ライフサイエンスコーパス: C-fiber

1 sy fibers (MFs) from the dentate gyrus and A/C fibers.

2 to deeper layers of the dorsal horn than did C fibers.

3 ure during aglycemia in A fibers, but not in C fibers.

4 heal administration of DEPs activated airway C-fibers.

5 n mechanical threshold in half of sensitized C-fibers.

6 In addition, dynorphin is present in some C-fibers.

7 sm and lost completely following ablation of C-fibers.

8 via inhibiting the release of glutamate from C-fibers.

9 letal muscle, cardiac muscle and TTX-treated C-fibers.

10 sory fiber activation, including nociceptive C-fibers.

11 of myelinated Adelta-fibers and unmyelinated C-fibers.

12 after electrical stimulation of dorsal root C-fibers.

13 conduction in distal axons of somatosensory C-fibers.

14 e damage, by analogy to somatic pain-sensing C-fibers.

15 ect excitatory input from different afferent C-fibers.

16 resent in the Golgi apparatus of both A- and C-fibers.

17 e, physiologically characterized nociceptive C-fibers.

18 16-20 microm), a feature of nociceptive-like C-fibers.

19 , and activation of VR1 receptors on sensory C-fibers.

20 e antidromic activation of some unmyelinated C-fibers.

21 ivation and sensitization of a proportion of C-fibers.

22 ecause all stimuli were too weak to activate C-fibers.

23 ct expression of Gi-DREADDs to predominantly C-fibers.

24 receptor potential ankyrin-1 on nociceptive C-fibers.

25 stimulation (HFS) at intensities recruiting C-fibers.

26 ing "nociceptor-like" mouse bronchopulmonary C-fibers.

27 ntials in myelinated A, but not unmyelinated C-fibers.

28 mediated, direct depolarization of BT/BM and CD fibers.

29 paclitaxel pretreatment: Abeta, 17%, p<0.05; C-fiber, 23%, p<0.05).

30 All nociceptive C-fibers (31 of 33 C-fibers studied) were excited by ET-

31 (cisplatin pretreatment: Abeta, 22%, p<0.01; C-fiber, 33%, p<0.01.

32 ed action potential discharge in nociceptive C-fibers (41/44) and nodose Adelta fibres (29/30) that a

33 ring rates 50% lower than those in wild-type C-fibers across a wide range of force intensities.

34 n addition, the role of afferent A-fiber and C-fiber activation of CVNs was examined.

35 n vivo and in acute spinal cord slices where C-fiber activation was mimicked by capsaicin challenge.

36 Inhibition of TRPV1 further reduced C-fiber activation.

37 dly suppressed following ablation of sensory C-fiber activity (using in vitro capsaicin desensitizati

38 rom a direct inhibitory effect on peripheral C-fiber activity caused by the selective inhibition of a

39 us activity (0.2-3.4 Hz) in 34% of cutaneous C-fibers adjacent to the tumor (9-17 d after implantatio

40 CFA inflammation significantly reduced C fiber ADS at 1 and 2 Hz stimulation rates.

41 hat sex/inflammation-dependent regulation of C fiber ADS can, by controlling the temporal relay of no

42 rothelium, that in turn could act on bladder C-fiber afferent nerves to alter their firing properties

43 ats pretreated with capsaicin to desensitize C-fiber afferent nerves.

44 ated with unmyelinated axons, VR1 identifies C-fiber afferent pathways within the brainstem.

45 ivity developed in approximately half of the C fiber afferents.

46 ctivity in itch-specific, mechanoinsensitive C-fiber afferents (CMi).

47 frequency spontaneous activity in 25% of the C-fiber afferents 8-10 d after the lesion compared with

48 sufficient to induce spontaneous activity in C-fiber afferents and behavioral signs of mechanical hyp

49 hed that exposure to kainate will depolarize C-fiber afferents arising from these cells.

50 r techniques were used to record from single C-fiber afferents in the L4 spinal nerve.

51 ea pig model, inhibited activation of single C-fiber afferents in vivo and depolarization of human an

52 sults show that the sensitivity of pulmonary C-fiber afferents to both mechanical and chemical stimul

53 er chemical desensitization of local sensory C-fiber afferents using capsaicin.

54 , trypsin did not evoke action potentials in C-fiber afferents whose receptive fields were located in

55 a direct interaction between DEP and airway C-fiber afferents.

56 ce of spontaneous activity in high-threshold C-fiber afferents.

57 nsory nerves, presumably the thermosensitive C-fiber afferents.

58 neurons are peripherin positive and produce C fibers, although a small portion produce Adelta fibers

59 wed that hypotonic solution activated 54% of C-fibers, an effect enhanced by the hyperalgesic inflamm

60 bers and isolectin B4 (IB4) for unmyelinated C fibers and both labels were quantified in the dorsal h

61 This involves activation of C fibers and mast cells, release of substance P and hist

62 In addition, at synapses between C fibers and NK1R+ neurons, NMDA receptor activation ini

63 Yet, both unmyelinated C fibers and particularly the morphologically distinct,

64 sualize fibers consistent with autonomic and C fibers and pulmonary neuroendocrine cells.

65 The destruction of sensory C fibers and sympathetic innervation will remove anti-in

66 tamatergic transporter profiles of DCN A and C fibers and their relationship to calcitonin gene-relat

67 These data provide evidence that both C-fiber and A-fiber nociceptors may encode high-intensit

68 Maximum C-fiber and endothelium-independent CuBF did not differ

69 ontrol neuronal excitability, in small-sized C-fiber and medium-sized Adelta fiber DRG neurons includ

70 At this stage, C-fiber and smooth muscle function are still preserved.

71 ng from activation of vagal bronchopulmonary C-fibers and Adelta afferents.

72 e C-type neuron soma and along nonmyelinated C-fibers and at nerve endings in the skin.

73 wered thresholds of electrical activation of C-fibers and increased current densities of TTX-sensitiv

74 aneous activity and sensitization to heat in C-fibers and increased innervation of cutaneous structur

75 e synaptic strength between primary afferent C-fibers and lamina I neurons, the first synaptic relay

76 that mGlu4 are located both on unmyelinated C-fibers and spinal neurons terminals in the inner lamin

77 release of sensory neurokinins from afferent C-fibers and that this release occurs independently of t

78 synapse formation between this population of C-fibers and their targets in the spinal cord dorsal hor

79 ia antidromic activation of the unmyelinated C-fibers and/or the small myelinated fibers.

80 ulants and lung inflation on vagal pulmonary C fibers, and if so, whether the excitabilities of other

81 orsal root axons, but rarely in unmyelinated C-fibers, and heavily expressed in the dorsal horn by la

82 nd possibly the NR2C subunits, found only in C-fibers, and the diheteromer NR1/NR2B, present in the G

83 Here we show that C-fibers, and their associated small-diameter neurons in

84 (Calca/Cgrpalpha), specific to pain-sensing C-fibers, and tyrosine hydroxylase (Th), specific to low

85 ic Kv1.4 channels predominate in A delta and C fibers arising from these cells.

86 s involved the release of neuropeptides from C fibers, as capsaicin treatment inhibited the responses

87 oid receptor 1 (TRPV1), expressed on sensory C-fibers, as playing an important endogenous protective

88 roup at day 10, the SAAs of both Adelta- and C-fibers at the "ascending" phase of microcontractions w

89 ogressive thermal hyperalgesia and prevented C-fiber atrophy, degeneration, and loss.

90 ound that CASP6 is expressed specifically in C-fiber axonal terminals in the superficial spinal cord

91 ential spatial distribution of NaV1.8 within C-fiber axons, being functionally more prominent in the

92 decreases in conduction velocity typical of C-fiber axons.SIGNIFICANCE STATEMENT Small-diameter dors

93 ypertrophy and increases the excitability of C-fiber bladder afferent neurons by suppressing IA chann

94 and larger in size than capsaicin-sensitive C-fiber bladder afferent neurons.

95 that ZD6169 can activate K(ATP) channels in C-fiber bladder afferents and suppress afferent activity

96 a-fiber blockade, but not capsaicin-mediated C-fiber blockade, also reduced chemotherapy-induced ongo

97 This study asked whether C-fiber bundles contain axons arising from more than one

98 r QX-314 with capsaicin persistently reduces C-fiber but not A-fiber compound action potentials and t

99 al overlap between spike trains in MFs and A/C fibers, but also depended on the temporal order of the

100 nge the baseline activity of vagal pulmonary C fibers, but it markedly enhanced the stimulatory effec

101 ow-frequency electrocutaneous stimulation at C-fiber, but not A-fiber, strength produced behavioral s

102 lear type II afferents of two genes found in C-fibers: calcitonin-related polypeptide alpha (Calca/Cg

103 Neurofilament-negative C-fiber cells comprise approximately 70% of bladder and

104 ically characterize a small subpopulation of C-fiber cells that express high levels of TRPV1 (HE TRPV

105 of mechanically insensitive, heat-sensitive C-fibers (CH) that contain the heat transducing TRPV1 (t

106 hat mechanically insensitive, heat-sensitive C-fibers (CHs) that contain TRPV1 increase in prevalence

107 receptive field of 43 mechano-heat-sensitive C-fiber (CMH) nociceptors.

108 The C-fiber component of the sciatic nerve compound action p

109 00 microm TTX after SNL, whereas both A- and C-fiber components of sciatic nerve CAP were blocked (>9

110 thed cutaneous nerves completely blocked the C-fiber compound action potential at concentrations that

111 n primates that a substantial portion of the C-fiber compound action potential in distal peripheral n

112 C fibers conduct successive action potentials at progres

113 red nerve function, we measured unmyelinated C-fiber conduction velocities (CV) in nerves of SIV-infe

114 IV-infected macaques had significantly lower C-fiber conduction velocity in sural nerves than uninfec

115 r than those required to block normal A- and C-fiber conduction.

116 ever, even with SCS at ten times MT, CAPs of C-fibers could not be detected in the tibial nerve.

117 ct the axotomy-induced decrease in polymodal C-fiber (CPM) heat threshold, but transiently prevented

118 C-fiber cross-over pathways comprised an average of 9% o

119 ycin A increased excitability in nociceptive C-fibers, decreasing the mechanical threshold by 50% and

120 Here we determined the uniqueness of this C-fiber deficit by performing a quantitative anatomical

121 We suggest that the selective cutaneous C-fiber deficit in the cutaneous nerves of naked mole-ra

122 naked mole-rat (Heterocephalus glaber) has a C-fiber deficit manifested as a substantially lower C:A-

123 In addition, this C-fiber dependency is likely related to neuropeptide sub

124 rization temperature decreases (37-4 degrees C) fiber diameter and pore size increase, whereas hydrog

125 In contrast, C-fibers did not express detectable levels of Kv7.2 or K

126 C fibers display activity-dependent slowing (ADS), where

127 ial cells (neuroendocrine cells) and sensory C fibers distributed to pulmonary airways, blood vessels

128 me for peak itch sensation for subjects with C-fiber-dominated itch matches the time for the peak res

129 iffers between subjects with A-fiber- versus C-fiber-dominated itch, (3) cowhage activates a subpopul

130 capsaicin in rats activated PI3K and ERK in C-fiber DRG neurons and epidermal nerve fibers.

131 Specifically, C-fiber-driven spinal hyperexcitability enables A fibers

132 nducting, small-diameter unmyelinated axons (C fibers) during aglycemia.

133 a minute of an intense noxious peripheral or C-fiber electrical stimulus, many phosphoERK-positive ne

134 Detection at the C-fiber electrode was found to have some differences in

135 hase particles were used for separation, and C-fiber electrodes were used for detection.

136 ong all types of innervation, with epidermal C-fiber endings preferentially diminishing earlier than

137 yl)methylamine hydrobromide (TCB-2) enhanced C-fiber-evoked dorsal horn potentials after SNL, which w

138 KF 38393 concentration-dependently depressed C-fiber-evoked potentials in rats receiving spinal nerve

139 erve induced long-term potentiation (LTP) of C-fiber-evoked potentials, revealing a constituent role

140 of synaptic long-term potentiation (LTP) of C-fiber-evoked potentials.

141 nosynaptic Adelta-fiber but not monosynaptic C-fiber-evoked responses.

142 C-fibers expressing heat-sensitive TRPV1 channels are pr

143 Inhaled tiotropium blocked cough and single C-fiber firing in the guinea pig to the transient recept

144 PPT-A) gene, from unmyelinated nerve fibers (C-fibers) following noxious stimuli.

145 The SAAs of Adelta- or C-fibers from the L6 dorsal roots were recorded during b

146 pathway to CVNs may be more complex than the C-fiber GABAergic pathway.

147 ry cycle phenomenon a biophysical model of a C-fiber has been developed.

148 -diameter unmyelinated group C nerve fibers (C-fibers) has limited effects on mechanical allodynia.

149 H2O2 also induced PKC-dependent nociceptive C-fiber hyperexcitability and PKC translocation.

150 ts also were completely lacking in cutaneous C-fibers immunoreactive for substance P and calcitonin g

151 lts further support the role of unmyelinated C fibers in injury-induced modulation of spinal GABAergi

152 the dorsal horn termination of unmyelinated C fibers in lamina II of the dorsal horn, using nerve in

153 ool to study the role of capsaicin-sensitive C fibers in pain.

154 the dorsal horn: selective block of afferent C fibers in postnatal week 2, using perisciatic injectio

155 g preparation of individual bronchopulmonary C fibers in the mouse.

156 Antidromic CAPs of C-fibers in dorsal roots were evoked by SCS at >or=90% o

157 Mechanical threshold of C-fibers in ethanol fed rats was lowered, and the number

158 ncrease in peripheral conduction velocity of C-fibers in GDNF-OE mice was measured, other electrophys

159 k propagation of action potentials in A- and C-fibers in sciatic nerve as well as skeletal muscle in

160 hyperalgesia and enhanced responsiveness in C-fibers in the rat.

161 extent, was also observed in the nociceptive C-fibers in the Remak bundles of sciatic nerves; however

162 to examine the role of afferent A-fibers and C-fibers in the synaptic activation of CVNs.

163 C-fibers in tumor-bearing mice exhibited a mean decrease

164 However, A fibers, but not C fibers, in the injured L5 spinal nerve have been shown

165 The absence of TRPV4-ATP-mediated effects on C-fibers indicates a distinct neurobiology for this ion

166 ng the increase in excitability of pulmonary C fibers induced by alveolar hypercapnia or constant inf

167 nhibits the hyperresponsiveness of pulmonary C fibers induced by inflammatory mediators such as prost

168 hyperresponsiveness to capsaicin of the same C fibers induced by PGE2 infusion was markedly attenuate

169 Further, C-fiber-induced spinal long-term potentiation (LTP) in v

170 Virtually all small neurons and C-fiber innervation requires TrkA to develop, but TrkC-r

171 inflammation reduced ADS in the monosynaptic C fiber input to lamina I neurokinin 1 receptor-expressi

172 neurons predominantly received monosynaptic C-fiber input (69%) with a smaller proportion receiving

173 nt a SG neural module by which a nociceptive C-fiber input to transient central cells is modified by

174 na II central neurons, with dorsal root (DR) C-fiber input, monosynaptically excited lamina II vertic

175 low threshold A fibers, whereas nociceptive C-fiber inputs mature gradually over the first postnatal

176 ic inhibition depends upon the maturation of C-fiber inputs to the dorsal horn: selective block of af

177 pses in lamina II but excluded from those at C-fiber inputs, a view supported by our immunohistochemi

178 ization evoked by dorsal root stimulation at C-fiber intensity was abolished by the mu agonist [D-Ala

179 roduced by the same injury [application of a C-fiber irritant, mustard oil (MO), to the hindpaw].

180 suggest that aberrant activity in uninjured C-fibers is a necessary component of pain associated wit

181 It has been repeatedly reported that C-fiber laser-evoked potentials (C-LEPs) become detectab

182 Repetitive activation of primary afferent C fibers leads to a synaptic strengthening of nociceptiv

183 xons, similar to the "dying back" pattern of C-fiber loss seen in patients with HIV-SN.

184 elinated sensory neurons (nonpeptidergic and C-fiber low-threshold mechanoreceptor neurons) resistant

185 ed by glycinergic inhibition and that A- and C-fibers low threshold mechanoreceptors (LTMRs) terminat

186 immunoreactivity did not colocalize with the C-fiber markers calcitonin gene-related peptide (CGRP),

187 ofound, long-lasting, segmental analgesia to C-fiber mediated pain in the rat.

188 heral capsaicin administration, a measure of C fiber-mediated central sensitization.

189 cotinic exposure prolongs superior laryngeal C-fiber-mediated apnea and bradycardia through enhancing

190 ments, we investigated the effects of TTX on C-fiber-mediated compound action potentials (C-CAPs) of

191 Endothelial, smooth muscle, and C-fiber-mediated cutaneous blood flow (CuBF) were record

192 transient central cells is modified by other C-fiber messages.

193 We also demonstrate a progressive delay of C fiber monosynaptic transmission to the spinal cord tha

194 were shown to receive high-threshold (Adelta/C fiber) monosynaptic input, whereas lamina III NK1R+ ne

195 fiber function in the hind paw, sural nerve C-fiber morphometry, sciatic nerve neurotrophins, and th

196 n and targets novel populations of Abeta and C fiber nerve afferents.

197 Activation of C-fiber nerve endings by pressure was attributable to st

198 of 20-HETE that, in turn, activates TRPV1 on C-fiber nerve endings resulting in depolarization of ner

199 matory response can also be evoked by direct C-fiber nerve stimulation in infant, but not adult, mice

200 nd adult DRGs that give rise to unmyelinated C-fibers (neurofilament 200 negative).

201 Percentages of nociceptive-type C-fiber neurons (C-nociceptors) with SA increased in int

202 ereas it was decreased in small unmyelinated C-fiber neurons as a result of diabetes.

203 rent neurons, consist of a smaller number of C-fiber neurons containing a higher percentage of IB4-po

204 was detected in a higher percentage (49%) of C-fiber neurons innervating the distal urethra than in t

205 he responsiveness of Adelta neurons, but not C-fiber neurons, as reflected in a decrease in the perce

206 n in the DRG was mainly found in small-sized C-fiber neurons.

207 rin and isolectin B4 markers of unmyelinated C-fiber neurons; 68% colabeled with antibodies to TRPV1

208 /kg morphine which preferentially attenuates C fiber nociception.

209 amine acting on the histamine H1 receptor in C-fiber nociceptive neurons.

210 of ionotropic and metabotropic receptors by C-fiber nociceptor afferents activates ERK via both PKA

211 n induces p38 MAPK activation in the soma of C fiber nociceptors in the dorsal root ganglion (DRG) af

212 ation channel is characteristic of polymodal C-fiber nociceptors and is sensitive to noxious heat, ir

213 Electrophysiological studies show that most C-fiber nociceptors are polymodal (i.e., respond to mult

214 C-fiber nociceptors do not appear to play a major role i

215 C-fiber nociceptors from Trpa1(-/-) mice exhibited actio

216 We demonstrated recently that uninjured C-fiber nociceptors in the L4 spinal nerve develop spont

217 an ex vivo preparation showed that cutaneous C-fiber nociceptors of ART-OE mice had reduced heat thre

218 -response function of mechanically sensitive C-fiber nociceptors to punctate mechanical stimuli appli

219 Following each action potential, C-fiber nociceptors undergo cyclical changes in excitabi

220 For A-fiber and C-fiber nociceptors, we systemically measured the respon

221 s molecular markers normally associated with C-fiber nociceptors.

222 redominantly expressed in a subpopulation of C-fiber nociceptors.

223 a large stimulus range for both A-fiber and C-fiber nociceptors.

224 ongoing/spontaneous firing (SF) in adult DRG C-fiber nociceptors.

225 , suggesting preferential MC4R expression in C-fiber nonpeptidergic neurons.

226 ggesting that the A partial differential and C fibers of the corneal innervation are affected differe

227 itionally, is distributed along unmyelinated C-fibers of sensory neurons.

228 presumably of unmyelinated primary afferent (C fiber) origin, stained for calcitonin gene-related pep

229 BB/Wor-rats, resulting in the prevention of C-fiber pathology and nociceptive sensory nerve dysfunct

230 ack of hair follicles alone accounts for the C-fiber paucity by using as a model a mouse that loses v

231 Pulmonary C fibers (PCFs) are involved in the generation of airway

232 nins evoked by CS-induced activation of lung C fibers play a primary role in this augmented response.

233 C-fibers predominantly contained either alpha2 or alpha3

234 ally spaced in the SG, contain GABA, receive C-fiber primary afferent input, and upregulate c-Fos pro

235 rat spinal slice preparations, activation of C-fiber primary afferents by a brief exposure of capsaic

236 Toll-like receptor 7 (TLR7) was expressed in C-fiber primary sensory neurons and was important for in

237 conduction velocities of Abeta, Adelta, and C fibers recorded in dorsal roots, the mean threshold in

238 Multiple cutaneous sensory C-fiber-released neuropeptides were evaluated for their

239 th long SCs processes and reduced numbers of C-fibers/Remak bundle.

240 y and late responses, mediated by Adelta and C fibers, respectively, based on required stimulation st

241 o group differences could be detected in the C-fiber response or smooth muscle vasodilation (p value

242 inute, 2 minutes) significantly enhanced the C-fiber response to capsaicin injection.

243 (2) infusion also significantly enhanced the C-fiber response to constant-pressure lung inflation (tr

244 l recordings from skin afferents showed that C-fiber responses to heat and C- and Adelta-fiber respon

245 ffects of PGE(2) were found on the pulmonary C-fiber responses to injections of lactic acid and adeno

246 In a separate series of experiments, C-fiber responses to injections of phenyl biguanide and

247 temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit

248 axons that are critical for Schwann cell and C-fiber sensory neuron survival.

249 C-fiber sensory neurons comprise nociceptors and smaller

250 At later stages, C-fiber sensory neurons die by apoptosis, a process that

251 ent activity related to nociception or other C-fiber signaling are subject to integration/modulation

252 at pulses concomitantly activate Adelta- and C-fiber skin nociceptors, and elicit a typical double se

253 al vanilloid 1 (TRPV1) of superior laryngeal C fibers (SLCFs) could induce bradycardia and apnea and

254 second postnatal week with the maturation of C-fiber spinal input, which triggers postsynaptic change

255 he descending modulation of cutaneous-evoked C-fiber spinal nociceptive responses from the brainstem.

256 (pCREB) in spinal cord slices in response to C-fiber stimulation is suppressed by preventing ERK acti

257 Finally, intrathecal RvD2 reversed C-fiber stimulation-evoked long-term potentiation in the

258 Molecular mechanisms underlying C-fiber stimulation-induced ERK (extracellular signal-re

259 ent of polysynaptic EPSP, and EPSP evoked at C-fiber strength, was seen in the absence of gamma-amino

260 All nociceptive C-fibers (31 of 33 C-fibers studied) were excited by ET-1 (1-20 nmol) in a

261 PC5 deletion and a shift in mechanosensitive C-fiber subtypes.

262 modulatory effects on transmission at spinal C-fiber synapses by dose dependently acting on distinct

263 effects of buprenorphine on transmission at C-fiber synapses in rat spinal cord dorsal horn in vivo.

264 fferent pathway to lamina II, nonpeptidergic C-fiber synapses in the deeper half of lamina II (IIi) c

265 rin, whereas the majority of the peptidergic C-fiber synapses in the outer half of lamina II (IIo) co

266 e amplitude of capsaicin-induced mEPSCs from C-fiber synapses was unaltered.

267 glia was indispensible for LTP induction at C-fiber synapses with spinal lamina I neurons.

268 ssociated with calcium-impermeable AMPARs at C-fiber synapses, it is required for the translocation o

269 buprenorphine reduced the strength of spinal C-fiber synapses.

270 ced an enhancement of transmission at spinal C-fiber synapses.

271 th these markers was observed in a subset of C-fiber synapses.

272 izations similar in size and distribution to C-fiber tactile afferent receptive fields, suggesting th

273 C-fiber tactile afferents are a subpopulation of unmyeli

274 en transported to peripheral but not central C fiber terminals.

275 here it is located in dense core vesicles in C-fiber terminals.

276 f the cat, VIP terminals originate only from C-fibers, terminate primarily in laminae I and V, and ex

277 at a class of low-threshold mechanosensitive C fibers that innervate the hairy skin represent the neu

278 umans, and match the responses of peripheral C-fibers that have similar selectivity.

279 n the percentage of mechanically insensitive C-fibers that responded to heat (CHs) after regeneration

280 nsist of myelinated Adelta- and unmyelinated C-fibers, the neuronal cell bodies of which correspond t

281 enuates the hyperresponsiveness of pulmonary C fibers to both chemical stimuli and lung inflation.

282 of action potentials relayed by nociceptive C fibers to the spinal cord.

283 fibers, especially small A delta fibers and C fibers, to relatively mild, short-duration hyperglycem

284 4, and LD2, kainate receptors are present on C-fiber-type neurons projecting to lamina II of spinal c

285 the terminals of individual bronchopulmonary C-fibers using a mouse ex vivo lung-vagal ganglia prepar

286 aicalein (10 micromol/L), desensitization of C-fibers using capsaicin (1 micromol/L, 20 minutes), or

287 In mammalian peripheral nerves, unmyelinated C-fibers usually outnumber myelinated A-fibers.

288 Capsaicin, which inactivates C-fibers, was used to examine the role of afferent A-fib

289 were found to be Abeta and Adelta fibers (no C fibers were detected).

290 rge Abeta myelinated fibers and unmyelinated C fibers were most affected by chemotherapy, whereas sen

291 noxious radiant heat mediated by Adelta and C fibers were similar in animals infected with proenkeph

292 C-fibers were characterized as nociceptors or non-nocice

293 ere attenuated, but SAAs of both Adelta- and C-fibers were intermittently enhanced by propagation of

294 e major subtypes in the corresponding A- and C-fibers were Na(V)1.6 and 1.7, respectively.

295 In contrast, SAAs of C-fibers were not significantly different between the gr

296 human vagus and firing of Adelta-fibers (not C-fibers), which was inhibited by TRPV4 and P2X3 recepto

297 depends on activation of COX-1 and COX-2 in C-fibers, which contribute to the induction and maintena

298 , specific to low-threshold mechanoreceptive C-fibers, which was shown previously to be a selective b

299 Npy2r neurons are largely slow-conducting C fibers, while P2ry1 neurons are largely fast-conductin

300 II interneurons receive prominent input from C fibers, while receiving little input from A delta fibe