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 elated peptide and substance P released from C-fibres.

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

7 olarization and activation of vagal afferent C-fibres.

8 duced action potential discharge in tracheal C-fibres.

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

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

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

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

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

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

15 ulated pathway primarily involving polymodal C-fibres.

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

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

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

19 nchopulmonary nerves, namely slow conducting C-fibres.

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

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

22 potential discharge in most jugular ganglion 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 ct of serotonin on capsaicin-sensitive vagal C-fibre afferent nerves was evaluated in an ex vivo vaga

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 activated following stimulation of pulmonary C-fibre afferents.

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

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

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

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

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

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

59 ot able to activate any of the airway nodose C-fibres analysed.

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

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

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

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

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

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

66 ind up was observed across the DH during the C-fibre and post-discharge latencies following 0.5 Hz st

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 < 20 microm) JNC neurons consistent with the C-fibre cell bodies display VR1 immunoreactivity.

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

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

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

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

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

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

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

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

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

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

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

112 S1P activation of nodose C-fibres does not occur in S1PR3 knockout mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

126 ng/50 mul) significantly reduced Adelta- and C-fibre-evoked activity in deep and superficial DH.

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

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

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

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

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

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

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

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

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

136 believed to arise from damage to nociceptive C fibres in diabetic neuropathy (DN).

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

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

139 imulation (lasting for 15-60 s) of pulmonary C-fibres in a concentration-dependent manner.

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

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

142 stimulatory effect on vagal bronchopulmonary C-fibres in anaesthetized rats.

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

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

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

146 for its ability to stimulate vagal afferent C-fibres in mouse lungs.

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

148 Single-unit activities of bronchopulmonary C-fibres in response to inhalation challenges of SO(2) (

149 osphate (S1P) strongly activates mouse vagal C-fibres in the airways.

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 NA inhibited C fibre input to transient central neurones.

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

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

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

168 S1P activation of nodose C-fibres is inhibited by a S1PR3 antagonist.

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

170 n, and stimulation of vagal bronchopulmonary C-fibres is primarily responsible.

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

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

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

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 pothesis that S1P may play a role in evoking C-fibre-mediated airway sensations and reflexes that are

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

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

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

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

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

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

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

185 Airway-specific nodose and jugular C-fibre neurons express mRNA coding for the S1P receptor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 12 of these had conduction velocities in the C-fibre range (< 2.5 m s(-1)).

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

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

214 Cardiopulmonary C fibre receptor stimulation elicits apnoea and rapid sh

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

216 Cardiopulmonary C fibre receptors were stimulated by right atrial inject

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

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

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

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

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

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

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

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

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

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

227 0 microl) reduced evoked Abeta-, Adelta- and C-fibre responses of spinal neurones in control rats (58

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

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

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

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

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

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

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

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

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

237 ptor antagonists prevented capsaicin-induced C fibre stimulation.

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

239 his study, we tested the hypothesis that the C-fibre stimulation was caused by SO(2) -induced local t

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

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

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

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

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

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

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

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

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

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

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

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

252 or tachykinin release from bronchopulmonary C-fibre terminals.

253 and tachykinin release from bronchopulmonary C-fibre terminals.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 ments containing small numbers of identified C fibre units.

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

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

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

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

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

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

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

276 Action potential generation by S1P in nodose C-fibres was effectively inhibited by the S1PR3 antagoni

277 effect of inhaled SO(2) on bronchopulmonary C-fibres was generated by acidification of fluid and/or

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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