ライフサイエンスコーパス: nociceptor

1 r the ganglion or peripheral terminal of the nociceptor.

2 k of dependence on the isolectin B4-positive nociceptor.

3 oupled MOR to the peripheral terminal of the nociceptor.

4 luble repellents sensed by the polymodal ASH nociceptors.

5 he somatic surface and cytoplasm of Kv4.3(+) nociceptors.

6 ens by spatial contrast activation of single nociceptors.

7 us heat in a subpopulation of high-threshold nociceptors.

8 ut can also lead to pain hypersensitivity in nociceptors.

9 Runx1 prior to maturation of nonpeptidergic nociceptors.

10 ated influx of extracellular Ca(2+) in mouse nociceptors.

11 .8(+) sensory neurons that are predominantly nociceptors.

12 centuated repetitive spiking in putative DRG nociceptors.

13 activation of TRPV4 and hyperexcitability of nociceptors.

14 peptide and isolectin B4, and thus represent nociceptors.

15 owth and excitability of Ret+ nonpeptidergic nociceptors.

16 tes Venus::PPK from the sensory dendrites of nociceptors.

17 spontaneous firing (SF) in adult DRG C-fiber nociceptors.

18 or) had no effect on the excitability of non-nociceptors.

19 exes to thermal activation of either A- or C-nociceptors.

20 ZBTB20 regulates TRP channels expression in nociceptors.

21 ity of fibromyalgia patients have abnormal C nociceptors.

22 lphaCGRP in LDCV mobilization in peptidergic nociceptors.

23 signaling in peptidergic and nonpeptidergic nociceptors.

24 ed in two distinct subsets of nonpeptidergic nociceptors.

25 R, suggesting they are not corneal polymodal nociceptors.

26 rce of IL-23, is in close contact with these nociceptors.

27 ion by modulating TRP channels expression in nociceptors.

28 s selectively expressed in IB4 binding rat C-nociceptors.

29 sitive TRP channels to function as polymodal nociceptors.

30 correlate of migraine headache in meningeal nociceptors.

31 e responses through activation of multimodal nociceptors.

32 1 (TRPV1), a Ca(2+)-permeable ion channel in nociceptors.

33 and exposure and sensitization of epithelial nociceptors.

34 1 pathway in Schwann cells, but not TRPA1 in nociceptors.

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

36 nisms underlying the effects of capsaicin on nociceptors.

37 s spinal inputs from unsensitized peripheral nociceptors.

38 ostmitotic differentiation of nonpeptidergic nociceptors, a major nociceptor subtype.

39 Nociceptors accomplish this task through the expression

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

41 fected withdrawal responses to both A- and C-nociceptor activation and this could be reversed by intr

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

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

44 G EP3R blockade also affected responses to A-nociceptor activation, but only in arthritic animals.

45 ide dynamic-range neurons evoked by C- vs. A-nociceptor activation.

46 olds to preferential C-nociceptor, but not A-nociceptor, activation and raised thermal withdrawal thr

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

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

49 released from peptidergic CGRP/somatostatin+ nociceptors acutely depresses neuronal transmission in S

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

51 chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting t

52 Our results indicate that nociceptors amplify pathological adaptive immune respons

53 Therefore, peripheral mechanical nociceptors and Abeta mechanoreceptors, together with sp

54 ansmission (T) neurons receiving inputs from nociceptors and Abeta mechanoreceptors, with Abeta input

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

56 K(+) channels in the transduction of cold by nociceptors and in cold-induced pain.

57 neuraminidase inhibits native T-currents in nociceptors and in so doing completely and selectively r

58 the TRPV1 channel found in primary afferent nociceptors and is activated by other noxious stimuli.

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

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

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

62 lude that TREK2 hyperpolarizes IB4 binding C-nociceptors and limits pathological spontaneous pain.

63 IP/DPPL ternary complexes in ISA -expressing nociceptors and pain-modulating spinal interneurons.

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

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

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

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

68 We determined that Prdm12 is expressed in nociceptors and their progenitors and participates in th

69 Nociceptors and their terminals in superficial dorsal ho

70 human induced pluripotent stem cell-derived nociceptors and TRKB-dependant SH-SY5Y cells.

71 how the complement system communicates with nociceptors and which ion channels and receptors are inv

72 gh suture branches of intracranial meningeal nociceptors and/or somatic branches of the occipital ner

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

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

75 comitantly activate Adelta- and C-fiber skin nociceptors, and elicit a typical double sensation: an i

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

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

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

79 Nociceptors are a particular subtype of dorsal root gang

80 Nociceptors are a subpopulation of dorsal root ganglia (

81 In primates, C-fibre polymodal nociceptors are broadly classified into two groups based

82 Peripheral nociceptors are excited by the activation of membrane re

83 Primary nociceptors are the first neurons involved in the comple

84 odulating TrkA or Ret pathways in developing nociceptors are unknown.

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

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

87 ting and the physiology of TRPA1 function in nociceptors, as well as for potential clinical applicati

88 WAS) have implicated SCN10A, which encodes a nociceptor-associated voltage-gated sodium channel subun

89 sion in SDH signaling to nonpeptidergic IB4+ nociceptors at glomeruli in LIIid.

90 l root ganglion (DRG) neurons, which include nociceptors, at the cellular level.

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

92 ers were characterized as nociceptors or non-nociceptors based upon conduction velocity and response

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

94 al reflex (EMG) thresholds to preferential C-nociceptor, but not A-nociceptor, activation and raised

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

96 4F complex to regulate the sensitization of nociceptors, but the details of this process are ill def

97 proalgesic TRPV1 potentiation in peptidergic nociceptors by abrogating its Ca(2+)-dependent exocytoti

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

99 Activation of visceral nociceptors by inflammatory mediators contributes to vis

100 -diameter DRG neurons, most likely cutaneous nociceptors by virtue of their binding the isolectin IB4

101 ese findings indicate that TRPV1(+)Nav1.8(+) nociceptors, by interacting with DDCs, regulate the IL-2

102 7) and reveal a tethered ligand that excites nociceptors, causing neurogenic inflammation and pain.

103 el superfamily, was recently identified as a nociceptor channel in the somatosensory system, where it

104 ection of IL-23 bypassed the requirement for nociceptor communication with DDCs and restored the infl

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

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

107 pendency of peripheral nerves, especially of nociceptors, correlates with receptive properties.

108 ctive pharmacological or genetic ablation of nociceptors, DDCs failed to produce IL-23 in imiquimod-e

109 ll excitatory ionic current that resulted in nociceptor depolarization and action potential firing.

110 A- and C-fibre nociceptors detect noxious stimulation, and have distinc

111 are the key sensory transducers that confer nociceptors distinct sensory modalities.

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

113 C) by ablating several different classes of nociceptor early in development.

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

115 In vivo, more hyperpolarized C-nociceptor Ems were associated with higher cytoplasmic e

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

117 lowering impulse activity in the peripheral nociceptor endings underlying pain.

118 t in vivo via descending pathways, leaving A-nociceptor-evoked reflexes largely unaffected.

119 All causes of congenital painlessness affect nociceptors, evolutionarily conserved specialist neurons

120 distinct group of lipid molecules that lower nociceptor excitability and attenuate nociception in per

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

122 ceptor plays a key role in the modulation of nociceptor excitability.

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

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

125 ponents of the inflammatory milieu eliciting nociceptor excitation and pain hypersensitivity.

126 Many silent nociceptors exhibit hyperexcitability resembling that in

127 sted whether these two distinct pruriceptive nociceptors exhibited an enhanced excitability after the

128 and MAS-related GPCR member A3 (MRGPRA3), in nociceptors expressing transient receptor potential vani

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

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

131 opeptides and channels in peptidergic C-type nociceptors facilitates a rapid modulation of pain signa

132 mouse colonic sensory neurons, and visceral nociceptor fibers in mouse and human nerve-gut preparati

133 tion of HA in rats decreases capsaicin joint nociceptor fibres discharge.

134 TRPV1 is a polymodal nociceptor for diverse physical and chemical stimuli tha

135 cessing of information arising from A- vs. C-nociceptors; for example, inhibition of the cyclooxygena

136 The central processes of primary nociceptors form synaptic connections with the second-or

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

138 suggest that therapies targeted at balancing nociceptor GRK2 and EPAC1 levels have promise for the pr

139 carrageenan induced a sustained decrease in nociceptor GRK2, whereas priming with the PKCepsilon ago

140 piratory tract, but its role as a peripheral nociceptor has not been explored.

141 While nociceptors have been described in lower vertebrates and

142 Nociceptors have been suggested to play a key role in th

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

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

145 tivation stimulates mouse and human visceral nociceptors, highlighting P2Y-dependent mechanisms in th

146 S evoked by mitochondrial dysfunction caused nociceptor hyperexcitability via the translocation and a

147 Antimycin A-induced nociceptor hyperexcitability was independent of TRP anky

148 ia patients behaved normally, but the silent nociceptors in 76.6% of fibromyalgia patients exhibited

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

150 The sensitization of dorsal root ganglion nociceptors in BDL rats was associated with increased su

151 cal stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small-fiber neurop

152 neous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small-fiber neuropat

153 at conducting (sometimes called uninjured) C-nociceptors in neuropathic pain models with more hyperpo

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

155 Proalgesic sensitization of peripheral nociceptors in painful syndromes is a complex molecular

156 confined to a subpopulation of pure mechano-nociceptors in the cornea.

157 We obtained stable recordings of 186 C nociceptors in the fibromyalgia group, 114 from small-fi

158 The mechanosensitive nociceptors in the fibromyalgia patients behaved normall

159 display increased density of nonpeptidergic nociceptors in the footpad and exhibit enhanced sensitiv

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

161 ensory information from mechanoreceptors and nociceptors in the skin plays key roles in adaptive and

162 fferents, including mouse and human visceral nociceptors, in nerve-gut preparations.

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

164 COX-1 inhibition, whereas the encoding of C-nociceptor information by wide dynamic-range spinal neur

165 Thus, TNFR1 exerts a dual role in nociceptor information processing by suppressing TrkA an

166 Lung nociceptors initiate cough and bronchoconstriction.

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

168 ters spinal nociceptive reflexes evoked by C-nociceptor input in vivo via descending pathways, leavin

169 Dorsal horn neurons with stronger C-nociceptor input were affected by COX-1 inhibition to a

170 as associated with spinal sensitization to A-nociceptor inputs alone.

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

172 t facilitation on the spinal processing of C-nociceptor inputs in naive and arthritic animals, but ga

173 ts from spinal sensitization to peripheral A-nociceptor inputs.

174 be the first known peptide antagonist of the nociceptor ion channel transient receptor potential anky

175 cate that the excitability of nonpeptidergic nociceptors is enhanced.

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

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

178 lgesic priming, a form of neuroplasticity in nociceptors, is a model of the transition from acute to

179 Disruption of ZBTB20 in nociceptors led to a marked decrease in the expression l

180 iors and their specific expression in larval nociceptors led us to hypothesize that these DEG/ENaC su

181 d proinflammatory cytokines acting at muscle nociceptor level.

182 is crucial for NGF-dependent nonpeptidergic nociceptor maturation.

183 eta holocomplex formation and nonpeptidergic nociceptor maturation.

184 cific strategies for sustained inhibition of nociceptors may help transform pain science and clinical

185 However, the mechanisms behind nociceptor-mediated modulation of GABA signaling remain

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

187 ivity (SA) in peripheral branches of primary nociceptors near sites of injury.

188 buffers transmission of mechanical forces to nociceptor nerve endings thereby reducing pain.

189 sing mutagenized OSM-9 expressed in the head nociceptor neuron, ASH, we study nocifensive behaviour a

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

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

192 Moreover, the derived nociceptor neurons exhibited TrpV1 sensitization to the

193 In turn, nociceptor neurons release neuropeptides and neurotransm

194 extracellular miRNAs for rapid excitation of nociceptor neurons via toll-like receptor-7 (TLR7) and i

195 receptors and channels found in adult mouse nociceptor neurons, as well as native subtype diversity.

196 pain mediators via activating TLR7/TRPA1 in nociceptor neurons.

197 fibroblasts into noxious stimulus-detecting (nociceptor) neurons.

198 (scRNA-seq) analysis of mouse nonpeptidergic nociceptors (NP), peptidergic nociceptors (PEP), and lar

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

200 Microneurography was used to record C nociceptors of 30 female patients meeting criteria for f

201 ogenetic strategy to bidirectionally control nociceptors of nontransgenic mice.

202 owever, this epithelium is not innervated by nociceptors of somatosensory ganglia, which detect damag

203 We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sen

204 Activation of the nociceptors "opens" the gate through concomitant excitat

205 neal afferent neurons that are not polymodal nociceptors or cold-sensing neurons, and is likely confi

206 rochemically distinct from corneal polymodal nociceptors or cold-sensing neurons.

207 C-fibers were characterized as nociceptors or non-nociceptors based upon conduction vel

208 ng either exon 37a (selectively expressed in nociceptors) or 37b in the proximal C terminus, reveal t

209 s not known, however, if cephalopods possess nociceptors, or whether their somatic sensory neurons ex

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

211 nonpeptidergic nociceptors (NP), peptidergic nociceptors (PEP), and large myelinated sensory neurons

212 These data suggest that a subset of nociceptor PKC isoforms differentially contribute to spo

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

214 tional initiation of Runx1 in nonpeptidergic nociceptor precursors is dependent on the homeodomain tr

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

216 ic animals, but gains in effects on spinal A-nociceptor processing from a region of secondary hyperse

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

218 mechanisms involved in the sensitization of nociceptors produced by repeated activation of mu-opioid

219 gic or the MrgprD+/non-peptidergic subset of nociceptors produced selective, modality-specific defici

220 Different functional classes of nociceptors project their axons to distinct target zones

221 educed expression of GPCR kinase 2 (GRK2) in nociceptors promotes cAMP signaling to the guanine nucle

222 Type II afferents may be the cochlea's nociceptors, prompting avoidance of further damage to th

223 This study aimed to investigate the role of nociceptor protein kinase C (PKC) isoforms in PIPN.

224 s are divided into three functional classes (nociceptors/pruritoceptors, mechanoreceptors and proprio

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

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

227 Primary nociceptors relay painful touch information from the per

228 Specifically, TrkA+ peptidergic nociceptors require TNF-alpha-TNFR1 forward signaling to

229 signaling in peptidergic and nonpeptidergic nociceptors, respectively.

230 d ASK gustatory neurons, and the ASH and ADL nociceptors, respond to a rise in CO2 with a rise in Ca(

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

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

233 Acute peripheral nociceptor sensitization drives spinal sensitization and

234 clude that acute inflammation and peripheral nociceptor sensitization in hind foot hairy skin, but no

235 lts suggest that the mechanical inflammatory nociceptor sensitization is dependent on glutamate relea

236 , a neurotransmitter known to be involved in nociceptor sensitization, is present in human tears.

237 relate tear serotonin levels, as a marker of nociceptor sensitization, to facets of dry eye (DE), inc

238 critically linked to inflammation-associated nociceptor sensitization.

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

240 Nociceptor sensory neurons detect immune mediators to pr

241 Nociceptor sensory neurons protect organisms from danger

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

243 Em, and (3) spontaneous pain behavior and C-nociceptor SF rate suggested that TREK2 knockdown might

244 lly, the mice lacking ZBTB20 specifically in nociceptors showed a defect in nociception and pain sens

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

246 macrophages and initiation of macrophage-to-nociceptor signaling.

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

248 capitulated the expression of quintessential nociceptor-specific functional receptors and channels fo

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

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

251 es significantly to pain mechanisms, and the nociceptor-specific P2X3 ATP receptor channel is conside

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

253 al horn neurons in response to both A- and C-nociceptor stimulation.

254 arge-pore ion channels to specifically block nociceptors, substantially reduced ovalbumin- or house-d

255 ation of nonpeptidergic nociceptors, a major nociceptor subtype.

256 ydes and ketones act as agonists to activate nociceptors such as TRPV1 and TRPA1 and elicit trigemina

257 nd cause cold-resistant hyperexcitability of nociceptors, suggesting a mechanistic basis for the temp

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

259 the inflammatory sensitization of peripheral nociceptor terminals to mechanical stimulation.

260 din E2 (PGE2) is presented to the peripheral nociceptor terminals, but also when it is presented intr

261 lgesia likely involve reversible ablation of nociceptor terminals.

262 e vicinity of the peripheral terminal of the nociceptor that induces priming-PKCepsilon activator, NG

263 in receptor TRPV1 ion channel is a polymodal nociceptor that responds to heat with exquisite sensitiv

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

265 peralgesic priming, a neuroplastic change in nociceptors that markedly prolongs inflammatory mediator

266 light a novel modality of cross talk between nociceptors that may be relevant for discrimination of p

267 amed and in turn activates trigeminovascular nociceptors that reach the affected periosteum through s

268 strate that mechanically sensitive polymodal nociceptors that respond either quickly (QC) or slowly (

269 all population of CGRP-expressing myelinated nociceptors that we now identify as the somatosensory ne

270 v1.1-expressing fibres are modality-specific nociceptors: their activation elicits robust pain behavi

271 This extracellular cGMP acts on and inhibits nociceptors, thereby reducing nociception.

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

273 of periodontitis by activation of trigeminal nociceptors through TLR4 should be explored.

274 the vicinity of the peripheral terminal of a nociceptor to its cell body that, in turn, induces a sig

275 nd PKA, which activates TRPV4 and sensitizes nociceptors to cause inflammation and pain.

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

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

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

279 by activated immune cells, acts directly on nociceptors to induce the release of vasoactive intestin

280 a mechanism specifically used by peptidergic nociceptors to potentiate their excitability.

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

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

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

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

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

286 tested the hypothesis that BoNT-A can block nociceptor transduction.

287 Histamine sensitizes the nociceptor transient reporter potential channel V1 (TRPV

288 al mechanism underlying sensitization of all nociceptor types or is subtype-specific remains controve

289 Following each action potential, C-fiber nociceptors undergo cyclical changes in excitability, in

290 released from peptidergic CGRP/somatostatin+ nociceptors upon capsaicin stimulation exert a tonic inh

291 The primary afferent nociceptor was used as a model system to study mechanism

292 as well as a small population of peptidergic nociceptors, whereas DPP6 is absent in sensory neurons.

293 ecify the elaborate branching pattern of PVD nociceptors, whereas high MEC-3 is correlated with the s

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

295 ansmission to trigger peptidergic trigeminal nociceptors, which link SCCs to the neurogenic inflammat

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

297 gically, the use dependence of TRPV2 confers nociceptors with a hypersensitivity to heat and thus pro

298 rgic airway inflammation, we stimulated lung nociceptors with capsaicin and observed increased neurop

299 (SA) generated in the cell bodies of primary nociceptors within dorsal root ganglia (DRG) has been fo

300 3 is expressed in a subset of nonpeptidergic nociceptors within the dorsal root ganglion (DRG), and k