar spinal cord play an important role in the control of ere

128 ecific Trpa1 disruption in a mouse brainstem-spinal cord preparation impedes the amplitude augmentati

129 s demonstrated that GPR160 inhibition in the spinal cord prevented and reversed neuropathic pain in m

130 rgets for interventions to improve brain and spinal cord remyelination, paving the way for the transl

131 anical mechanisms contributing to successful spinal cord repair in adult zebrafish are, however, curr

132 e studies into the role of mechanosensing in spinal cord repair.

133 natures of the dorsal root ganglia (DRG) and spinal cord response, not observed at the nerve injectio

134 ion of ZIKV infection in the mouse brain and spinal cord resulting in massive neurodegeneration of in

135 n females, after cystometry c-Fos neurons in spinal cord segments L5-S2 were concentrated in the sacr

136 aviors with two-photon microscopy in ex vivo spinal cord slices from CX3CR1-GFP mice complemented wit

137 Enhancing the efficacy of spinal cord stimulation (SCS) is needed to alleviate the

138 ple with upper-limb amputation that epidural spinal cord stimulation (SCS), a common clinical techniq

139 d closed-loop versus fixed-output, open-loop spinal cord stimulation for the treatment of chronic bac

140 A novel spinal cord stimulation system provides the first in viv

141 l pain relief up to 12 months than open-loop spinal cord stimulation.

142 contrast, adult zebrafish are able to repair spinal cord tissue and restore motor function after comp

143 ive mapping of the spatiotemporal changes of spinal cord tissue stiffness in regenerating adult zebra

144 During regeneration after transection, the spinal cord tissues displayed a significant increase of

145 NK cells in post-mortem ALS motor cortex and spinal cord tissues, and the expression of NKG2D ligands

146 ect CB2 upregulation on postmortem human ALS spinal cord tissues.

147 through descending pathways to hindbrain and spinal cord to activate muscle and generate movement.

148 vivo two-photon Ca(2+) imaging of the mouse spinal cord to establish that NK1R and the gastrin-relea

149 switch redirected disease pathology from the spinal cord to the brain.

150 ue and restore motor function after complete spinal cord transection owing to a complex cellular resp

151 e injury (n = 64, 21.9%) including brain and spinal cord trauma.

152 Similarly, myelination in the spinal cord was disorganized after exposure at 2 dpf but

153 Labeling throughout the brainstem and spinal cord were very similar for the two antibodies and

154 nd that MOL type 2 (MOL2) is enriched in the spinal cord when compared to the brain, while MOL types

155 homogeneous delivery throughout the cervical spinal cord white and gray matter and brain motor center

156 nd microglia activation were observed in the spinal cord white matter of 7-month-old Hri(-/-) mice as

157 MENT Interneuron (IN) diversity empowers the spinal cord with the computation flexibility required to

158 sychosine levels in the rodent brainstem and spinal cord, and a significantly shorter life-span of th

159 gnaling triggers the release of Wnt5a in the spinal cord, and inhibition of spinal Wnt5a signaling at

160 um), diencephalon, mesencephalon, hindbrain, spinal cord, and retina.

161 dulated by projections from the brain to the spinal cord, but the neural substrates for top-down sens

162 ein prevents immune-cell infiltration in the spinal cord, decreases integrin expression in antigen-sp

163 eatures of excitatory synapses in the lumbar spinal cord, detailing synaptic diversity that is depend

164 detect PI16 expression in neurons or glia in spinal cord, DRG, and nerve.

165 e ependyma changes after injury of the adult spinal cord, functionally resembling the immature active

166 nerated by a neural network, situated in the spinal cord, known as the locomotor central pattern gene

167 As the resident macrophages of the brain and spinal cord, microglia are crucial for the phagocytosis

168 In the zebrafish spinal cord, neural progenitors form stereotypic pattern

169 In the developing spinal cord, Onecut transcription factors control the di

170 In the spinal cord, the central canal forms through a poorly un

171 We show NK1R mRNA expression in human spinal cord, underscoring the translational relevance of

172 he dorsal white matter tract of the cervical spinal cord, we found that both lesioned dorsal and inta

173 fers from the striatum, locus coeruleus, and spinal cord, where multiple peptidases metabolize enkeph

174 ipsilateral projections of CS neurons in the spinal cord, while other studies demonstrate that CS pro

175 expression of programmed-death-ligand-1) in spinal cord-draining lymph nodes and decreases the numbe

176 ntricular organ and the central canal of the spinal cord.

177 m the brain through the central canal of the spinal cord.

178 nal trigeminal nucleus and all levels of the spinal cord.

179 of excitatory synapses throughout the lumbar spinal cord.

180 ential targets to improve self-repair of the spinal cord.

181 the lesion site of completely transected rat spinal cord.

182 ed MBP ligand in the brain compared with the spinal cord.

183 NMDARs and their synaptic trafficking in the spinal cord.

184 r matrix that ligate the severed ends of the spinal cord.

185 nt inhibition between motoneurons within the spinal cord.

186 the white matter of the motor cortex and the spinal cord.

187 anosensory stimuli are represented along the spinal cord.

188 al root entry zone (DREZ) to extend into the spinal cord.

189 f presynaptic and postsynaptic NMDARs in the spinal cord.

190 neurogenesis profiles of V3 INs in the mouse spinal cord.

191 xpressing LJA5 neurons through the brain and spinal cord.

192 in the optic nerve, corpus callosum, and the spinal cord.

193 oot ganglia (DRG) and the dorsal horn of the spinal cord.

194 ndamental to reestablish motor control after spinal-cord injury (SCI).

195 Grafts of spinal-cord-derived neural progenitor cells (NPCs) enabl

196 Further, immunohistochemical analyses of the spinal cords of treated animals showed significantly low

197 r activity of various frequencies in upright spinal cords prepared from male and female neonatal mice

198 t 12-13 or 19 weeks of age, and their lumbar spinal cords were processed for histo- and immunohistoch

199 Background Spinal digital subtraction angiography (DSA) exposes pat

200 Conclusion Antiscatter grid removal during spinal digital subtraction angiography decreased partici

201 Because endogenous levels of spinal dopamine are low, this excitatory dopaminergic pa

202 tor (NK1R; encoded by Tacr1) is expressed in spinal dorsal horn neurons and has been suggested to med

203 sociated with enhanced neuronal responses in spinal dorsal horn neurons.

204 s of evoked EPSCs and puff NMDAR currents in spinal dorsal horn neurons.

205 ocking the Wnt5a-Ryk/Ror2 interaction in the spinal dorsal horn prevented spine remodeling and signif

206 se 5 (Cdk5) in dorsal root ganglia (DRG) and spinal dorsal horn.

207 prospective study included adults undergoing spinal DSA between January and December 2016.

208 We did not observe any lymphatic vessels in spinal dura mater.

209 ge may persistently constrain the ability of spinal DYN interneurons to limit ascending nociceptive t

210 Within the cervical and lumbar spinal enlargements, central pattern generator (CPG) cir

211 We found that spinal ERalpha-positive neurons are largely excitatory i

212 ynthetic urine (SU), and artificial cerebral spinal fluid (aCSF) using ethyl acetate as the extractio

213 We tested 46 plasma samples and 36 cerebral spinal fluid (CSF) samples taken from patients with suba

214 High spinal fluid protein was found in 27/32 (78%) cases.

215 irus 2 from nasopharyngeal swab and cerebral spinal fluid.

216 As rates of spinal fusion continue to increase, rates of complicatio

217 Spinal fusion is one of the most common procedures perfo

218 he recovery of locomotor functions following spinal hemisection, using chemogenetic tools to selectiv

219 1.14), pelvic (HR, 1.10; 99% CI, 1.02-1.19), spinal (HR, 1.18; 99% CI, 1.10-1.27), and wrist (HR, 1.0

220 ere eczema (compared with those without) for spinal (HR, 2.09; 99% CI, 1.66-2.65), pelvic (HR, 1.66;

221 and immunohistochemical evidence of reduced spinal inflammation and fibrosis following SCI as compar

222 pport the hypothesis that Acomys has reduced spinal inflammation and fibrosis following SCI.

223 modulation would play a role in setting the spinal inhibitory tone and influencing sensory signaling

224 best promote recovery.SIGNIFICANCE STATEMENT Spinal injuries that remove sensation from the hand, can

225 rological outcomes were assessed by American Spinal Injury Association (ASIA), or International Stand

226 In opossums spinal injury early in development results in spontaneou

227 a putative role for miR-21 in the microglial spinal injury response.

228 to sensorimotor cortex dysfunction above the spinal injury site.

229 lone, propelling axon growth well beyond the spinal injury site.

230 Outcome data at 1 year after spinal injury were available for 1031 patients (66.6%).

231 al motor score from baseline to 1 year after spinal injury.

232 ng and afferent drives project onto the same spinal interneuronal networks that encode locomotor musc

233 Many spinal interneurons, including those identified as proje

234 essive glial activation and vulnerability of spinal interneurons.

235 ited further dissection of their function in spinal itch circuitry.

236 able to differentiate between nonneoplastic spinal lesions and malignant lesions.

237 usion MRI, and histopathologic diagnosis for spinal lesions.

238 networks, having an excitatory effect at the spinal level and an inhibitory effect at the cortical le

239 processing has emerged, showing that, at the spinal level, oxytocin blocks pain transmission.

240 very last instructions sent by the brain to spinal locomotor circuits.

241 hibited alterations of locomotor pattern and spinal locomotor network activity, likely resulting from

242 s') may require functional reorganization of spinal mechanisms to perform APAs.

243 quality, nondiagnostic biopsy, and extensive spinal metastasis or prior kyphoplasty.

244 We also observed these changes in spinal MNs of an independent ALS mouse model caused by a

245 sequencing to identify molecular changes in spinal MNs of TDP-43-driven ALS at motor symptom onset.

246 ndamental electrophysiological properties of spinal motoneurons follows the same rostro-caudal sequen

247 nd also for conferring optimal protection to spinal motor neurons from ischemic spinal cord injury (I

248 he orderly recruitment of different types of spinal motor neurons.

249 Spinal muscular atrophy (SMA) is a motor neuron disease.

250 e SMA motor phenotype.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is a neurodegenerative dis

251 Spinal muscular atrophy (SMA) is a neuromuscular disorde

252 for measuring SMN1 and SMN2 copy numbers in spinal muscular atrophy (SMA) samples has not been repor

253 data in a large cohort of 199 patients with spinal muscular atrophy (SMA) type III assessed using th

254 nk between amyotrophic lateral sclerosis and spinal muscular atrophy (SMA), and 3 mutations of the AS

255 k between two motor neuron diseases, ALS and spinal muscular atrophy (SMA).

256 ul application of virus-mediated GT to treat spinal muscular atrophy is a significant milestone, serv

257 in rats with mechanical allodynia induced by spinal nerve ligation (SNL).

258 he compound action potential recorded in the spinal nerves, as well as the paw withdrawal threshold.

259 dose-dependent control of neuromodulators on spinal network output and advances our understanding of

260 however, how the specific receptors regulate spinal network output in mammals is poorly understood.

261 ity, which is a characteristic of developing spinal networks operating in a low excitability state, w

262 Descending command neurons instruct spinal networks to execute basic locomotor functions, su

263 ed in parallel the excitability cortical and spinal networks, having an excitatory effect at the spin

264 mechanism underlying zippering during mouse spinal neural tube closure.

265 havior in mice and that the majority of NK1R spinal neurons are local interneurons.

266 and chemogenetic activation of Tacr1(CreER) spinal neurons increases itch behavior in male and femal

267 We demonstrate neurokinin-1 receptor (NK1R) spinal neurons mediate itch behavior in mice and that th

268 elied heavily on neurotoxic ablation of NK1R spinal neurons, which limited further dissection of thei

269 , which can form functional connections with spinal neurons.

270 We show that pharmacological activation of spinal NK1R and chemogenetic activation of Tacr1(CreER)

271 mice, whereas pharmacological inhibition of spinal NK1R suppresses itch behavior.

272 ergic transmission and activating descending spinal noradrenergic mechanisms.

273 to measure basic cardiovascular physiology, spinal oxygenation, mitochondrial function, and tissue p

274 and confirm whether EA attenuates VH through spinal PAR-2 activation and CGRP release, goats received

275 mmunoreactive-cells and expression-levels of spinal PAR-2, CGRP and c-Fos in the EA group were greate

276 Here, we quantified this spinal pathology at 3 and 7 months of age revealing sign

277 d to the digestive periphery via cranial and spinal pathways; we show that, among these pathways, the

278 via canonical and noncanonical signaling in spinal processing of nociception in a number of patholog

279 lutamate co-release and convergent output to spinal-projecting premotor neurons in the brainstem.

280 brachial nucleus (lPBN) is a major target of spinal projection neurons conveying nociceptive input in

281 m the periphery are channelled through these spinal projection neurons en route to the brain.

282 rficial Tacr1(CreER) dorsal horn neurons are spinal projection neurons, and thus the majority of Tacr

283 ted that central neurons mediating vestibulo-spinal reflexes and self-motion perception optimally enc

284 ilar to all mammals studied to date exhibits spinal scarring following SCI.

285 Therefore, our results show that spinal sensorimotor circuits generate backward locomotio

286 verall reduction of neuronal activity in the spinal sensory-motor circuit.

287 uron death, and reduced neuronal activity in spinal sensory-motor circuits.

288 These data reveal a key principle in spinal somatosensory processing, namely, sensorimotor re

289 inhibitory synaptic transmission within the spinal superficial dorsal horn (SDH) that include a redu

290 ined with non-invasive stimulation targeting spinal synapses further promotes functional recovery.

291 te that targeted non-invasive stimulation of spinal synapses might represent an effective strategy to

292 vel of alpha2delta-1-bound GluN1 proteins in spinal synaptosomes.

293 solid phase extraction by packed sorbent (in spinal syringe format) followed by HPLC-UV.

294 maturation of premotor descending and local spinal systems.

295 This unilateral section of the dorsal spinal tract provides a realistic model in which axonal

296 t treadmill speeds before and after complete spinal transection in six adult cats (three males and th

297 rapid respiratory muscle recovery following spinal trauma occurs through oxygen transport, metabolic

298 Spinal treatment can restore diaphragm function in all a

299 B), caudal pressor area, and lamina I of the spinal trigeminal nucleus and all levels of the spinal c

300 Wnt5a in the spinal cord, and inhibition of spinal Wnt5a signaling attenuates the functional impact