ライフサイエンスコーパス: nociceptor

1 -threshold mechanosensors and high-threshold nociceptors.

2 hes are initiated by activation of meningeal nociceptors.

3 have higher translational efficiency in DRG nociceptors.

4 l, nonselective), ablating AITC detection by nociceptors.

5 oid-mediated forms of synaptic plasticity in nociceptors.

6 M is mediated by both IB4(+) and peptidergic nociceptors.

7 ver, mediated by both IB4(+) and peptidergic nociceptors.

8 wo alternative isoforms, are co-expressed in nociceptors.

9 priming is dependent on a different class of nociceptors.

10 vier of induced pluripotent stem cell (iPSC) nociceptors.

11 ens by spatial contrast activation of single nociceptors.

12 e responses through activation of multimodal nociceptors.

13 ue immune responses are regulated in part by nociceptors.

14 bodies and the intact peripheral endings of nociceptors.

15 1 (TRPV1), a Ca(2+)-permeable ion channel in nociceptors.

16 and exposure and sensitization of epithelial nociceptors.

17 1 pathway in Schwann cells, but not TRPA1 in nociceptors.

18 downstream CD44, the cognate HA receptor, in nociceptors.

19 as harsh touch in both the TRNs and the PVD nociceptors.

20 nisms underlying the effects of capsaicin on nociceptors.

21 s spinal inputs from unsensitized peripheral nociceptors.

22 n SCI-nociceptors to a level similar to sham-nociceptors.

23 elta-opioid receptors (DOPr) in endosomes of nociceptors.

24 ialized in detecting painful stimuli, termed nociceptors.

25 IB4-positive (IB4+) and IB4-negative (IB4-)] nociceptors.

26 sts inhibited mechanically sensitive colonic nociceptors.

27 olutions after heat sterilization, activates nociceptors.

28 s of neurons: peptidergic and nonpeptidergic nociceptors.

29 Cgamma1), and phosphoinositide 3-kinase, in nociceptors.

30 Nociceptor ablation alters local immune responses at per

31 Nociceptors accomplish this task through the expression

32 1) NMDA receptor mediated LTP is observed in nociceptors across both vertebrate and invertebrate phyl

33 iception, we sparsely traced non-peptidergic nociceptors across the body using a newly generated Mrgp

34 dulation of nociceptors and demonstrate that nociceptor activation drives both protective pain behavi

35 ophage colony stimulating factor (GM-CSF) in nociceptor activation in male and female mice.

36 ade of vlPAG EP3R raised EMG thresholds to C-nociceptor activation in the area of secondary hypersens

37 t 40-50 mA, greatly exceeding thresholds for nociceptor activation reported for both humans [9] and h

38 ated Peptide (iCGRP) release as a measure of nociceptor activation, and we found that each dicarbonyl

39 temperatures, where tissue damage causes pan-nociceptor activation.

40 ustard oil, stimuli known to evoke sustained nociceptor activity and sensitization following tissue d

41 K(+) channels, which act to reduce nociceptor activity, have been suggested to be novel dru

42 vity with the region that receives orofacial nociceptor afferents, the spinal trigeminal nucleus.

43 aberrant pain signaling and sensitization of nociceptors after peripheral nerve injury.

44 nsiveness and blocks spontaneous activity of nociceptors after SCI.

45 ce neurogenic inflammation(1,2), but whether nociceptors also interact with the immune system remains

46 increased activity of T-type channels in SCI-nociceptors and chronic neuropathic pain following SCI.

47 ive epineural optogenetic neuromodulation of nociceptors and demonstrate that nociceptor activation d

48 pressed by a subset of mouse non-peptidergic nociceptors and functions as the molecular receptor for

49 of HbAA-BERK mice produced sensitization of nociceptors and hyperalgesia.

50 The physical proximity of nociceptors and immune cells allows for direct local int

51 These results reveal a link between nociceptors and immune cells, which might have implicati

52 ctional consequences of interactions between nociceptors and immune cells.

53 a liposome shell for targeting DOPr-positive nociceptors and incorporated into a mesoporous silica co

54 um channel Na(v)1.7, which is present in DRG nociceptors and is essential in pain signaling.

55 nel that is expressed on a major subclass of nociceptors and is found in many orofacial tissues, incl

56 ain pathway expressed in Adelta- and C-fibre nociceptors and is responsible for the thermal hyperalge

57 ve shown Kv4.3 in a subset of nonpeptidergic nociceptors and Kv4.2/Kv4.3 in certain spinal lamina II

58 e that several reactive dicarbonyls activate nociceptors and potentiate inflammatory mediators.

59 ht to arise from increased transmission from nociceptors and recruitment of 'silent' afferents.

60 can down-regulate TRPV1 channel activity in nociceptors and reduce their synaptic transmission, the

61 ISA s) have been recorded from the somata of nociceptors and spinal lamina II excitatory interneurons

62 are also found on the peripheral endings of nociceptors and their activation there produces meaningf

63 Basal sensitivity is controlled in nociceptors, and allodynia involves TrkB(+) light-touch

64 ggest that type II afferents may be cochlear nociceptors, and can be excited by ATP released during t

65 ormation from baroreceptors, chemoreceptors, nociceptors, and circulating hormones, and is modulated

66 rimary afferents, including TRPV1-expressing nociceptors, and formed GABAergic, bicuculline-sensitive

67 ce of a functional GM-CSF receptor in murine nociceptors, and suggest an indirect mechanism of action

68 migraine depends on activation of meningeal nociceptors, and that for selected patients, activation

69 al novel transcripts were altered in injured nociceptors, and the global signature of these LCM-captu

70 Nociceptors are a particular subtype of dorsal root gang

71 Nociceptors are a subpopulation of dorsal root ganglia (

72 chanical stimuli, MRGPRD- and TRPV1-positive nociceptors are required to elicit reflexive and coping

73 Nociceptors are sensitized by inflammatory mediators pro

74 Sensory neurons, termed nociceptors, are derived from dorsal root ganglia (DRG)

75 channels, present in the peripheral parts of nociceptors, are strongly inhibited by microOR activatio

76 These findings identify Adelta meningeal nociceptors as a likely site of action of fremanezumab i

77 l sciatic nerve ligation, TRPA1 silencing in nociceptors attenuated mechanical allodynia, without aff

78 Regardless of whether the nociceptors become active before or after the induction

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

80 l depletion of small-diameter sensory nerves/nociceptors benefits the condition, but the mechanisms a

81 ciceptors that enhances our understanding of nociceptor biology.SIGNIFICANCE STATEMENT The DRG and tr

82 analysis revealed that MORs are expressed by nociceptors, but not by spinal microglia.

83 4F complex to regulate the sensitization of nociceptors, but the details of this process are ill def

84 ctivation of Adelta but not C-type meningeal nociceptors by CSD.

85 which may contribute to the sensitization of nociceptors by cytokines in pain development.

86 ibition of cAMP and promote hyperactivity of nociceptors by enhancing C-Raf activity.

87 ial ankyrin 1 (TRPA1) channels, expressed by nociceptors, contribute to neuropathic pain.

88 Injury-induced sensitization of nociceptors contributes to pain states and the developme

89 male and female mouse mechano- and polymodal nociceptor corneal neurons display rapidly, intermediate

90 The mechanisms and significance of nociceptor-dependent modulation of LN function are unkno

91 l findings of differences between TG and DRG nociceptors described in the literature but also suggest

92 TRPV1+ nociceptors directly respond to STm by releasing calcito

93 Consistent with this finding, rat nociceptors display decreased Cirl1 expression during al

94 SF applied directly to magnetically purified nociceptors does not induce any transcriptional changes

95 etic approaches indicated that HDM-activated nociceptors drive the development of allergic skin infla

96 ciceptor-to-SON transmission; stimulation of nociceptors during development sensitizes nociceptor pre

97 es a myriad of noxious chemical stimuli into nociceptor electrical excitation and neuropeptide releas

98 notypic screening paradigms that make use of nociceptor electrophysiology.

99 Deletion of MORs specifically in nociceptors eliminated morphine tolerance, OIH and prono

100 receptor in small-diameter primary afferent nociceptor enables chemogenetic inhibition of mechanical

101 Our results demonstrate sex differences in nociceptor-enriched translatomes and reveal unexpected s

102 and calcium channels, thereby blocking both nociceptor excitability and pro-inflammatory peptide rel

103 omes, which provided sustained inhibition of nociceptor excitability and relief from inflammatory pai

104 eIF4E is a critical mechanism for changes in nociceptor excitability that drive the development of ch

105 PV1) receptor is a well-known contributor to nociceptor excitability.

106 ation pathways are key factors in changes in nociceptor excitability.

107 res including fin clipping, PIT tagging, and nociceptor excitation via injection of acetic acid subcu

108 CIP patient-derived iPSC nociceptors exhibited an inability to properly respond t

109 all retrogradely labeled neurons, including nociceptors, express the recently characterized mechanos

110 both high-threshold cold thermoreceptors and nociceptors expressing TRPM8, providing a general model

111 old CSNs and in a subpopulation of polymodal nociceptors expressing TRPM8, providing a general molecu

112 des, which preferentially activate large non-nociceptor fibers.

113 Here, we propose that mast cells and nociceptors form a single regulatory unit in both physio

114 Nociceptors from migraine patients with the F139WfsX2 mu

115 This SCI effect is mimicked in nociceptors from naive animals by a modest 5 min depolar

116 ) (PGE(2)) were observed, when compared with nociceptors from opioid naive rats.

117 nd quantitative differences between cultured nociceptors from opioid-naive and opioid-primed animals,

118 rons) depends on activation of the meningeal nociceptors from their receptors in the dura.

119 dorsal root ganglia neurons corresponding to nociceptors (from rats of either sex), stimulation at fr

120 itable state and spontaneous activity of SCI-nociceptors have been proposed as a possible underlying

121 rexcitable state and spontaneous activity of nociceptors have been suggested to play a critical role

122 arbors of plantar paw and trunk innervating nociceptors have distinct morphologies in the spinal cor

123 t all cutaneous afferent subtypes, including nociceptors have strongly reduced mechanosensitivity upo

124 ERK activity maintain a depolarized RMP and nociceptor hyperactivity after SCI, providing a self-rei

125 einforcing mechanism to persistently promote nociceptor hyperexcitability and limit the therapeutic e

126 ge-gated sodium channel Na(v)1.8 that induce nociceptor hyperexcitability increase resurgent currents

127 A conorphin agonist inhibited colonic nociceptors in a mouse tissue model of chronic visceral

128 e and chemically depleted the small-diameter nociceptors in a selective manner.

129 xyquin, can reduce the spontaneous firing of nociceptors in an in vitro human pain model.

130 acterize mRNA translation in Scn10a-positive nociceptors in chemotherapy-induced neuropathic pain (CI

131 roneurography revealed an absence of C-fiber nociceptors in CIP patients, reflected in a reduced cort

132 hyperalgesia, and decreased sensitization of nociceptors in HbSS-BERK mice.

133 a comprehensive translational profile of DRG nociceptors in naive mice and at the peak of neuropathic

134 been made to reveal the molecular profile of nociceptors in normal conditions, little is known about

135 Recent evidence has implicated a role of nociceptors in OIH.

136 tion in the weakly IB4-binding population of nociceptors in OIH.

137 Yet, the role of nociceptors in regulating sterile cutaneous inflammation

138 uickly induce hyperexcitability of uninjured nociceptors in the adjacent DRG that drives an outburst

139 FN-alpha and IFN-beta) might act directly on nociceptors in the dorsal root ganglion (DRG) to cause p

140 a two-way crosstalk between macrophages and nociceptors in the peripheral nervous system, which may

141 al plasticity, including hypersensitivity of nociceptors in the presence of inflammatory mediators, o

142 ique functional links between mast cells and nociceptors in the skin.

143 compare mRNA translation in Scn10a-positive nociceptors in the TG and DRG of male and female mice.

144 Nociceptors in these tissues are critical first neurons

145 While nociceptors in these two tissues show a high degree of f

146 ay differentially drive plasticity states in nociceptors in these two tissues.

147 ion, in the weakly IB4-binding population of nociceptors, in OIH.SIGNIFICANCE STATEMENT Clinically us

148 cellular and molecular mechanisms of OIH in nociceptors, in vitro, subcutaneous administration of an

149 of high-potassium solution (20 mm, K20), in nociceptors incubated with beta-estradiol.

150 ceptors (MORs) expressed by primary afferent nociceptors initiate tolerance and OIH development.

151 epend on persistent hyperactivity in primary nociceptors (injury-detecting sensory neurons), associat

152 ry neuron subsets, predominantly peptidergic nociceptors, innervate LNs, distinct from those innervat

153 pened TRPV1- and TRPA1-mediated responses in nociceptors innervating the inflamed paw, but not in tho

154 Therefore, the spinal sensitization to A-nociceptor inputs associated with secondary hypersensiti

155 Here, we discuss the role of nociceptor interactions with the immune system in pain a

156 cate that the excitability of nonpeptidergic nociceptors is enhanced.

157 months after SCI and long after isolation of nociceptors is surprising.

158 a specific population of DRG neurons (e.g., nociceptors) is an effective strategy to reveal new mech

159 erspike T-type calcium current recorded from nociceptors isolated from SCI rats showing TTA-P2-induce

160 erspike T-type calcium current recorded from nociceptors isolated from SCI rats without TTA-P2-induce

161 ation of an alternative exon specifically in nociceptors, likely permits CTCF binding and expression

162 Nociceptors located in the trigeminal ganglion (TG) and

163 Downstream of M cells, nociceptors maintain levels of segmentous filamentous ba

164 calcitonin gene-related protein (peptidergic nociceptor marker; CGRP), and/or neurofilament 200 (myel

165 nd exposure of the large population of molar nociceptors may trigger prolonged or abnormal activation

166 g induced by opioids are mediated by similar nociceptor mechanisms.

167 rm trigeminal thermoreceptors and orosensory nociceptors; menthol attenuates cool thermoresponses.

168 sion of an inhibitory (Gi-coupled) DREADD in nociceptors might enable ligand-dependent analgesia.

169 nerve fibers responding to noxious stimuli (nociceptors) modulate immunity in a variety of tissues,

170 culture, providing evidence for the role of nociceptor MOR-mediated calcium signaling and peripheral

171 HDM allergens, activation of TRPV1(+)Tac1(+) nociceptor-MRGPRB2(+) mast cell sensory clusters represe

172 d provide evidence for the important role of nociceptor mu-opioid receptor-mediated calcium signaling

173 Recordings of mechano- and polymodal-nociceptor nerve terminals in the corneal surface of Pie

174 Therefore, the dialog between nociceptor neurons and the immune system is a fundamenta

175 y clear that active crosstalk occurs between nociceptor neurons and the immune system to regulate pai

176 dium and calcium channels in pain-initiating nociceptor neurons are attractive targets for new analge

177 Here, we find that nociceptor neurons critically mediate host defense again

178 Nociceptor neurons drive granulocyte colony-stimulating

179 trast, mechanical responses of somatosensory nociceptor neurons evoking pain, remain intact or are on

180 These findings reveal a major role for nociceptor neurons in sensing and defending against ente

181 In turn, nociceptor neurons release neuropeptides and neurotransm

182 c priming (opioid-primed rats), long-lasting nociceptor neuroplasticity manifested as prolongation of

183 We report on an in vitro model of nociceptor neuroplasticity mediating this opioid-induced

184 hyperalgesic priming, a form of maladaptive nociceptor neuroplasticity, resulting in pain chronifica

185 , in vivo administration of fentanyl induces nociceptor neuroplasticity, which persists in culture, p

186 In conclusion, we propose that nociceptors not only play a crucial role in inflammation

187 ing effect of 100 nm PGE(2) in strongly IB4+ nociceptors, not attenuated by inhibitors of Type I and

188 regulated by estrogen receptor alpha in the nociceptor of female rats.

189 ditional restoration of IL-1R1 expression in nociceptors of IL-1R1-knockout mice induced pain behavio

190 nding only to mechanical force (pure mechano-nociceptor) or also exhibiting TRPV1 (transient receptor

191 nel Kcnt1 (Slack) is abundantly expressed in nociceptor (pain-sensing) neurons of the dorsal root gan

192 r of the labeled neurons do not appear to be nociceptors, perhaps insinuating a role for them in disc

193 consequence of the antidromic activation of nociceptor peripheral terminals.

194 oportion of patients with the irritable (IR) nociceptor phenotype were responders to intravenous lido

195 7 times greater (95% CI 1.4-53.8) for the IR nociceptor phenotype.

196 portant contributing factor to mechanisms of nociceptor plasticity and the development of chronic pai

197 Using this iPSC nociceptor platform, we found that some Na(V)1.7 blocker

198 To uncover the nociceptor population mediating opioid-induced hyperalge

199 tured from rats primed with fentanyl, robust nociceptor population-specific changes in sensitization

200 ic priming (OIHP), in male rats, to identify nociceptor populations involved and its maintenance mech

201 Mutant mice have normal nociceptor populations, which, however, display decrease

202 Pain-perceptual nociceptors (PPN) are essential sensory neurons that rec

203 of nociceptors during development sensitizes nociceptor presynapses to this feedback inhibition.

204 ion of the Il1r1 gene specifically in TRPV1+ nociceptors prevented the development of mechanical allo

205 rats, there is enhanced control of spinal A-nociceptor processing through PG EP3 receptors.

206 High frequency stimulation (HFS) of nociceptors produced a persistent increase in synaptic t

207 Dorsal root ganglia nociceptors protect against STm colonization, invasion,

208 ighly expressed in MRGPRD(+) non-peptidergic nociceptors, raising the possibility of whether TRPC3 fu

209 geminal nerve fibers, for example, polymodal nociceptors, rather than through taste buds.

210 Nociceptors regulate the density of microfold (M) cells

211 Upon activation, nociceptors release neuropeptides from their terminals t

212 aporin (which deplete IB4(+) and peptidergic nociceptors, respectively), or their combination, preven

213 nsive and warm-responsive thermosensors, and nociceptors (responsive only to temperatures >=43-45 deg

214 g mice that express channelrhodopsin only in nociceptors resulted in behaviors characteristic of pain

215 of the transcriptomic profile of the injured nociceptors revealed oxidative stress as a key biologica

216 mily V member 1) immunoreactivity (polymodal nociceptor) revealed that they express Piezo2.

217 ing the female-selective role of PRL/PRLR in nociceptor sensitization and in pathological pain condit

218 eceptor (PRLR) in primary afferents promotes nociceptor sensitization and pain in a female-selective

219 acting kinases (MNKs) 1/2 is a key factor in nociceptor sensitization and the development of chronic

220 hesia during surgery, preventing the chronic nociceptor sensitization associated with such injuries,

221 -eIF4E signaling), which is known to produce nociceptor sensitization in inflammatory and neuropathic

222 l mechanisms through which type I IFNs cause nociceptor sensitization with implications for understan

223 olecular-weight hyaluronan (HMWH) attenuates nociceptor sensitization, in the setting of inflammation

224 e its function, with consequent increases in nociceptor sensitization.

225 se (MAPK) pathways blocks the development of nociceptor sensitization.

226 CD44, for the treatment of pain generated by nociceptor sensitization.SIGNIFICANCE STATEMENT High-mol

227 Activation of nociceptor sensory neurons by noxious stimuli both trigg

228 Nociceptor sensory neurons detect immune mediators to pr

229 Nociceptor sensory neurons protect organisms from danger

230 Gut-innervating nociceptor sensory neurons respond to noxious stimuli by

231 It is mediated by nociceptor sensory neurons that innervate the skin, join

232 y neurons-olfactory chemosensory neurons and nociceptor sensory neurons-detect bacterial toxins, form

233 sed in DRGs of HbSS-BERK mice and sensitizes nociceptors (sensory neurons that respond to noxious sti

234 Nociceptors, sensory neurons in the DRG that detect dama

235 Nociceptors, sensory neurons that detect damage or poten

236 gic tone within the dorsal horn could obtund nociceptor signaling to the brain and serve as analgesic

237 also transforms a subpopulation of polymodal nociceptors signaling pain into neurons activated by mil

238 transduction of mechanical forces by corneal nociceptors.SIGNIFICANCE STATEMENT The cornea is a richl

239 we identified a conopeptide that targets the nociceptor-specific ion channel ASIC3.

240 of referred hyperalgesia using a conditional nociceptor-specific NaV 1.7 knockout mouse (NaV 1.7(Nav1

241 Furthermore, the sensitization-regulated nociceptors (SRN) can greatly assist pain-sensitive huma

242 ratory responses evoked by inhalation of the nociceptor stimulant capsaicin.

243 mate receptor-induced sensitization of TRPA1 nociceptors stimulates targeted modification of the rece

244 lated peptide (CGRP), a marker for polymodal nociceptors, suggesting that trigeminal general mucosal

245 gle-cell transcriptomics atlas and nominated nociceptor target populations and interaction modalities

246 odel, we observed that chemical depletion of nociceptor terminals did not alter the early phase of th

247 (1 mug, i.d.), in the vicinity of peripheral nociceptor terminals, it produced mechanical hyperalgesi

248 lgesia likely involve reversible ablation of nociceptor terminals.

249 o within a specific subset of small-diameter nociceptors that bind isolectin B4.

250 ptome and translatome activity in TG and DRG nociceptors that enhances our understanding of nocicepto

251 mechanosensitive primary afferent meningeal nociceptors that innervate the cranial dura, using singl

252 headache may involve activation of meningeal nociceptors that innervate the posterior 1/3 of the dura

253 ht to map the origin and course of meningeal nociceptors that innervate the posterior dura overlying

254 mechanism driving changes in excitability of nociceptors that is critical for the generation of chron

255 uces neuroplasticity in weakly IB4+ and IB4- nociceptors that persists in vitro and has properties of

256 unrecognized differences between TG and DRG nociceptors that provide new insight into how injury may

257 about possible sex differences in peripheral nociceptors, the fundamental building blocks of pain tra

258 Barrier tissues are heavily innervated by nociceptors, the sensory neurons that detect noxious sti

259 Unlike other nociceptors, these HTMRs are fast-conducting Adelta-fibe

260 s of warm-responding neurons and shifted the nociceptor threshold to lower temperatures.

261 ng protease-activated receptor-2 (PAR(2)) on nociceptors through distinct mechanisms.

262 granulation of mast cells contiguous to such nociceptors, through the release of substance P and the

263 e injury plays a primary role in driving SCI-nociceptors to a hyperexcitable state and contributes to

264 the injury plays a major role in driving SCI-nociceptors to a hyperexcitable state and for promoting

265 ionic mechanisms responsible for driving SCI-nociceptors to a hyperexcitable state and for triggering

266 ing in response to current injections in SCI-nociceptors to a level similar to sham-nociceptors.

267 ngly understood that pathogens interact with nociceptors to alert organisms to infection as well as t

268 lications for the relative capacity of these nociceptors to be sensitized upon injury.

269 itis released opioids that activated DOPr on nociceptors to cause a sustained decrease in excitabilit

270 urons, and specific receptors are present in nociceptors to detect danger signals from infections.

271 ing pathway modulating the susceptibility of nociceptors to develop plasticity may contribute to our

272 which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters tha

273 acts at both peptidergic and nonpeptidergic nociceptors to induce mechanical hyperalgesia that is pr

274 sitive neurons, CIRL dampens the response of nociceptors to mechanical stimulation.

275 produced by viral infection, act directly on nociceptors to produce pain sensitization.

276 el pore-forming subunit Kv4.3 in a subset of nociceptors to selectively inhibit mechanical hypersensi

277 rine signals to activate TRPA1 of ensheathed nociceptors to sustain mechanical allodynia.

278 tal noxious input modifies transmission from nociceptors to their SONs, but not from mechanosensors t

279 ic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli.

280 ONs activate serotonergic neurons to inhibit nociceptor-to-SON transmission; stimulation of nocicepto

281 In male rats, we first evaluated the role of nociceptor Toll-like receptor 4 (TLR4) in OIH and primin

282 treated murine macrophages was able to drive nociceptor transcription.

283 n Nav1.8-positive neurons, most of which are nociceptors, translatomes would differ by sex.

284 We also found that conditioned medium from nociceptors treated with the well established pain media

285 sustains allodynia by paracrine targeting of nociceptor TRPA1.

286 en used to preferentially activate cutaneous nociceptors, unlike conventional large area-electrodes,

287 in both liver and Schwann cells surrounding nociceptors was required for TRPA1-induced mechanical al

288 also expressed in high-threshold mechanical nociceptors where it adjusts nocifensive behaviour under

289 olectin B4-positive (IB4(+)) and peptidergic nociceptors, whereas priming is dependent on a different

290 M is mediated by both IB4(+) and peptidergic nociceptors, whereas priming is not dependent on the sam

291 ease activity directly activated peptidergic nociceptors, which are neuropeptide-producing nociceptiv

292 This process relies on nociceptors, which are specialized neurons that detect a

293 arises due to a profound loss of functional nociceptors, which is more pronounced than that reported

294 lso innervated by a low density of Mrgprd(+) nociceptors, while individual arbors in different locati

295 ion of dissociated dorsal root ganglia (DRG) nociceptors with 1 nM BPA increases the frequency of act

296 flammation provoked a pronounced increase in nociceptors with functional co-expression of TRPM3, TRPV

297 ity in induced pluripotent stem cell derived nociceptors with the C110R mutation and preserved TRESK

298 ltages during the interspike interval in SCI-nociceptors, with a modest contribution (~10-15%) from t

299 3 is expressed in a subset of nonpeptidergic nociceptors within the dorsal root ganglion (DRG), and k

300 l arbors of somatosensory neurons, including nociceptors, yet the developmental origins and functiona