ライフサイエンスコーパス: C-fibre

1 ors; 14 were A fibres and the remainder were C fibres.

2 greater increase in mechano-sensitivity than C fibres.

3 m ms(-1) indicating a mixture of A-delta and C fibres.

4 resemble those previously described in human C fibres.

5 duced action potential discharge in tracheal C-fibres.

6 thod for the study of mouse bronchopulmonary C-fibres.

7 (pH = 5) excited both TRPV1+/+ and TRPV1-/- C-fibres.

8 (P < 0.05) less persistent than in TRPV1+/+ C-fibres.

9 m) was restricted to the capsaicin-sensitive C-fibres.

10 d to evoke substantive discharge in TRPV1-/- C-fibres.

11 otential discharge in jugular but not nodose C-fibres.

12 role in the mechanical activation of nodose C-fibres.

13 tial discharge in nodose, but not in jugular C-fibres.

14 ly myelinated Adelta-fibres and unmyelinated C-fibres.

15 nchopulmonary nerves, namely slow conducting C-fibres.

16 ral cells were mediated by both A delta- and C-fibres.

17 ferent input predominantly from A delta- and C-fibres.

18 ulated pathway primarily involving polymodal C-fibres.

19 potential discharge in most jugular ganglion C-fibres.

20 elated peptide and substance P released from C-fibres.

21 e alters the excitability of vagal pulmonary C-fibres.

22 olarization and activation of vagal afferent C-fibres.

23 5-KARs play a limited role in inhibiting the C fibre-activated pathway.

24 ked changes in the impulse activity of vagal C-fibre-activated neurones in nucleus tractus solitarii

25 ness, and an involvement of bronchopulmonary C fibre activation has been suggested.

26 (0.1 microm) partially inhibited the nodose C-fibre activation by adenosine, and the combination of

27 conclude that TRPV1 is obligatory for vagal C-fibre activation by capsaicin and anandamide.

28 C-fibre activation induces a long-term potentiation (LTP

29 C-fibre activation may thus sensitize the cough reflex v

30 Application of the C-fibre activator mustard oil (MO) to the cutaneous rece

31 The augmented C fibre activity slowly declined but remained elevated e

32 Moreover, the inhibitory effects of IL-6 on C-fibre activity and neuronal hyperexcitability, suggest

33 By contrast, jugular A delta and C fibres adapted slowly to mechanical stimulation, were

34 ct of serotonin on capsaicin-sensitive vagal C-fibre afferent nerves was evaluated in an ex vivo vaga

35 iguus (NA) and (b) are involved in pulmonary C-fibre afferent-evoked excitation of CVPNs, by right-at

36 The pulmonary C-fibre afferent-evoked excitation of eight CVPNs was at

37 ted the increase in activity of twelve other C fibre afferents during 10 min of abdominal ischaemia f

38 enhanced the increased activity of 11 of 13 C fibre afferents during 10 min of ischaemia.

39 the increased activity in six of seven other C fibre afferents during ischaemia.

40 However, ischaemically sensitive C fibre afferents had a high threshold (86 +/- 12 mmHg,

41 results show that ischaemically insensitive C fibre afferents had a lower threshold in response to d

42 f PLL and PLA on single-unit pulmonary vagal C fibre afferents in anaesthetized, open-chest rats.

43 Nerve activity of single-unit C fibre afferents innervating duodenum, mesentery, pancr

44 Single-unit activity of C fibre afferents innervating the stomach, duodenum and

45 ge population of unmyelinated high-threshold C fibre afferents that innervate the urinary bladder.

46 rent cats did not alter the response of nine C fibre afferents to exogenous 5-HT (0.91 +/- 0.17 vs. 1

47 ically sensitive and insensitive sympathetic C fibre afferents to graded distension of the gastrointe

48 ttenuated the responses of five of six other C fibre afferents to histamine.

49 e activity of single-unit abdominal visceral C fibre afferents was measured from the right thoracic s

50 Ischaemically sensitive C fibre afferents were identified according to their res

51 Ischaemically sensitive C fibre afferents were identified according to their res

52 Ischaemically sensitive and insensitive C fibre afferents were identified according to their res

53 ween ischaemically sensitive and insensitive C fibre afferents with regard to their testing activity

54 rvated by low and high threshold sympathetic C fibre afferents, the latter having the distinct abilit

55 avenous injection of anandamide on pulmonary C-fibre afferents and the cardiorespiratory reflexes.

56 ed activity, can be activated when pulmonary C-fibre afferents are stimulated by right atrial injecti

57 ivation/sensitization of cardiac sympathetic C-fibre afferents during myocardial ischaemia.

58 stent with being activated only by pulmonary C-fibre afferents.

59 activated following stimulation of pulmonary C-fibre afferents.

60 chaemia in activation of cardiac sympathetic C-fibre afferents.

61 (3) expression within DRG neurons projecting C-fibre afferents.

62 agi, suggesting the involvement of pulmonary C-fibre afferents.

63 Tachykinin-containing, capsaicin-sensitive C-fibres also innervate the airways and have been implic

64 The jugular C-fibres also responded strongly to serotonin with actio

65 echanical sensitivity occurred in both A and C fibres, although A fibres showed a greater increase in

66 gi with capsaicin to block the conduction of C-fibres, anandamide no longer evoked these reflex respo

67 jugular ganglion contained equal numbers of C fibre and A delta fibre tracheal afferent somata.

68 e a selective degeneration of vagal afferent C fibres and has been used extensively to examine the si

69 s an intense stimulatory effect on pulmonary C fibres and potentiates their sensitivities to both lun

70 e be considered selective for vagal afferent C fibres and, consequently, care is needed when using pe

71 of the electrically evoked C-fibre, initial C-fibre and measures of neuronal hyperexcitability (post

72 ng several subtypes of functionally distinct C-fibres and A-fibres.

73 tic excitatory inputs from both A delta- and C-fibres and inhibitory inputs mediated by both fibre ty

74 and is found in the airway terminals of both C-fibres and RAR-like fibres.

75 ction potential discharge in airway afferent C-fibres and the consequent nocifensor reflexes.

76 eptive itch which includes both unmyelinated C-fibres and thinly myelinated Adelta nerve fibres.

77 via A-fibres or 'alarm' via TRPV1 expressing C-fibres and, accordingly, this pathway organization pro

78 ptors was more intense in both IB4-positive (C-fibre) and NF200-positive (A-fibre) neurons in DRG of

79 lated all 38 cardiac afferents (8 Adelta, 30 C-fibres) and the responses of these 38 afferents to che

80 ated all 39 cardiac afferents (8 Adelta-, 31 C-fibres) and the responses of these 39 afferents to che

81 d pathway that uses mechanically insensitive C-fibres, and a cowhage-stimulated pathway primarily inv

82 tive TRPV1-expressing vagal bronchopulmonary C-fibres, and are activated by electrophilic compounds s

83 All CQ sensitive nerves were C-fibres, and were also sensitive to histamine.

84 In the rat, eleven of the fifty-four C fibres antidromically stimulated had vasodilator actio

85 ferents terminating in laminae I-II and that C-fibres appear not to sprout outside their normal lamin

86 C-fibres are sensitive to mechanical stimuli and a range

87 eptive-like fibres include both A-fibres and C-fibres, are insensitive to P2X receptors agonist and m

88 ir site of origin also differs: upper airway C-fibres arise predominantly from the jugular ganglion a

89 of the peripheral terminals of A(delta) and C fibres at the site of inflammation.

90 V and 0.5 ms while a single AP propagates in C-fibre axons.

91 ociceptors (C-M nociceptors) with Adelta- or C-fibre axons.

92 We concluded that in vagal afferent C-fibres, BK evokes membrane depolarization and action p

93 he slowly inactivating mechanism, present in C-fibres but not in RAR-like fibres, is mediated by VR1.

94 he lactate ion, by itself, does not activate C fibres, but it seems to potentiate the stimulatory eff

95 The data indicate that C-fibres, but not A-fibres, conveyed low-threshold mecha

96 iated action potential discharge in TRPV1-/- C-fibres, but the response was significantly (P < 0.05)

97 The stimulation of C fibres by Ado was significantly attenuated by pretreat

98 e the immediate and transient stimulation of C fibres by capsaicin, the C fibre stimulation by Ado ha

99 ions to the stimulation of single pulmonary C fibres by lactic acid were examined in anaesthetized a

100 responsible for the activation of pulmonary C fibres by lactic acid, probably through a direct effec

101 The stimulation of C-fibres by anandamide was completely and reversibly blo

102 and selectively activates a subset of airway C-fibres by directly stimulating TRPA1.

103 aining the slowing of conduction velocity in C-fibres by the build-up of Na(+) channel inactivation.

104 Mechanically insensitive C-fibres (C-MIAs) are beta-alanine insensitive but vigor

105 ed the hypothesis that single vagal afferent C-fibres can be stimulated via either the adenosine A1 o

106 < 20 microm) JNC neurons consistent with the C-fibre cell bodies display VR1 immunoreactivity.

107 nt potassium current common to many putative C-fibre cell bodies.

108 as used to address the hypothesis that vagal C-fibres comprise at least two distinct phenotypes.

109 indicated minimal axonal loss (95% of A- and C-fibres conducting), consistent with the normal microsc

110 After the C-fibre conduction in both vagus nerves was blocked, rig

111 tion potential revealed that the mouse vagal C-fibre conduction velocities range from 0.3 to 1.5 m s(

112 btype of the vagal afferent bronchopulmonary C-fibres (conduction velocity < 0.7 ms(-1)) to the putat

113 Neither C-fibre cooling sensitive (n = 4) nor C-fibre low thresh

114 ed to respond to a variety of tests; and (d) C-fibre cooling-sensitive units (n = 4).

115 he baseline fibre activity (FA) of pulmonary C-fibres did not change significantly at M, but increase

116 ocked the bronchoconstriction-induced nodose C-fibre discharge.

117 P2X receptors, whereas lung specific jugular C-fibres do not.

118 (I.T.) instillation of PLL or PLA activated C fibre endings in a dose-dependent manner; for example,

119 ii (NTS) received input from cardiopulmonary C fibre endings supplied by the pulmonary versus systemi

120 ults suggest that input from cardiopulmonary C fibre endings, primarily supplied by the pulmonary cir

121 igher dose, failed to have any effect on the C fibre endings.

122 s, the sensitization of the bronchopulmonary C-fibre endings by chronic exposure to sidestream tobacc

123 ncreases the sensitivity of bronchopulmonary C-fibre endings, but the physiological relevance of this

124 more of the TRPV receptors, expressed on the C-fibre endings.

125 nificantly greater inhibition of Adelta- and C-fibre evoked neuronal responses compared to Abeta-fibr

126 en significantly reduced Abeta-, Adelta- and C-fibre evoked responses of spinal dorsal horn neurones

127 port that GABA(B)-receptor control of A- and C-fibre evoked responses of spinal neurones is not profo

128 pinal muscimol inhibited Abeta-, Adelta- and C-fibre evoked responses of spinal neurones to a similar

129 -discharge responses and the non-potentiated C-fibre evoked responses were significantly inhibited by

130 This sensitization was unlike the classic C fibre-evoked 'wind-up' observed in adult dorsal horn.

131 discharged tonically during cardiopulmonary C fibre-evoked apnoea and rapid shallow breathing, displ

132 rats to mechanical punctate stimuli and the C fibre-evoked neuronal responses were significantly red

133 ically evoked responses (Abeta-, Adelta- and C-fibre-evoked responses, postdischarge); however, respo

134 By contrast, a different population of C fibres expressing MRGPRD was activated by pinching but

135 The only C fibres found to have vasodilator actions were of the p

136 By contrast, C-fibres from nodose (inferior) neurones innervate prima

137 d with latencies consistent with A delta and C fibres, generally firing three or four times per stimu

138 Nine of the eleven vasoactive C fibres had receptive fields located on the foot or the

139 impulse activity on conduction in cutaneous C fibres have been examined in 46 microneurographic reco

140 Positive C-fibre high threshold mechanoreceptive (HTM) units had

141 ts form a minor functional class of afferent C fibre in the rat saphenous nerve, and are not found in

142 To assess the role of vagal pulmonary C fibres in evoking these adverse reactions, the effect

143 tidromic stimulation of identified cutaneous C fibres in fine filaments dissected from the saphenous

144 upt and intense discharge in vagal pulmonary C-fibres in a dose-dependent manner.

145 nt mechanism underlying the sensitisation of C-fibres in airway irritability.

146 ction of action potentials in sensory A- and C-fibres in many neurons was effectively abolished after

147 evoking action potential discharge in vagal C-fibres in mouse lungs is PAR1, and that this is a dire

148 The C-fibres in mouse lungs isolated from PAR1(-/-) animals

149 n to study the electrical activity of nodose C-fibres in response to bronchoconstriction.

150 Activation of vagal afferent sensory C-fibres in the lungs leads to reflex responses that pro

151 The results indicate that C-fibres in the mouse lungs are not homogeneous, but can

152 ARs) capable of activating respiratory vagal C-fibres in the mouse was investigated.

153 The data show that vagal C-fibres in the respiratory tract of the mouse are stron

154 al discharge of approximately 90% (28/31) of C-fibres in the TRPV1+/+ mice, but failed to activate br

155 de-derived neurones (nodose ganglia) project C-fibres in the vagus, and that these two C-fibre popula

156 ice, but failed to activate bronchopulmonary C-fibres in TRPV1-/- animals (n = 10).

157 elated inhibition of the electrically evoked C-fibre, initial C-fibre and measures of neuronal hypere

158 ifferentiates nociceptive from cold-specific C fibres innervating human hairy skin, as has previously

159 3 receptor agonist) stimulated the firing of C-fibres innervating the intestine.

160 ributed between nodose ganglion A-fibres and C-fibres innervating the lung.

161 hysiological experiments revealed that vagal C-fibres innervating the pulmonary system are derived fr

162 ensitive afferent neurones (both Adelta- and C-fibres) innervating the rostral trachea and larynx hav

163 5HT had inhibitory effects on Adelta and C fibre input to all types of SDH neurones.

164 DA receptors in transmitting cardiopulmonary C fibre input to such NTS neurones.

165 NA inhibited C fibre input to transient central neurones.

166 ion to a greater extent than those with weak C-fibre input.

167 -triphosphate (ATP, 30 microM) activated the C-fibres irrespective of the conduction velocities.

168 eline activity and excitability of pulmonary C-fibres is induced by intrathoracic hyperthermia, and t

169 radycardia evoked by activation of pulmonary C-fibres is not respiratory modulated.

170 acid-induced activation of bronchopulmonary C-fibres, it is not required for action potential discha

171 eus caudalis (Vc) from cells with Adelta and C-fibre latency responding to electrical stimulation of

172 either C-fibre cooling sensitive (n = 4) nor C-fibre low threshold mechanoreceptive (LTM) units (n =

173 oot ganglion sensory neurons associated with C-fibres, many of which are activated by tissue-damage,

174 The stimulation of pulmonary C fibres may play an important role in Ado-induced adver

175 C-fibre mediated post-discharge responses and the non-po

176 etween the values for Abeta-fibre-evoked and C-fibre mediated post-discharge responses of spinal dors

177 inhibiting transmission at both A delta and C fibre monosynaptic pathways, whereas presynaptic GluR5

178 us A beta fibre brush stimulus and a noxious C fibre (mustard oil) stimulus were extracellularly reco

179 In the canine lungs ATP activates vagal C fibre nerve terminals.

180 Nineteen of fifty-one C fibre neurones showed SP-LI.

181 nes possessing AHPslow in ferret nodose were C fibre neurones; all AHPslow neurones had conduction ve

182 ke the nerve terminals, lung specific nodose C-fibre neurones express functional P2X receptors, where

183 Fourteen of 34 C-fibre neurones showed CGRP-LI.

184 noted that TRPV1-positive neurons (presumed C-fibre neurons) expressed PAR1 and PAR3, whereas PAR2 a

185 urons and with AP rise time only in positive C-fibre neurons.

186 rons) and with dorsal root CVs in A- but not C-fibre neurons.

187 These included 10/21 C-fibre nociceptive neurones.

188 in the pain pathway expressed in Adelta- and C-fibre nociceptors and is responsible for the thermal h

189 fore recording both the number of responsive C-fibre nociceptors and their response magnitude increas

190 A- and C-fibre nociceptors detect noxious stimulation, and have

191 This was tested by examining AMS in C-fibre nociceptors following the application of axoplas

192 ivate the peripheral terminals of Adelta and C-fibre nociceptors in the skin.

193 The reduction in AP duration in C-fibre nociceptors was apparent both in high threshold

194 showed the following significant changes: in C-fibre nociceptors, decreased AP duration at base, AP r

195 vide the dominant inputs to NS neurones, and C-fibre nociceptors, which are the dominant inputs to HP

196 al sensory fibres are broadly categorized as C fibres (nociceptors) and A fibres (non-nociceptive; ra

197 ere greater in slowly conducting, especially C-fibre, nociceptors.

198 opulation of these fibres so that they, like C-fibres, now express substance P.

199 IC(3) expression is largely observed in thin C-fibres of DRG neurons after hindlimb ischaemia.

200 est that stimulation of nociceptive afferent C-fibres of the dura mater leads to a sensitization of s

201 No wind-up of either long latency C-fibre or short latency Adelta responses was seen durin

202 nnel subfamily V member 1 (TRPV1) expressing C-fibres] or only non-TRPV1 ST afferent inputs, and neve

203 Stimulation of pulmonary vagal C fibres (PCFs) inhibits inspiration but the response pa

204 In primates, C-fibre polymodal nociceptors are broadly classified int

205 preferentially expressed in the nociceptive C-fibre population innervating the lungs.

206 bradykinin application, but only the nodose C-fibre population responded with action potential disch

207 ct C-fibres in the vagus, and that these two C-fibre populations represent distinct phenotypes.

208 o inhibited, to a lesser degree, the initial C-fibre, post discharge and wind-up responses in sham-op

209 al responses and also potently inhibited the C-fibre, post discharge, input and wind-up evoked respon

210 12 of these had conduction velocities in the C-fibre range (< 2.5 m s(-1)).

211 nduction velocities (0.8-2.0 m s(-1)) in the C-fibre range.

212 The results indicate that cardiopulmonary C fibre receptor stimulation causes tonic firing of Edec

213 Cardiopulmonary C fibre receptor stimulation elicits apnoea and rapid sh

214 piratory (I) neurones during cardiopulmonary C fibre receptor-evoked apnoea and rapid shallow breathi

215 Cardiopulmonary C fibre receptors were stimulated by right atrial inject

216 om stimulation of the vagal bronchopulmonary C-fibre reflex.

217 The nodose C-fibres responded strongly to serotonin and this effect

218 The C-fibres responded to the gradual reduction of pH with p

219 within the lungs of both nodose and jugular C-fibres responded with action potential discharge to ca

220 P3) or P6, while by P10, 35 % of cells had a C fibre response.

221 lxanthine (DPCPX) and SCH 58261, blocked the C-fibre response to histamine, without inhibiting the br

222 (3) The C-fibre response to lung inflation was also significantl

223 (2) The C-fibre response to right-atrial injection of capsaicin

224 In contrast the C-fibre response to the transient approximately 3 s expo

225 rical stimulation of the GON was observed in C-fibre responses (P < 0.001).

226 0 microl) reduced evoked Abeta-, Adelta- and C-fibre responses of spinal neurones in control rats (58

227 Similar increases in the C-fibre responses to other chemical stimulants (e.g. ade

228 C-fibre responses to ozone were abolished by ruthenium r

229 t a reduction in GABA(A)-receptor control of C-fibre responses, in particular in relation to post-dis

230 n, block of expression or function of such a C-fibre-restricted sodium channel may have a selective a

231 ved) nociceptive-like fibres are exclusively C-fibres sensitive to a P2X receptors agonist and rarely

232 (4) The enhanced C-fibre sensitivity was not altered by pretreatment with

233 nt stimulation of C fibres by capsaicin, the C fibre stimulation by Ado had a latency of 6.5 +/- 0.3

234 y spike responses were evoked in response to C fibre stimulation in pups at postnatal day 3 (P3) or P

235 voked responses to single and repeated A and C fibre stimulation remained unaffected.

236 ptor antagonists prevented capsaicin-induced C fibre stimulation.

237 ion, suggesting a selective association with C-fibre stimulation and nociceptive second-order spinal

238 antly decrease pHa, nor did it stimulate any C fibres studied.

239 Among the 62 capsaicin-sensitive C-fibres studied (conduction velocity approximately 0.5

240 Depending on the C-fibre subtype both 5-HT3 and non-5-HT3 mechanisms are

241 passive origin of supernormality in all rat C fibre subtypes.

242 ike other molecularly defined mechanosensory C-fibre subtypes, MRGPRB4(+) neurons could not be detect

243 In conclusion, Ado stimulates pulmonary C fibre terminals through an activation of A1 receptors.

244 ly evoked action potential discharge in lung C-fibre terminals arising from the nodose ganglia, but f

245 The activation of mouse bronchopulmonary C-fibre terminals by 4ONE (10-100 microm) was mediated e

246 tory for action potential discharge in vagal C-fibre terminals evoked by capsaicin, anandamide, acid

247 annels, based on the absence of responses in C-fibre terminals from TRPA1 knockout mice.

248 enosine selectively depolarizes vagal nodose C-fibre terminals in the lungs to action potential thres

249 and distinct stimulatory effect on pulmonary C-fibre terminals, and this effect appears to be mediate

250 or tachykinin release from bronchopulmonary C-fibre terminals.

251 and tachykinin release from bronchopulmonary C-fibre terminals.

252 olite of Ado, did not activate any of eleven C fibres tested in six rats.

253 It has been suggested that primary afferent C-fibres that respond to innocuous tactile stimuli are i

254 ) stimulated approximately 93 % of pulmonary C-fibres that were activated by capsaicin at a much lowe

255 g kg-1) activated 68 % (73/107) of pulmonary C fibres; the total number of action potentials during a

256 n that all afferents were affected by chain (c) fibres, they were classified in four groups: b1b2c (4

257 hibited by stimuli that excite and sensitise C-fibres - this could be an important mechanism underlyi

258 atly enhanced the sensitivities of pulmonary C fibres to both lung inflation and chemical stimuli (e.

259 However, the response of C fibres to lactic acid was 134% stronger than that to f

260 studied by microneurography in single human C fibres to provide information about axonal membrane pr

261 (5) The response of pulmonary C-fibres to a progressive increase in T(it) in a ramp pa

262 ike fibres were slightly more sensitive than C-fibres to acidic solutions (pH threshold > 6.7).

263 jugular (superior) ganglion neurones project C-fibres to both the extrapulmonary airways (larynx, tra

264 The sensitivity of the bronchopulmonary C-fibres to the vanilloid receptor 1 (VR1) agonist capsa

265 e zone innervated by the terminals of single C fibre units.

266 ments containing small numbers of identified C fibre units.

267 Four (n = 6) unresponsive or unidentified C-fibre units were positive.

268 APs that were longer on average by 3 times (C-fibre units), 1.7 times (Adelta-fibre units) and 1.4 t

269 n LTM neurones in all CV ranges: by 3 times (C-fibre units), 6.3 times (Adelta-fibre units) and 3.6 t

270 LTM units made up about 8 % of identified C-fibre units, 36 % of identified Adelta-fibre units and

271 is a relevant endogenous activator of vagal C-fibres via an interaction with TRPA1, and at less rele

272 Overall, the population of nociceptive C fibres was evenly distributed over the saphenous nerve

273 tions, the effect of Ado on single pulmonary C fibres was studied in anaesthetized and artificially v

274 induced action potential discharge in nodose C-fibres was mimicked by either the selective A1 agonist

275 both noxious and innocuous, but only in the C-fibres was there an increase in spontaneous activity.

276 roperties in nociceptive and non-nociceptive C fibres, we studied impulse-dependent velocity changes

277 Furthermore, C fibres were activated only by right-atrial and not by

278 Cutaneous C fibres were classified, based primarily on their activ

279 All eleven vasoactive C fibres were nociceptive and comprised seven polymodal

280 the rabbit filaments a total of thirty-three C fibres were tested for their ability to produce antidr

281 tologically, nodose neurones projecting lung C-fibres were different from the jugular neurones in tha

282 Single-unit afferent activities of 88 C-fibres were recorded in anaesthetized and artificially

283 A total of 83 bronchopulmonary C-fibres were studied.

284 ity (CV) = 0.2-5.6 m s(-1), 8 Adelta- and 47 C-fibres) were identified.

285 se burst of afferent activities in pulmonary C fibres, whereas sodium lactate had no effect.

286 been attributed to the enhanced activity of C fibres, which increase the excitability of their posts

287 nces between different functional classes of C fibres, which resemble those previously described in h

288 There are two subtypes of respiratory C-fibres whose cell bodies reside within two distinct ga

289 tion potential amplitude in peripheral mouse C-fibres (wildtype).

290 ed action potential discharge in mouse vagal C-fibres with a peak frequency similar to that observed

291 t activation of capsaicin-sensitive TRPV1+/+ C-fibres with a threshold of 3-10 microm, but failed to

292 ia the trachea strongly activated vagal lung C-fibres with action potential discharge, recorded with

293 ly, bradykinin (1 microM) excited only those C-fibres with conduction velocities < 0.7 m s(-1).

294 Thus C-fibres with conduction velocities between 0.3 and 0.7

295 (-1) responded to capsaicin (1 microM) while C-fibres with conduction velocities between 0.7 and 1.5

296 action potential discharge in vagal afferent C-fibres with receptive fields in the trachea or main st