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1 DRG neuronal populations were identified by neurofilamen
2 DRG neurons of NGF(R100W/wt) mice are morphologically no
3 DRG neurons showed accumulation of cleaved caspase 3 (ap
9 ts of daily chemogenetic activation of adult DRG neurons for 12 weeks post-crush in vivo enhances axo
11 stem and indicate that loss of Jedi-1 alters DRG neuron activity indirectly through an intercellular
12 inct differences in mechanical allodynia and DRG gene expression, even though sex differences in IVD
13 ted TNF and CXCL1 in macrophage cultures and DRG tissues in both sexes, but these changes were compro
15 of future neural interface technologies and DRG-focused pharmaceutical therapies, and provide a rigo
16 veral findings of differences between TG and DRG nociceptors described in the literature but also sug
17 scriptome and translatome activity in TG and DRG nociceptors that enhances our understanding of nocic
18 usly unrecognized differences between TG and DRG nociceptors that provide new insight into how injury
20 located in the trigeminal ganglion (TG) and DRG are the primary sensors of damaging or potentially d
21 ments using pharmacological tools as well as DRG from ERbeta(-/-) mice indicate that this BPA effect
22 ransfected into the injured DRGs (defined as DRGs with injured spinal nerves) of living SNL rats.
24 lls in the injured nerve, but not axotomized DRGs, strongly express receptors for the cytokine GM-CSF
25 innervated by cervicovascular neurons in C2 DRG whose axons reach the posterior dura through multipl
26 in male rats, we found that neurons in C2-C3 DRGs innervate the dura of the posterior fossa; that nea
31 eleased in the exosomal fraction of cultured DRG following capsaicin activation of TRPV1 receptors.
32 e-cell patch clamp recordings using cultured DRG neurons and observed mechanically-activated (MA) cur
33 -Exos promoted neurite outgrowth of diabetic DRG neurons and migration of Schwann cells challenged by
34 normal, with no alteration in the different DRG subpopulations, whereas skin innervation is reduced.
41 how that the T790A mutation greatly enhances DRG neuron excitability by reducing current threshold an
44 ultured with human intrafusal muscle fibers, DRG organoid sensory neurons contact their peripheral ta
48 is of ex vivo H3K9ac ChIPseq and RNAseq from DRG followed by promoter acetylation and protein express
51 ptors, are derived from dorsal root ganglia (DRG) and can undergo changes in membrane excitability du
52 ed with degeneration in dorsal root ganglia (DRG) and sciatic nerve and abundance of Schwann cells.
53 cular signatures of the dorsal root ganglia (DRG) and spinal cord response, not observed at the nerve
56 lls and chick embryonic dorsal root ganglia (DRG) bodies, as well as the migration of Schwann cells.
61 esident GFAP(+) glia in dorsal root ganglia (DRG) known as satellite glial cells (SGCs) potentiate ne
62 evels in fibroblasts in dorsal root ganglia (DRG) meninges and in the epi/perineurium of the sciatic
64 cubation of dissociated dorsal root ganglia (DRG) nociceptors with 1 nM BPA increases the frequency o
65 regenerative ability of dorsal root ganglia (DRG) sensory neurons compared to EE or a conditioning in
66 ion response in bipolar dorsal root ganglia (DRG) sensory neurons, a regeneration-incompetent central
68 thologic changes in the dorsal root ganglia (DRG) through inflammation, altered metabolism, and neuro
69 from the autonomic and dorsal root ganglia (DRG) to the axon and any peripheral nerve fibre type.
71 ry culture and in mouse dorsal root ganglia (DRG), as determined by the characteristic senescence mar
72 well known to reside in dorsal root ganglia (DRG), the morphology and location of peripheral nerve en
73 on protein, we isolated dorsal root ganglia (DRG), the primary sensory cell body for peripheral nerve
85 nd the transcriptome of dorsal root ganglia (DRGs) provide possible explanations for the increase in
86 nscriptome profiling of dorsal root ganglia (DRGs) revealed 138 differentially regulated genes in Glu
89 ere upregulated in the dorsal root ganglion (DRG) after chronic compression of DRG (CCD), and some CX
90 rations, such as whole dorsal root ganglion (DRG) and hindpaw tissues, revealed only a few sex-depend
91 alyses of rodent whole dorsal root ganglion (DRG) have revealed sex differences, mostly in immune cel
93 have described a human dorsal root ganglion (DRG) neuron culture model and human induced pleuripotent
94 n of mammalian PATs in dorsal root ganglion (DRG) neurons and, strikingly, found that only two PATs,
95 creased RNA binding in dorsal root ganglion (DRG) neurons compared with wild-type and non-phosphoryla
96 Our study shows that dorsal root ganglion (DRG) neurons contain at least two major functional K(v)1
97 4 potassium current in dorsal root ganglion (DRG) neurons contributes to the hyperexcitability associ
98 channels (VGSC) on the dorsal root ganglion (DRG) neurons controlling electrical impulses may have ab
100 which is known to make dorsal root ganglion (DRG) neurons hyperexcitable, but different pain profiles
101 ic activation of adult dorsal root ganglion (DRG) neurons improves axon growth on an in vitro model o
102 PM3 expressed in mouse dorsal root ganglion (DRG) neurons is inhibited by agonists of the Gi-coupled
105 eage (Vglut3(lineage)) dorsal root ganglion (DRG) neurons play an important role in mechanosensation
106 8-15) and with primary dorsal root ganglion (DRG) neurons resulted in significant neurite outgrowth a
107 ) conductance of mouse dorsal root ganglion (DRG) neurons was examined by the whole-cell patch-clamp
108 ained ASIC currents in dorsal root ganglion (DRG) neurons were enhanced by naturally occurring endomo
109 and differentiation of dorsal root ganglion (DRG) neurons, and on adult DRG neuron sensitization to p
110 mall-diameter (<30 um) dorsal root ganglion (DRG) neurons, cultured from fentanyl-primed rats, and ra
111 0.5 nm) was applied to dorsal root ganglion (DRG) neurons, cultured from opioid-primed rats, it induc
112 gene transcription in dorsal root ganglion (DRG) neurons, which may contribute to nerve injury-induc
118 nociceptors within the dorsal root ganglion (DRG), and knockdown of Kv4.3 selectively induces mechani
119 evels of P2X(3) in the dorsal root ganglion (DRG), and the whole cell patch clamp was used to examine
120 adjacent uninjured L4 dorsal root ganglion (DRG), as revealed by both in vivo electrophysiological r
121 ns isolated from mouse dorsal root ganglion (DRG), native TRPM3 channels were inhibited by activating
122 own, but we found that dorsal root ganglion (DRG)-specific knockdown of Magi-1 attenuated thermal noc
124 on and duration of surgery as well as German DRG case-weight were significantly higher in the interve
125 Thus, based on the changes in dorsal horn, DRG and peripheral innervation, we suggest that the adul
126 ee-dimensional spatial organization of human DRG neural fibers and somata has not been quantitatively
127 simplex virus 1 (HSV-1) to infect the human DRG-derived neuronal cell line HD10.6 in order to study
129 erve injury-induced pain hypersensitivities, DRG DNMT1 contributes to neuropathic pain genesis partia
130 ct of fentanyl was reversed in weakly IB4(+) DRG neurons cultured from opioid-primed rats after in vi
135 vated MrgprD signaling to activate TRP-A1 in DRG neurons and in human embryonic kidney 293 cells, to
136 mulation of senescent-like neuronal cells in DRG is associated with cisplatin-induced peripheral neur
140 expression of all Kv4 complex components in DRG neurons is downregulated following spinal nerve liga
141 that increased Nav1.8 resurgent currents in DRG neurons greatly prolong action potential duration an
145 hibitors targeting key epigenetic enzymes in DRG neurons, we identified HDAC3 signalling as a novel c
147 d up-regulation of phosphorylated (p)-ERK in DRG was considerably reduced in the IL-6 knockout mice.
153 on of sustained ASIC currents was greater in DRG neurons isolated from rats with ligated femoral arte
154 e, we report that RUNX1, expressed highly in DRG, binds HSV-1 genome, represses transcription of nume
156 ANO1-containing multichannel nanodomains in DRG neurons and suggest that coupling between TRPV1 and
158 dergic and nonpeptidergic sensory neurons in DRG are potentially capable of detecting sensory stimuli
160 sterior fossa; that nearly half originate in DRG neurons containing CGRP and TRPV1; that nerve bundle
163 suppressed spontaneous action potentials in DRG neurons occurring in rats with CIPN, while intrathec
164 sodium channel Na(v)1.7, which is present in DRG nociceptors and is essential in pain signaling.
166 g that activation of adrenergic receptors in DRG neurons is preferentially linked to CaMKII activity.
167 bserved strong circadian reporter rhythms in DRG neurons which are highly entrainable by external cue
168 Type I IFNs stimulate JAK/STAT signaling in DRG neurons but this does not apparently result in PKR-e
169 Recently, we have revealed itch signaling in DRG neurons by which TRPC4 mediates itch to serotonergic
171 We have also shown that silencing TRPC4 in DRG and its inhibition by intradermal injections were al
172 injury in mice, miR-21-5p is upregulated in DRG neurons and both intrathecal delivery of a miR-21-5p
173 roduction of PGE(2)-G over that of PGE(2) in DRGs, decreased mechanical and thermal hyperalgesia, and
174 the hypotheses that PGE(2)-G is increased in DRGs of HbSS-BERK mice and sensitizes nociceptors (senso
176 membrane permeability showed much increased DRG concentrations at doses of 30 mpk PO, but, confoundi
177 rophages and neutrophils infiltrate infected DRGs and account for the development of herpetic neuralg
178 mmediately after plantar formalin injection, DRG neuronal activity increases substantially and this a
180 DNA methyltransferase DNMT3a in the injured DRG neurons via the activation of the transcription fact
181 attenuated hyperexcitability in the injured DRG neurons, and alleviated nerve injury-induced pain hy
182 upregulated DNMT1 expression in the injured DRG through the transcription factor cAMP response eleme
184 and DPP10 were transfected into the injured DRGs (defined as DRGs with injured spinal nerves) of liv
186 oss the dorsal root entry zone after injury, DRG neurons in which fidgetin was knocked down displayed
189 tive antagonist, Dendrotoxin-K, in several L-DRG subclasses (L1, L2, L3, and L5), suggesting the pres
190 expression in the male since fluorescent L4 DRG neurons, innervating the hindlimbs and lower back, w
195 aclitaxel treatment significantly lengthened DRG circadian periods, with little effects on the amplit
196 s showed that small-diameter Vglut3(lineage) DRG neurons fire menthol-evoked action potentials and ex
198 ctivity from primary afferents in the lumbar DRG using non-penetrating electrode arrays and to charac
202 t type I IFNRs are expressed in small/medium DRG neurons and that their activation produces neuronal
203 While different gene variants may modulate DRG neuron excitability and thereby contribute to interi
207 luorimetry analysis of male and female mouse DRG neurons demonstrated that the cooling compound menth
209 other voltage-gated sodium channels in mouse DRG are considered threshold channels because they produ
212 ast growth factor (FGF), FGF13, in the mouse DRG neurons selectively abolished heat nociception.
214 regulation, overexpression of RCAN1 in naive DRG neurons recapitulated the effects of pharmacological
215 transcriptional signature similar to native DRGs and display the main peripheral sensory neuronal an
216 fter oxaliplatin treatment in sciatic nerve, DRGs, or spinal cord tissue as revealed by untargeted an
217 al levels could be found in the inner 85% of DRG length, the outer-most 25-30% radially, and the dors
219 r is to review the bioelectrical behavior of DRG neurons, signaling complexity in sensory neurons, va
220 Our results demonstrated that clearance of DRG senescent neuronal cells reverses CIPN, suggesting t
221 ganglion (DRG) after chronic compression of DRG (CCD), and some CXCR4 immunopositive neurons were al
222 re we demonstrate a critical contribution of DRG macrophages, but not those at the nerve injury site,
223 rus in explanted ganglia and cryosections of DRG and the sacral sympathetic ganglia (SSG) from latent
225 ntribution to neuropathic pain, depletion of DRG macrophages reduces nerve injury-induced mechanical
231 hysiological changes during HSV infection of DRG neurons, which may have implications for understandi
232 cological inhibition or genetic knockdown of DRG DNMT1 alleviated nerve injury-induced pain hypersens
233 lations as well as computational modeling of DRG neuron subtypes were undertaken to assess the functi
237 ate a comprehensive translational profile of DRG nociceptors in naive mice and at the peak of neuropa
238 tro and caused defects in axon projection of DRG toward the spinal cord in vivo Furthermore, live-cel
246 it from genetic counseling and/or testing of DRGs, which may further inform personalized cancer surve
248 , we generate dorsal root ganglia organoids (DRG organoids) by in vitro differentiation of human iPSC
249 rized the expression of TRPC4 in peptidergic DRG neurons and showed that acute itch induced by seroto
251 )1.8 sodium channels in incoming presynaptic DRG axons is no longer sufficient to block activation of
254 egeneration, we plated dissociated adult rat DRGs transduced using AAV5-shRNA-fidgetin on a laminin s
257 results suggest that clearance of senescent DRG neuronal cells following platinum-based cancer treat
258 that from nonpainful SWN tumors, sensitized DRG neurons, causing increased sensitivity to depolariza
260 ments the mechanical responsiveness of small DRG neurons and potentially sensitizes group IV afferent
261 lated a subset of sensory neurons by sorting DRG neurons back-labeled from paw and thigh muscle.
264 ulk and single-cell RNA sequencing show that DRG organoids present a transcriptional signature simila
265 n vivo two-photon calcium imaging shows that DRG neuronal activity is higher in awake than anesthetiz
266 neuropathic pain, our findings suggest that DRG DNMT1 may be a potential target for neuropathic pain
267 in female cortical neurons, suggesting that DRG findings may be generalizable to other nervous syste
268 al density was fairly homogeneous across the DRG length, there was a distinct low density region in t
273 receptor expressed by satellite glia in the DRG involved in clearing apoptotic neurons during develo
277 ecreased population size (cell death) in the DRG of SIV-infected animals compared with uninfected ani
283 er, increased macrophage infiltration of the DRG was observed in response to the HFD, absent any pain
284 single-unit activity from the surface of the DRG, although with smaller signal to noise ratios (SNRs)
285 ociceptor biology.SIGNIFICANCE STATEMENT The DRG and trigeminal ganglion (TG) provide sensory informa
286 d 2, T cell-related signaling spreads to the DRG and spinal cord in females, but remains localized to
287 -penetrating arrays were not anchored to the DRG or surrounding tissues, the spike amplitudes did not
289 s induced by application of lidocaine to the DRG, thus pinpointing intermittent failure of spike prop
293 ere, we show that exposure of each opioid to DRG neurons resulted in potentiation of the sustained AS
294 duced CIPN caused macrophage infiltration to DRGs in both sexes, and this infiltration was not affect
298 ith sex differential expression in the whole DRG transcriptome and 66 genes whose messenger RNAs were
300 ated genes is higher in the TG compared with DRG, whereas several genes associated with the negative