ライフサイエンスコーパス: peripheral nerve injury

1 the mechanical hypersensitivity produced by peripheral nerve injury.

2 DF could contribute to pain generation after peripheral nerve injury.

3 to manage chronic neuropathic pain following peripheral nerve injury.

4 shown that it can also do this in mice after peripheral nerve injury.

5 te with pain behavior and inflammation after peripheral nerve injury.

6 y distinct degenerative insults: hypoxia and peripheral nerve injury.

7 he ipsilateral spinal cord dorsal horn after peripheral nerve injury.

8 t underlie successful regeneration following peripheral nerve injury.

9 R) are upregulated in spinal microglia after peripheral nerve injury.

10 hwann cells undergo phenotypic modulation in peripheral nerve injury.

11 h neuropeptide Y (NPY) and galanin following peripheral nerve injury.

12 pha9alpha10 nAChRs in the pathophysiology of peripheral nerve injury.

13 n of damaged axons in the early stages after peripheral nerve injury.

14 ms that contribute to neuropathic pain after peripheral nerve injury.

15 f spinal GABA(A)-receptor function following peripheral nerve injury.

16 sensory and motor neuron survival following peripheral nerve injury.

17 -H protein and mRNA are downregulated after peripheral nerve injury.

18 uting of the fibers into these laminae after peripheral nerve injury.

19 ithin the dorsal root ganglion (DRG) after a peripheral nerve injury.

20 ore robust, centrally mediated response than peripheral nerve injury.

21 rons become recoupled by gap junctions after peripheral nerve injury.

22 ic discharges and mechanical allodynia after peripheral nerve injury.

23 e etiology of mechanical allodynia following peripheral nerve injury.

24 lectrical properties that are observed after peripheral nerve injury.

25 les with gelatinases activity at the site of peripheral nerve injury.

26 hat matched patterns normally observed after peripheral nerve injury.

27 le in regulating motoneuron survival after a peripheral nerve injury.

28 KCgamma) show reduced neuropathic pain after peripheral nerve injury.

29 ritories are activated and proliferate after peripheral nerve injury.

30 neuronal plasticity after specific types of peripheral nerve injury.

31 ters the thermal hyperalgesic sensitivity to peripheral nerve injury.

32 following either peripheral inflammation or peripheral nerve injury.

33 echanical and thermal hypersensitivity after peripheral nerve injury.

34 le in regulating motoneuron survival after a peripheral nerve injury.

35 ant roles in the reactions of DRG neurons to peripheral nerve injury.

36 ng observed within sensory ganglia following peripheral nerve injury.

37 in the DRG at multiple time points following peripheral nerve injury.

38 ription factor CREB in the injured DRG after peripheral nerve injury.

39 d can persist after apparent resolution of a peripheral nerve injury.

40 (CGRP) decrease in the dorsal horn following peripheral nerve injury.

41 uting of sympathetic fibers in the DRG after peripheral nerve injury.

42 s (SGC) appeared specifically in response to peripheral nerve injury.

43 aling and sensitization of nociceptors after peripheral nerve injury.

44 tex (S1) exhibit synchronized activity after peripheral nerve injury.

45 on of excitatory neurotransmission following peripheral nerve injury.

46 in the mechanical hypersensitivity caused by peripheral nerve injury.

47 ation and neuropathic pain development after peripheral nerve injury.

48 k the degenerative process in a rat model of peripheral nerve injury.

49 or limit maladaptive sensory phenomena after peripheral nerve injury.

50 antinociceptive intervention in animals with peripheral nerve injury.

51 injured dorsal root ganglion (DRG) following peripheral nerve injury.

52 ffected by oxycodone withdrawal in mice with peripheral nerve injury.

53 neuropathic and inflammatory pain following peripheral nerve injury.

54 i silkworms can support axon regeneration in peripheral nerve injury.

55 get muscle is a determinant of outcome after peripheral nerve injury.

56 Sensation is essential for recovery after peripheral nerve injury.

57 al and behavioral alterations resulting from peripheral nerve injury.

58 gical changes in a neuropathic pain model of peripheral nerve injury.

59 o regeneration and functional recovery after peripheral nerve injury.

60 transition from acute to chronic pain after peripheral nerve injury.

61 mechanism for activation of autophagy after peripheral nerve injury.

62 tactile and cold allodynia remain following peripheral nerve injury.

63 -138 in adult sensory neurons in response to peripheral nerve injury.

64 amed rats differ from those in animals after peripheral nerve injury.

65 gy as well as similar inflammatory events of peripheral nerve injury.

66 d late-phase neuropathic pain behavior after peripheral nerve injury.

67 niscent of IRF8-driven reactive microglia in peripheral-nerve injury.

68 ctional rehabilitation following central and peripheral nerve injuries.

69 eat neurological diseases such as stroke and peripheral nerve injuries.

70 like expression in the spinal cord following peripheral nerve injuries.

71 re capable of dramatic reorganizations after peripheral nerve injuries.

72 y processing in excitatory neurons following peripheral nerve injuries.

73 d molecular therapies to improve outcomes of peripheral nerve injuries.

74 regeneration and muscle reinnervation after peripheral nerve injuries.

75 Peripheral nerve injury accounts for roughly 2.8% of all

76 Neuropathic pain accompanies peripheral nerve injury after a wide variety of insults

77 plete (i.e. sciatic nerve transection (SNT)) peripheral nerve injury altered the mean threshold inten

78 We conclude that, following peripheral nerve injury, an immediate acute immune respo

79 Peripheral nerve injuries and neuropathies lead to profo

80 is also implicated in neuropathic pain after peripheral nerve injury and apoptosis after spinal cord

81 are upregulated by sensory neurons following peripheral nerve injury and appear to participate in neu

82 ore, to the reduced levels of cAMP following peripheral nerve injury and are likely critical to the p

83 wann cells readily dedifferentiate following peripheral nerve injury and become repair cells.

84 le spindle-motoneurone connection both after peripheral nerve injury and during development.

85 ative of persistent pain in rodent models of peripheral nerve injury and inflammation and prevented n

86 changes in cortical circuits also accompany peripheral nerve injury and may represent additional the

87 dynamics in the dorsal horn associated with peripheral nerve injury and pain.

88 sensory hypersensitivity in mouse models of peripheral nerve injury and peripheral inflammation.

89 to 208) accelerated axon regeneration after peripheral nerve injury and promoted regrowth of reticul

90 A detailed background of peripheral nerve injury and repair pathology, and an in-

91 nation during both development and following peripheral nerve injury and repair.

92 ctivity is microglial cells activated by the peripheral nerve injury and secreting the enzyme, as a r

93 o a peripheral nerve can mimic the effect of peripheral nerve injury and significantly increase the n

94 Both surgically induced peripheral nerve injury and statin-associated muscle dam

95 in higher-order spinal sensory neurons after peripheral nerve injury and suggest a link between misex

96 ate the efficacy of hMDSPC-based therapy for peripheral nerve injury and suggest that hMDSPC transpla

97 mouse Celf2 expression is upregulated after peripheral nerve injury and that Celf2 mutant mice are d

98 inal cord dorsal horn could change following peripheral nerve injury and that the Hippo signaling pat

99 ibute to efficient axonal regeneration after peripheral nerve injury and, when grafted to the central

100 els of axonal PTBP1 increased markedly after peripheral nerve injury, and it associates in axons with

101 the spinal first sensory synapse induced by peripheral nerve injury, and presynaptic NMDARs might be

102 ntribute to mechanical allodynia produced by peripheral nerve injury, and that they do so in a sex-de

103 ease in analgesic potency and efficacy after peripheral nerve injury, and their effects are blocked b

104 ical hypersensitivity in the mouse models of peripheral nerve injury- and paclitaxel-induced neuropat

105 Peripheral nerve injuries are prevalent, yet strategies

106 al applications in regenerative medicine for peripheral nerve injury as regenerating nerves follow th

107 in CSF samples increased significantly after peripheral nerve injury, associated with spinal microgli

108 ays a role in the early neuronal response to peripheral nerve injury at sites distal to the cell body

109 which is dramatically upregulated following peripheral nerve injury at the site of injury, in the do

110 After peripheral nerve injury at the spinal nerve level, some

111 can normalize redox signaling at the site of peripheral nerve injury, attenuating subsequent neuropat

112 ve axonal regeneration in superimposed acute peripheral nerve injury attributable to tissue-damaging

113 After peripheral nerve injury, axons are able to regenerate, a

114 hared with an important repair program after peripheral nerve injury, but lead to neural perturbation

115 d neuronal function in development and after peripheral nerve injury, but little is known regarding i

116 suggests that A-fibre sprouting arise after peripheral nerve injury, but mainly from small calibre A

117 ry sensory neurons readily regenerates after peripheral nerve injury, but the central branch, which c

118 alter spinal glial activation resulting from peripheral nerve injury by specific manipulation of IL-6

119 Peripheral nerve injuries can be extremely debilitating,

120 Peripheral nerve injury can cause debilitating disease a

121 Peripheral nerve injury can lead to a persistent neuropa

122 Peripheral nerve injury can occur in patients with COVID

123 nization of essential motor circuits after a peripheral nerve injury can result in permanent motor de

124 Peripheral nerve injury can trigger neuropathic pain in

125 Different peripheral nerve injuries cause neuropathic pain through

126 Our findings demonstrate that a peripheral nerve injury causes activated microglia withi

127 Peripheral nerve injury causes sensory dysfunctions that

128 Peripheral nerve injury causes spontaneous and long-last

129 Peripheral nerve injury causes spontaneous electrical ac

130 eurial hypoxia in a mouse model of traumatic peripheral nerve injury, causing painful mononeuropathy.

131 Pain resulting from peripheral nerve injury, characterised by ongoing pain,

132 Here we show that following peripheral nerve injury, cholinergic neurons in the ante

133 al root ganglion neurons using two models of peripheral nerve injury: chronic constriction injury (CC

134 m of abnormal spontaneous activity following peripheral nerve injury: clusters of adjacent DRG neuron

135 at transcription factors induced early after peripheral nerve injury confer the cellular plasticity r

136 ement cascade in spinal cord microglia after peripheral nerve injury contributes to neuropathic pain

137 croglia in the spinal cord dorsal horn after peripheral nerve injury contributes to the development o

138 Here we show that peripheral nerve injury decreased agrin expression in th

139 brain injury, ischemia, spinal cord injury, peripheral nerve injury, demyelinating disease, neuromus

140 Following peripheral nerve injury, denervated tissues can be reinn

141 a, as a marker of neuropathic pain following peripheral nerve injury, did not require microglial STIN

142 Here we present novel evidence that peripheral nerve injury diminishes glycine-mediated inhi

143 Moreover, unilateral peripheral nerve injury evokes parallel, but smaller eff

144 Following peripheral nerve injury, extracellular adenosine 5'-trip

145 SGC, which promotes axon regeneration after peripheral nerve injury, failed to occur after central a

146 Neuropathic pain accompanies peripheral nerve injury following a variety of insults i

147 After peripheral nerve injury, following frequencies were incr

148 rophage metabolism can enhance recovery from peripheral nerve injuries, for which there are currently

149 lia (DRG), the primary sensory cell body for peripheral nerve injury generated hypersensitivity, and

150 Progress in experimental studies of root and peripheral nerve injuries has identified potential candi

151 Poor functional recovery found after peripheral nerve injury has been attributed to the misdi

152 hich time resolution of the hyperalgesia and peripheral nerve injury has occurred according to previo

153 Current approaches for treating peripheral nerve injury have resulted in promising, yet

154 Using both in vivo and in vitro models for peripheral nerve injury, here we show that inhibition of

155 In animals with peripheral nerve injury, however, the antinociceptive po

156 in the mechanisms of neuropathic pain after peripheral nerve injury; however, how central GRs and NM

157 Peripheral nerve injury in a rat model (spinal nerve lig

158 e cortical "recovery" that typically follows peripheral nerve injury in adult monkeys is apparently d

159 Peripheral nerve injury in diabetes can manifest as prog

160 then discuss the pathways that contribute to peripheral nerve injury in DN.

161 eriences associated with limb amputation and peripheral nerve injury in humans.

162 echanical hypersensitivity (allodynia) after peripheral nerve injury in male and female mice.

163 cord microglia at chronic time points after peripheral nerve injury in mice.

164 Peripheral nerve injury in neonatal rats results in the

165 Peripheral nerve injury in rodents results in hypersensi

166 scular junctions and hastened recovery after peripheral nerve injury in wild type mice.

167 ehavior were significantly exacerbated after peripheral nerve injury in Wistar-Kyoto (WKY) rats, a ge

168 Pathophysiological responses to peripheral nerve injury include alterations in the activ

169 Peripheral nerve injury increased Kcna2 antisense RNA ex

170 Here, we report that peripheral nerve injury increases expression of the DNA

171 Peripheral nerve injury increases nNOS expression in fib

172 response of CX(3)CR1-deficient microglia to peripheral nerve injury indicates unimpaired neuronal-gl

173 n causes delayed axon degeneration following peripheral nerve injury, indicating that it participates

174 We found that peripheral nerve injury induced de novo expression of co

175 The fact that peripheral nerve injury induced de novo GRP expression i

176 Unexpectedly, however, peripheral nerve injury induced significant GRP expressi

177 These findings indicate that peripheral nerve injury induced time-dependent and regio

178 h-clamp recording technique, we investigated peripheral nerve injury-induced changes in excitatory sy

179 Peripheral nerve injury-induced chronic neuropathic pain

180 rc8a), a VRAC essential subunit, had reduced peripheral nerve injury-induced increase in extracellula

181 Peripheral nerve injury-induced intrinsic immune respons

182 al horn (lamina II) neurons before and after peripheral nerve injury-induced pain.

183 Mechanistically, peripheral nerve injury induces DNA demethylation and up

184 Peripheral nerve injury induces increased expression of

185 Peripheral nerve injury induces long-term pro-inflammato

186 Here, we show that peripheral nerve injury induces microglial engulfment of

187 Peripheral nerve injury induces permanent alterations in

188 Interestingly, peripheral nerve injury induces tactile allodynia and up

189 Peripheral nerve injury induces upregulation of the calc

190 nerve injury, few studies have examined how peripheral nerve injury influences spinal somatosensory

191 Finally, after partial peripheral nerve injury, innocuous stimulation (brush) i

192 Following peripheral nerve injury, innocuous stimuli activated thi

193 However, if the neurons are conditioned by a peripheral nerve injury into an actively growing state,

194 Activation of spinal microglia following peripheral nerve injury is a central component of neurop

195 Peripheral nerve injury is a debilitating condition.

196 Neuropathic pain caused by peripheral nerve injury is a debilitating neurological c

197 Peripheral nerve injury is a major neurological disorder

198 Peripheral nerve injury is a prevalent clinical problem

199 he activation of dorsal horn microglia after peripheral nerve injury is a significant expansion and p

200 demonstrate using immunohistochemistry that peripheral nerve injury is also sufficient to alter the

201 Herein, we show that peripheral nerve injury is associated with activation of

202 Neuropathic pain following peripheral nerve injury is associated with hyperexcitabi

203 Motor axon regeneration following peripheral nerve injury is critical for motor recovery b

204 on of microglia in the spinal cord following peripheral nerve injury is critical for the development

205 ge accumulation in the sensory ganglia after peripheral nerve injury is due to the local proliferatio

206 iately regulated inflammatory response after peripheral nerve injury is essential for axon regenerati

207 A critical step for functional recovery from peripheral nerve injury is for regenerating axons to con

208 Peripheral nerve injury is known to induce changes in th

209 Peripheral nerve injury is known to upregulate the rapid

210 o find that cold hypersensitivity induced by peripheral nerve injury is reduced in eIF4E(S209A) and M

211 A rapid proinflammatory response after peripheral nerve injury is required for clearance of tis

212 Recovery of motor and sensory function after peripheral nerve injury is suboptimal, even after approp

213 ion offered by voluntary wheel running after peripheral nerve injury is unknown.

214 Peripheral nerve injury leads to deficient recovery of s

215 In summary, these results indicated that peripheral nerve injury leads to sNAMs proliferation in

216 Peripheral nerve injury leads to various injury-induced

217 Peripheral nerve injury led to inferred microglia-driven

218 Following peripheral nerve injury, low threshold mechanoreceptive

219 After peripheral nerve injury, macrophages infiltrate the dege

220 ific subcellular redistribution of PN3 after peripheral nerve injury may be an important factor in es

221 herapeutic enhancement of regeneration after peripheral nerve injury may require a combination of fac

222 These RNA-Seq data analyses indicate that peripheral nerve injury may result in highly selective m

223 Following peripheral nerve injury, microglia in the S1 maintain ra

224 various types of gait deficit due to: (a) a peripheral nerve injury model with increasing degrees of

225 horn of the spinal cord in response to three peripheral nerve injury models of neuropathic pain.

226 s mechanical and thermal hypersensitivity in peripheral nerve injury models of neuropathic pain.

227 eus accumbens (NAc) neurons in mouse and rat peripheral nerve injury models of neuropathic pain.

228 subject to divergent plasticity in different peripheral nerve injury models, reflecting the complexit

229 While a regeneration-competent peripheral nerve injury mounts a regenerative gene expre

230 There is consensus that, distal to peripheral nerve injury, myelin and Remak cells reorgani

231 f central GRs in nociceptive behaviors after peripheral nerve injury (neuropathic pain behaviors) rem

232 After peripheral nerve injury, neurotrophins play a key role i

233 her central nervous system manifestations of peripheral nerve injury nor functional bowel disorders a

234 Traumatic peripheral nerve injuries often produce permanent functi

235 ated cognitive decline, Parkinson's disease, peripheral nerve injury, optic nerve degeneration, and d

236 d NMDAR-dependent persistent pain induced by peripheral nerve injury or injection of Complete Freund'

237 (DRG) neurones of rat alters as a result of peripheral nerve injury or localized inflammation.

238 ptible to myelination diseases such as adult peripheral nerve injury or multiple sclerosis.

239 may render the spinal neurons vulnerable to peripheral nerve injury or neuropathic pain stimuli.

240 Peripheral Nerve Injuries (PNI) affect more than 20 mill

241 Millions of people worldwide are affected by peripheral nerve injuries (PNI), involving billions of d

242 Peripheral nerve injury (PNI) and the limitations of cur

243 States continues to increase, evaluation of peripheral nerve injury (PNI) in the presence of pre-exi

244 Functional restoration following major peripheral nerve injury (PNI) is challenging, given slow

245 Functional recovery after a peripheral nerve injury (PNI) is often poor.

246 Incomplete functional recovery after peripheral nerve injury (PNI) often results in devastati

247 Peripheral Nerve Injury (PNI) represents a major clinica

248 animals with spared nerve injury, a model of peripheral nerve injury (PNI)-induced neuropathic pain.

249 e anterior cingulate cortex contralateral to peripheral nerve injury prevented exacerbation of mechan

250 he anterior cingular cortex contralateral to peripheral nerve injury prevented the exacerbation of me

251 mill training in the first 2 weeks following peripheral nerve injury produces a marked enhancement of

252 In normal animals, peripheral nerve injury produces a persistent, neuropath

253 Our findings suggest that peripheral nerve injury promotes CB2 expression in prima

254 elta1-dependent pathway activated by TSP4 or peripheral nerve injury promotes exaggerated presynaptic

255 Peripheral nerve injury reduces NECAB2, but not NECAB1,

256 drenoceptor agonist clonidine at the site of peripheral nerve injury reduces pain behavior and local

257 Currently, diagnosis and monitoring of peripheral nerve injury relies on clinical and electrodi

258 primary somatosensory cortex (S1) caused by peripheral nerve injury require neuron-microglial signal

259 In contrast, peripheral nerve injury resulted in a persistent suppres

260 Peripheral nerve injury results in axonal degeneration a

261 In a recent study, it was shown that peripheral nerve injury results in increased NKCC1 activ

262 Partial peripheral nerve injury results in pain-like behavioral

263 Peripheral nerve injury results in persistent motor defi

264 f GCS in wild-type mice, following transient peripheral nerve injury, reversed the overexpression of

265 In peripheral nerve injury, Schwann cells (SCs) must surviv

266 After a peripheral nerve injury, Schwann cells (SCs), the myelin

267 After peripheral nerve injury, Schwann cells transition from a

268 n this study, we hypothesized that (1) after peripheral nerve injury, second-order dorsal horn neuron

269 Peripheral nerve injury sensitizes a complex network of

270 After peripheral nerve injury, sensory neurons switch to a reg

271 In humans with peripheral nerve injuries, shorter wait times to decompr

272 Neuropathic pain caused by peripheral nerve injuries significantly affects sensory

273 during development of SC lineage and during peripheral nerve injury, so we sought to study their fun

274 rats with a hypersensitivity state following peripheral nerve injury, spinal administration of an NO

275 It has been shown recently that in models of peripheral nerve injury, spinal cord microglia can becom

276 Peripheral nerve injury stimulates neuronal expression o

277 rved behavior in the rotarod, water maze and peripheral nerve injury tests was possibly affected by i

278 tive in alleviating mechanical allodynia for peripheral nerve injury than nerve root injury, suggesti

279 In severe proximal peripheral nerve injuries that require long-distance axo

280 re observed in the rat spinal cord following peripheral nerve injuries that result in neuropathic pai

281 ndergo a similar transcriptional response to peripheral nerve injury that both promotes axonal regene

282 the aim of this study is to examine whether peripheral nerve injury that causes neuropathic pain mod

283 play an unique role in neuroplasticity after peripheral nerve injury that may contribute to allodynia

284 r RNA elevation in rat spinal cord following peripheral nerve injury that results in pain behaviors s

285 In the weeks following unilateral peripheral nerve injury, the deprived primary somatosens

286 After peripheral nerve injury, there is an increase in the pop

287 tion as distal stimulators in a rat model of peripheral nerve injuries, thereby demonstrating the pot

288 A representative application is in treating peripheral nerve injuries through targeted stimulation a

289 Robust axon regeneration occurs after peripheral nerve injury through coordinated activation o

290 adult dorsal root ganglion neurons following peripheral nerve injury, triggering selective degenerati

291 Peripheral nerve injury upregulated DNMT1 expression in

292 d nerve conduction examinations, evidence of peripheral nerve injury was seen.

293 ning can affect the functional outcome after peripheral nerve injury, we assessed the effect of up-co

294 sal horn of the spinal cord is reduced after peripheral nerve injury, we have studied synaptic transm

295 pression and function of spinal NMDARs after peripheral nerve injury were modulated by central GRs.

296 untered in lumbar DRGs in standard models of peripheral nerve injury were not observed in diabetic mi

297 ase in synthesis of NGF within the DRG after peripheral nerve injury, which contributes to the recove

298 st a role for NP-1 in the axonal response to peripheral nerve injury, which may be specific to a part

299 Patients with peripheral nerve injuries would highly likely suffer fro

300 in mice and rats after optic nerve injury or peripheral nerve injury, yet the mechanisms underlying i