ライフサイエンスコーパス: DRG

1 DRG membranes isolated from SCI animals revealed a novel

2 DRG neuron membrane stiffness was not significantly affe

3 ChIP2, and DPP10 are coexpressed in Kv4.3(+) DRG neurons, but whether they participate in Kv4.3-media

4 on, siRNA knockdown of Panx1 expression in a DRG cell line significantly reduced caspase-1 release in

5 Overall, our work uncovers a DRG neuron-microglia interaction that responds to G-CSF

6 s rubric to identify a drug that accelerates DRG neurite outgrowth in vitro and optic nerve outgrowth

7 to studies and screens using VTD to activate DRG neurons.

8 lthough normally at very low levels in adult DRG neurons, Neto2 protein expression can be upregulated

9 ted these features in cultured mouse CNS and DRG neurons.

10 DRG membrane, Slack channel endocytosis, and DRG neuronal hyperexcitability after PKA activation.

11 ique prolonged exposure in sciatic nerve and DRG.

12 creased CGRP release from sciatic nerves and DRGs, and a reduction in mechanical and thermal pain hyp

13 ransfected into the injured DRGs (defined as DRGs with injured spinal nerves) of living SNL rats.

14 RNA and protein expression in the axotomized DRG and attenuated the development of nerve injury-induc

15 genetic silencing of Kcna2 in the axotomized DRG.

16 icient to inhibit P2X3 activation in bladder DRG neurons and to alleviate bladder overactivity in Pir

17 paclitaxel-induced spontaneous discharges by DRG neurons to promote recovery from CIPN.

18 rmal growth patterns in mutant SPTLC1(C133W) DRG.

19 ferent nerve activity, and c-Fos-IR in C2-C4 DRG neurons ipsilateral to the CL316,243 injections vers

20 ta1 were significantly increased in the CAIA DRGs as compared to controls, both 15 and 47 days after

21 levels of Ube3a-ATS Analysis of single-cell DRG transcriptomes further suggested that Ube3a is expre

22 Complementarily, DRG neurons isolated from segments where patients had a

23 y beta-alanine is also unchanged in cultured DRG neurons from TrpC3 null mice compared to wild type.

24 In cultured DRG neurons, chelating calcium early in the process of W

25 knockdown alters axon branching in cultured DRG neurons.

26 eleased in the exosomal fraction of cultured DRG following capsaicin activation of TRPV1 receptors.

27 T2DM), dyslipidemia and hyperglycemia damage DRG neurons and induce mitochondrial dysfunction; howeve

28 d action potential firing in FGF13-deficient DRG neurons.

29 on to spike repolarization in small-diameter DRG neurons and undergo frequency-dependent reduction, l

30 Sensitization of cultured small-diameter DRG neurons by prostaglandin E2 is also prevented and re

31 nosensory afferent fibres and small-diameter DRG neurons possessed lower functional TRPV1 receptor re

32 ological inhibition of CaN in small-diameter DRG neurons slowed repolarization of the somatic action

33 Histopathology showed diminished DRG pathology with natalizumab treatment, including decr

34 oot ganglion (DRG) neuron numbers, but fewer DRG neurons expressed the SAI markers TrkB, TrkC, and Re

35 e dorsal root ganglion (DRG) is critical for DRG neuronal excitability and neuropathic pain genesis.

36 was upregulated in the dorsal root ganglia (DRG) after nerve injury, which was further validated for

37 ut all persisted in the dorsal root ganglia (DRG) and sciatic nerve (SN) for up to 72 hours.

38 ed with degeneration in dorsal root ganglia (DRG) and sciatic nerve and abundance of Schwann cells.

39 To define which dorsal root ganglia (DRG) are activated by BAT SNS stimulation, indicated by

40 sensory neurons in the dorsal root ganglia (DRG) are the initial transducers of sensory stimuli, inc

41 t, we found that mutant dorsal root ganglia (DRG) during growth in vitro exhibit increased neurite le

42 sensory neurons of the dorsal root ganglia (DRG) express kainate receptors (KARs), a subfamily of gl

43 nduced mutation affects dorsal root ganglia (DRG) formation in ouchless mutant zebrafish larvae.

44 mary nociceptors within dorsal root ganglia (DRG) has been found to make major contributions to chron

45 t neurons isolated from dorsal root ganglia (DRG) innervating the lower gastrointestinal tract, where

46 ene constructs into the dorsal root ganglia (DRG) is a powerful but challenging therapeutic strategy

47 ated monocytes into the dorsal root ganglia (DRG) is critical for pathology in HIV peripheral neuropa

48 mall diameter (<27 mum) dorsal root ganglia (DRG) neurons and on miniature (m)EPSCs recorded from lar

49 that Schwann cells and dorsal root ganglia (DRG) neurons developed abnormally in mz-smn mutants.

50 nction mutations render dorsal root ganglia (DRG) neurons hyperexcitable.

51 TATEMENT Small-diameter dorsal root ganglia (DRG) neurons mediating nociception and other sensory mod

52 are a subpopulation of dorsal root ganglia (DRG) neurons that detect noxious stimuli and signal pain

53 mall diameter (<27 mum) dorsal root ganglia (DRG) neurons.

54 s upon hyperactivity in dorsal root ganglia (DRG) neurons.

55 tem, spinal nerves, and dorsal root ganglia (DRG) of rhesus macaques that were inoculated intrathecal

56 sult in transduction of dorsal root ganglia (DRG) or trigeminal ganglia (TG), respectively.

57 roRNAs (miRs) occurs in dorsal root ganglia (DRG) sensory neurons.

58 ve (SN), the lumbar 4/5 dorsal root ganglia (DRG), and the trigeminal ganglia (TG) of streptozotocin-

59 endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain.

60 well known to reside in dorsal root ganglia (DRG), the morphology and location of peripheral nerve en

61 er of T cells in lumbar dorsal root ganglia (DRG), where CD8(+) T cells were the major subset.

62 afferent neurons of the dorsal root ganglia (DRG).

63 n vivo, specifically to dorsal root ganglia (DRG).

64 mur and the ipsilateral dorsal root ganglia (DRG).

65 inflammatory markers in dorsal root ganglia (DRGs) and spinal cord up to 2 wk after intervention.

66 expression profiling of dorsal root ganglia (DRGs) combined with multi-level bioinformatic analyses a

67 sponses to capsaicin in dorsal root ganglia (DRGs) following application of supernatants generated fr

68 n of different types of dorsal root ganglia (DRGs) neurons after sciatic nerve injury in the rat.

69 Z-octadecenoic acid) in dorsal root ganglia (DRGs) of paclitaxel-treated mice as a model of CIPNP.

70 ression is increased in dorsal root ganglia (DRGs) of paclitaxel-treated rats.

71 wth from chicken or rat dorsal root ganglia (DRGs).

72 hose cell bodies lie in dorsal root ganglia (DRGs).

73 ere upregulated in the dorsal root ganglion (DRG) after chronic compression of DRG (CCD), and some CX

74 ulation of MORs in the dorsal root ganglion (DRG) and diminishes the opioid effect on neuropathic pai

75 and DPP10 in adult rat dorsal root ganglion (DRG) and spinal cord by immunohistochemistry.

76 in colonic tissue and dorsal root ganglion (DRG) cells isolated from 3- and 24-month animals, and im

77 PO due to insufficient dorsal root ganglion (DRG) exposure attributed to poor membrane permeability.

78 nd is characterized by dorsal root ganglion (DRG) inflammation and intraepidermal nerve fiber density

79 l subunit Kcna2 in the dorsal root ganglion (DRG) is critical for DRG neuronal excitability and neuro

80 erkel cells had normal dorsal root ganglion (DRG) neuron numbers, but fewer DRG neurons expressed the

81 to acutely dissociated dorsal root ganglion (DRG) neuron somata.

82 lays a central role in dorsal root ganglion (DRG) neuronal cell survival and neurotransmission by tra

83 4 potassium current in dorsal root ganglion (DRG) neurons contributes to the hyperexcitability associ

84 rons; adult miR-155 KO dorsal root ganglion (DRG) neurons extend 44% longer neurites than WT neurons.

85 um channel NaV1.7 make dorsal root ganglion (DRG) neurons hyperexcitable.

86 alysis, we categorized dorsal root ganglion (DRG) neurons into different subtypes and discovered co-r

87 PM3 expressed in mouse dorsal root ganglion (DRG) neurons is inhibited by agonists of the Gi-coupled

88 terization of isolated dorsal root ganglion (DRG) neurons revealed that RPRFamide increases their exc

89 studies on dissociated dorsal root ganglion (DRG) neurons revealed the peptide's putative molecular t

90 particular subtype of dorsal root ganglion (DRG) neurons that detect noxious stimuli and elicit pain

91 eneration assay in rat dorsal root ganglion (DRG) neurons using a trophic factor withdrawal paradigm.

92 um channels (VGSCs) in dorsal root ganglion (DRG) neurons were sensitized in a rat model of LDH.

93 In rat dorsal root ganglion (DRG) neurons, exposure to E-2 in acidic solutions signif

94 gene transcription in dorsal root ganglion (DRG) neurons, which may contribute to nerve injury-induc

95 on of TRPM8 in sensory dorsal root ganglion (DRG) neurons.

96 el V1 (TRPV1)-positive dorsal root ganglion (DRG) neurons.

97 rced in Pirt-deficient dorsal root ganglion (DRG) neurons.

98 S and CIM0216 in mouse dorsal root ganglion (DRG) neurons.

99 roxylmethylcytosine in dorsal root ganglion (DRG) neurons.

100 ells exposed to G-CSF, dorsal root ganglion (DRG) nociceptors become hyperexcitable.

101 ural tissues including dorsal root ganglion (DRG) produce PD-L1 that can potently inhibit acute and c

102 ion of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic termina

103 branch development of dorsal root ganglion (DRG) sensory neurons.

104 nociceptors within the dorsal root ganglion (DRG), and knockdown of Kv4.3 selectively induces mechani

105 nnel expression in the dorsal root ganglion (DRG), but little is known about the epigenetic mechanism

106 al inflammation of the dorsal root ganglion (DRG), we observed marked increases in mechanical and col

107 ensing) neurons of the dorsal root ganglion (DRG), where they transmit the large outward conductance

108 ession of ASIC3 in the dorsal root ganglion (DRG).

109 A-fiber neurons in the dorsal root ganglion (DRG).

110 nociceptive neurons of dorsal root ganglion (DRG).

111 edian and ulnar nerves/dorsal root ganglion (DRG)/spinal cord (SC) recording preparation.

112 ces in viral load at dorsal root ganglionic (DRG) neurons at day 4 postinfection (p.i.) for both viru

113 Notably, although eribulin exhibited greater DRG and SN penetration than paclitaxel, the neurotoxicit

114 Despite the functional importance, how DRG neurons function at a population level is unclear du

115 RPV1 responses directly in dissociated human DRG neurons.

116 tial knockdown of SHANK3 expression in human DRG neurons abrogates TRPV1 function.

117 also shows that Nav1.7 is increased in human DRG neurons only in dermatomes where patients are experi

118 ProTx II decreased firing frequency in human DRGs with spontaneous action potentials.

119 sed nociceptive neuron excitability in human DRGs.

120 os immunoreactivity (IR), we prelabeled IBAT DRG innervating neurons by injecting the retrograde trac

121 pathway that links CaN, RCAN1, and Kv3.4 in DRG neurons.

122 hed by TRPM8 antagonists, and were absent in DRG and TG neurons isolated from Trpm8(-/-) mice.

123 Accordingly, in DRG neurons, HA decreases TRPV1-mediated impulse firing

124 PD-1 activation in DRG nociceptive neurons by PD-L1 induced phosphorylation

125 Pharmacological inhibition of Akt in DRG neuron-Schwann cell cocultures dramatically decrease

126 ibited inward currents induced by CIM0216 in DRG neurons, and nocifensive responses elicited by this

127 expression of all Kv4 complex components in DRG neurons is downregulated following spinal nerve liga

128 induced spontaneous pain, inward currents in DRG neurons, and synaptic currents in spinal cord neuron

129 paclitaxel-induced spontaneous discharges in DRG neurons.

130 In mice lacking Ehmt2 in DRG neurons, nerve injury failed to reduce the expressio

131 reases Kv current, increases excitability in DRG neurons and leads to spinal cord central sensitizati

132 tolloid-like 2 (Neto2) is also expressed in DRG.

133 d chemokine C-C motif ligand 2 expression in DRG neurons and macrophage infiltration into DRGs, and m

134 thymine DNA glycosylase-dependent fashion in DRG neurons.

135 ster ovary cells, supporting our findings in DRG neurons.

136 sonance imaging; and assessment of firing in DRG neurons carrying S241T mutant channels.

137 d in neonatal DRG and modifies KAR gating in DRG neurons in a developmentally regulated fashion in mi

138 he potentiation was significantly greater in DRG neurons isolated from rats whose femoral arteries we

139 are promoted by persistent hyperactivity in DRG neurons.

140 ting ectopic firing and hyperexcitability in DRG neurons, however little is known regarding the role

141 A1, diminished AYP-induced calcium influx in DRG neurons and the scratching behavior in mice.

142 ddition, G9a inhibition or Ehmt2 knockout in DRG neurons normalized nerve injury-induced reduction in

143 roles of cytoskeleton and membrane lipids in DRG neuron mechanics.

144 d late), and SIVp28(+) (late) macrophages in DRG tissues.

145 reduced the number of motile mitochondria in DRG axons, but physiologic concentrations of glucose did

146 and energetically challenged mitochondria in DRG neurons.

147 suppressed spontaneous action potentials in DRG neurons occurring in rats with CIPN, while intrathec

148 ttle information on VTD response profiles in DRG neurons and how they relate to neuronal subtypes.

149 we detected recombinant human FXN protein in DRG.

150 g that activation of adrenergic receptors in DRG neurons is preferentially linked to CaMKII activity.

151 and glucose on mitochondrial trafficking in DRG neurons remains unknown.

152 The activity of TRPM3 in DRG neurons is also negatively modulated by tonic, const

153 injury in mice, miR-21-5p is upregulated in DRG neurons and both intrathecal delivery of a miR-21-5p

154 ed to the C7 ventral ramus and visualized in DRG and spinal cord sections colabeled for CGRP and SP.

155 uppressed expression of NaV1.7 and NaV1.8 in DRGs of LDH rats.

156 telmisartan reduces EpOME concentrations in DRGs and in plasma and reverses mechanical hypersensitiv

157 oportion of cold-sensitive neurons (CSNs) in DRGs contributing to the sciatic nerve, and a decrease i

158 FAP), and the fractalkine receptor CX3CR1 in DRGs.

159 ediates leukocyte traffic, was diminished in DRGs of all natalizumab-treated animals.

160 ne maternal and paternal Ube3a expression in DRGs neurons and to evaluate whether nociceptive respons

161 The number of CD3(+) T lymphocytes in DRGs was not affected by natalizumab treatment.

162 expression and function of Nav1.7 protein in DRGs from male rats with paclitaxel-related CIPN and fro

163 also decreased downstream TrkB signaling in DRGs, and altered the expression of genes associated wit

164 We propose that CD8(+) T cells increase DRG IL-10 receptor expression and that IL-10 suppresses

165 membrane permeability showed much increased DRG concentrations at doses of 30 mpk PO, but, confoundi

166 Paclitaxel increased DRG IL-10 receptor expression and this effect requires C

167 these results suggest that palmitate induces DRG neuron mitochondrial depolarization, inhibiting axon

168 rophages and neutrophils infiltrate infected DRGs and account for the development of herpetic neuralg

169 Cytokine profiling in locally inflamed DRG showed increases in pro-inflammatory Type 1 cytokine

170 and rescues Kcna2 expression in the injured DRG and attenuates neuropathic pain.

171 fully reversed MOR expression in the injured DRG and potentiated the morphine effect on pain hypersen

172 DNA methyltransferase DNMT3a in the injured DRG neurons via the activation of the transcription fact

173 and DPP10 were transfected into the injured DRGs (defined as DRGs with injured spinal nerves) of liv

174 IP1, and DPP10 surface levels in the injured DRGs.

175 e inactivation curve, of hindpaw innervating DRG neurons, which is retrogradely labeled by DiI.

176 ith NaV1.7 and NaV1.8 in hindpaw-innervating DRG neurons.

177 DRG neurons and macrophage infiltration into DRGs, and microglia activation in spinal dorsal horns in

178 , comparable to the levels obtained by intra-DRG injection (81.3% +/- 5.1%, p = 0.82) but much higher

179 The current delivery methods of direct intra-DRG injection and intrathecal injection have several dis

180 t alter the excitability of acutely isolated DRG neurons.

181 ated gene; approximately 50% more injured KO DRG neurons expressed SPRR1A versus WT neurons.

182 entered the spinal nerves near the L4 and L5 DRG.

183 expression of CNR1 in L6-S2, but not L4-L5, DRGs.

184 ve injury upregulated CXCL12 in lumbar L4-L6 DRGs, and this upregulation caused migration of i.t.-inj

185 eductions in pain behaviors induced by local DRG inflammation (a rat model of low back pain) and by a

186 tability of sensory neurons induced by local DRG inflammation observed 4 d later.

187 cing established pain behaviors in the local DRG inflammation model.

188 blocking sympathetic sprouting in the local DRGs or hindpaw was the sole mechanism.

189 a reduction in all components in the lumbar DRGs.

190 tions of dextran-amine made into lumbosacral DRGs (L5-S2).

191 In cultured male DRG neurons, IP3 (100 mum) potentiated depolarization-in

192 he regenerative effects of cAMP in mammalian DRG neurons.

193 diameter proprioceptive and mechanosensitive DRG neurons expressed maternal Ube3a and paternal Ube3a-

194 mitochondrial transport, primary adult mouse DRG neuron cultures were treated with physiologic concen

195 nct lipoxygenase inhibitors as well as mouse DRG neurons lacking expression of 12/15-lipoxygenase dis

196 cium in zebrafish neurons and cultured mouse DRG neurons.

197 -induced calcium responses in cultured mouse DRG neurons.

198 1) can affect the excitability of male mouse DRG neurons.

199 ast growth factor (FGF), FGF13, in the mouse DRG neurons selectively abolished heat nociception.

200 s, predominantly in A-fiber neurons of mouse DRGs.

201 y correlated with CMS coding guidance and MS-DRG introduction after adjustment for comorbidity and ot

202 medical severity diagnosis-related group (MS-DRG) systems on sepsis trends.

203 2007); and (3) after the introduction of MS-DRG (October 2007 to December 2010).

204 guidance for new sepsis ICD-9 coding and MS-DRGs.

205 regulation, overexpression of RCAN1 in naive DRG neurons recapitulated the effects of pharmacological

206 eto2 protein is highly expressed in neonatal DRG and modifies KAR gating in DRG neurons in a developm

207 KARs in neonatal DRG require the GluK1 subunit as a necessary constituent

208 eter non-peptidergic neurons in the neonatal DRG express functional kainate receptors (KARs), one of

209 sly monitor the activities of >1,600 neurons/DRG in live mice and discovered a striking neuronal coup

210 dividual injured and non-injured nociceptive DRG neurons and to define their gene profiling in rat sp

211 About 70% of DRG neurons respond to 30-100 muM VTD.

212 xpression was detected in 82.8% +/- 1.70% of DRG neurons, comparable to the levels obtained by intra-

213 neuronal cell body throughout the bundles of DRG axons.

214 ganglion (DRG) after chronic compression of DRG (CCD), and some CXCR4 immunopositive neurons were al

215 MET-1 reduced the excitability of DRG neurons by significantly increasing rheobase, decrea

216 evant thermal stimuli on the excitability of DRG neurons expressing mutant and WT Nav1.7 channels, su

217 eria can directly impact the excitability of DRG neurons, through PAR-4 activation.

218 ated the effects of MET-1 on excitability of DRG neurons.

219 ess the effect of carbamazepine on firing of DRG neurons carrying S241T mutant channels.

220 Firing of DRG neurons expressing the S241T NaV1.7 mutant channel i

221 nce of SCI-induced SA in a large fraction of DRG neurons and the persistence of this SA long after di

222 o2 assembly is critical to KAR modulation of DRG neuron process outgrowth.SIGNIFICANCE STATEMENT Pain

223 gene regulation in a specific population of DRG neurons (e.g., nociceptors) is an effective strategy

224 th and neuropathy in different population of DRG neurons.

225 expression in a heterogeneous population of DRG neurons.

226 tro and caused defects in axon projection of DRG toward the spinal cord in vivo Furthermore, live-cel

227 is required for robust axon regeneration of DRG neurons and behavioral recovery.

228 The response of DRG neurons expressing Nav1.7-A1632G mutant channels upo

229 he endoplasmic reticulum and cell surface of DRG neurons.

230 the injection site survived at the border of DRGs for more than 2 months.

231 psin G recapitulated the effects of MET-1 on DRG neurons.

232 ted the effects of substrate availability on DRG neurons.

233 ors abrogated the effect of MET-1 effects on DRG neuron rheobase.

234 mth, the effects of increased temperature on DRG neurons expressing mutant Nav1.7 channels have not b

235 ession by neurofilament(+) and peripherin(+) DRG neurons was similar.

236 ons received TRP channel M8 (TRPM8)-positive DRG inputs as well as novel TRPV1(+) DRG inputs that wer

237 itability when activated in cultured primary DRG neurons.

238 the DRG membrane, reduces IKNa, and produces DRG neuronal hyperexcitability when activated in culture

239 by which i.t. BMSCs target CXCL12-producing DRGs to elicit neuroprotection and sustained neuropathic

240 n mechanotransduction in neurite-bearing Pv+ DRG neurons through localized elastic matrix movements a

241 imuli and impairs mechanotransduction in Pv+ DRG neurons because of substrate deformation-induced neu

242 ing frequencies and the number of active rat DRG neurons expressing Nav1.7-A1632G mutant channels, wh

243 e neuron-specific activator of Cdk5, and rat DRG neurons transduced with HSV overexpressing p35 can o

244 that action potentials of small-diameter rat DRG neurons showed spike broadening at frequencies as lo

245 ly increase these parameters slightly in rat DRG neurons expressing Nav1.7 WT channels.

246 threshold, and enhanced evoked firing in rat DRG neurons expressing Nav1.7-A1632G mutant channels.

247 Whole-cell patch-clamp recordings in rat DRG neurons revealed that paclitaxel induced an enhancem

248 recordings further revealed that intact rat DRG neurons expressing Nav1.7-A1632G mutant channels are

249 f terminal synaptic vesicles in isolated rat DRG neurons.

250 nd expression of the TRPV1 receptor in L6-S2 DRG neurons.

251 Tissue injury can sensitize DRG neurons, causing heightened pain sensitivity, often

252 C387(+)) monocytes is associated with severe DRG pathology and loss of intraepidermal nerve fibers in

253 increase of caspase-6 (CASP6) in small-sized DRG neurons and its functional role in SNI- and paclitax

254 showed that Nav1.7 was upregulated in small DRG neuron somata, especially those also expressing calc

255 anodine in low concentration (2 nM) to small DRG neurons cultured from females, significantly potenti

256 of gap junctions in glial cells surrounding DRG neurons.

257 We found that DRG neurons had a plasma membrane tension of approximate

258 Finally, we observed that DRG neurons are the only Munc18-1 KO neurons that do not

259 Here we show that DRG neuron cell bodies release extracellular vesicles, i

260 strategy for sensory disorders affecting the DRG and their peripheral processes.

261 that targeting the CBS-H2S signaling at the DRG level might represent a novel therapeutic strategy f

262 Slack channel expression at the DRG membrane is necessary for their characteristic firin

263 h and modulation of glutamate release at the DRG-dorsal horn synapse.

264 growth and regulate glutamate release at the DRG-dorsal horn synapse.

265 eu, PKA internalizes Slack channels from the DRG membrane, reduces IKNa, and produces DRG neuronal hy

266 nts a new form of neuronal plasticity in the DRG and contributes to pain hypersensitivity by "hijacki

267 the native regulator of CaN 1 (RCAN1) in the DRG at the transcript and protein levels.

268 ction in the expression level of MORs in the DRG but not in the spinal cord.

269 v current, and increased excitability in the DRG neurons and led to spinal cord central sensitization

270 mRNA is co-localized with Kcna2 mRNA in the DRG neurons.

271 Primary sensory neurons in the DRG play an essential role in initiating pain by detecti

272 n rate of >90% of the sensory neurons in the DRG that innervate the footpad.

273 In the DRG, we found colocalization of KChIP1, KChIP2, and DPP1

274 onditional deletion of maternal Ube3a in the DRG.

275 imethylation in the promoter of Oprm1 in the DRG.

276 ociceptive neurons was also increased in the DRG.

277 f inflammatory macrophage recruitment in the DRG.

278 c pain by repressing Kcna2 expression in the DRG.

279 Here, we investigated the DRG and spinal cord expression of the putative primary a

280 sent in the corresponding cell bodies of the DRG or the cranial TG.

281 er, increased macrophage infiltration of the DRG was observed in response to the HFD, absent any pain

282 is essential for clathrin recruitment to the DRG membrane, Slack channel endocytosis, and DRG neurona

283 nocyte, but not T lymphocyte, traffic to the DRG results in decreased inflammation and pathology, sup

284 local environmental factors found within the DRG.

285 n of the ADP-responsive P2Y1 receptor in the DRGs.

286 ons of dextran-amine were made into thoracic DRGs (T8-T12).

287 proach, PEI/DNA polyplexes were delivered to DRG neurons without nerve injury.

288 disadvantages, including potential injury to DRG neurons and low transfection efficiency, respectivel

289 used for the delivery of therapeutic mRNA to DRG.

290 d safety of delivering PEI/DNA polyplexes to DRG neurons via spinal nerve injection.

291 n a high-fat diet (HFD) for 6 weeks prior to DRG inflammation.

292 robiota derived from a human donor signal to DRG neurons.

293 n caused migration of i.t.-injected BMSCs to DRGs through the CXCL12 receptor CXCR4, which was expres

294 Palmitate-treated DRG neurons also exhibited a reduction in mitochondrial

295 hondrial depolarization in palmitate-treated DRG neurons.

296 ositive DRG inputs as well as novel TRPV1(+) DRG inputs that were selectively activated by intense co

297 ced Slack-mediated IKNa expression underlies DRG neuronal sensitization.

298 inated fibers without affecting unmyelinated DRG neurons.

299 While DRG neurons express MCT1, myelinating Schwann cells (SCs

300 ession patterns found previously using whole DRG tissue following SNI.