ライフサイエンスコーパス: hyperalgesia

1 prolongation of prostaglandin E(2) (PGE(2)) hyperalgesia.

2 s Adjuvant)-induced inflammation and thermal hyperalgesia.

3 the degeneration of these fibers that drives hyperalgesia.

4 ortex mediated the effect of value on nocebo hyperalgesia.

5 ut a significant correlation with behavioral hyperalgesia.

6 ted intake, highly motivated responding, and hyperalgesia.

7 and migraine pain, as well as opioid-induced hyperalgesia.

8 o baseline but partially recovered from peak hyperalgesia.

9 attenuated neuronal coupling and mechanical hyperalgesia.

10 decoy receptor) markedly reduced CCI-induced hyperalgesia.

11 CRF-CRFR1 signaling in CeA in stress-induced hyperalgesia.

12 IFN-alpha by a neutralizing antibody induced hyperalgesia.

13 bitor GNF-5837 prevented C5a-induced thermal hyperalgesia.

14 provides a mechanism for peripheral thermal hyperalgesia.

15 tra-CeA CRF infusion mimicked stress-induced hyperalgesia.

16 iezo2 contributes to inflammatory mechanical hyperalgesia.

17 assessed by measuring thermal and mechanical hyperalgesia.

18 tors (CRFR1s) reduces stress-induced thermal hyperalgesia.

19 of noxious heat and in inflammatory thermal hyperalgesia.

20 peralgesia during remission from CFA-induced hyperalgesia.

21 optosis mice abolished C5a-dependent thermal hyperalgesia.

22 ked prolongation of prostaglandin E2-induced hyperalgesia.

23 itaxel-induced mechanical allodynia and heat hyperalgesia.

24 tal role in inflammatory pain and mechanical hyperalgesia.

25 s a potent inflammatory mediator that causes hyperalgesia.

26 icated in mediating enhanced translation and hyperalgesia.

27 der basal conditions and during inflammatory hyperalgesia.

28 kedly prolongs inflammatory mediator-induced hyperalgesia.

29 on or extinction of conditioned analgesia or hyperalgesia.

30 t mechanisms modulating comorbid anxiety and hyperalgesia.

31 a pivotal role in stress-induced anxiety and hyperalgesia.

32 mportant role in the peripheral inflammatory hyperalgesia.

33 ical role in the development of inflammatory hyperalgesia.

34 iceptive sensitivities and developed similar hyperalgesia.

35 ct centrally mediated referred allodynia and hyperalgesia.

36 hanges and associated morphine tolerance and hyperalgesia.

37 sitivity in two mouse models of inflammatory hyperalgesia.

38 pretreatment with 46 prevented NPFF-induced hyperalgesia.

39 ensor and integrator of inflammation-induced hyperalgesia.

40 esting their importance for the PGE2-induced hyperalgesia.

41 effect on an equivalent thermal inflammatory hyperalgesia.

42 unction intact, yet alleviates some forms of hyperalgesia.

43 ients, including persistent inflammation and hyperalgesia.

44 s converge onto TRPV1, leading to mechanical hyperalgesia.

45 for both opioid analgesia and opioid-induced hyperalgesia.

46 ce produced sensitization of nociceptors and hyperalgesia.

47 asked in persistent inflammation to maintain hyperalgesia.

48 , indicating a role of opioid involvement in hyperalgesia.

49 d abolishes chronic opioid treatment-induced hyperalgesia.

50 idence that LHb M-channels may contribute to hyperalgesia.

51 prolongation of prostaglandin E(2) (PGE(2)) hyperalgesia.

52 increased serotonin production, and visceral hyperalgesia.

53 rol (PGE(2)-G); PGE(2)-G is known to produce hyperalgesia.

54 ated by nerve conduction slowing and thermal hyperalgesia.

55 time of adult reincision blocks the enhanced hyperalgesia.

56 vity, possibly giving rise to opioid-induced hyperalgesia.

57 on, attenuating inflammatory and neuropathic hyperalgesia.

58 but could also be correlated with behavioral hyperalgesia.

59 velopment of chemotherapy-induced mechanical hyperalgesia.

60 xant and ataxic effects, reversed mechanical hyperalgesia 24h after injury, while it was devoid of cl

61 In adults, acute physiological stress causes hyperalgesia [5-7], and increased background stress incr

62 rked prolongation of prostaglandin E2 (PGE2) hyperalgesia, a key feature of hyperalgesic priming.

63 ristine cause pronounced mechanical and heat hyperalgesia, a significant decrease in tail compound ne

64 al hypersensitivity, including allodynia and hyperalgesia, abnormal colonic transit, and psychologic

65 repeat restraint stress each led to visceral hyperalgesia, accompanied by mucosal inflammation and im

66 ninjured L4 nerve in the development of heat hyperalgesia after L5 nerve injury.

67 neurons and investigated specific states of hyperalgesia after persistent inflammation.

68 play a role in the development of mechanical hyperalgesia after persistent inflammation.

69 r treatment significantly diminished thermal hyperalgesia after SCI as measured by the Plantar test.

70 icroM) affected tactile allodynia or thermal hyperalgesia after SNL, but it increases cold allodynia

71 Mechanical hyperalgesia after spared nerve injury was also reduced

72 to the mouse hindpaw produced strong thermal hyperalgesia, an effect that was absent in TRPV1 knock-o

73 Rats develop hyperalgesia and allodynia in the hind paw after L5 spin

74 rathecal bumetanide significantly attenuated hyperalgesia and allodynia induced by paclitaxel.

75 y kinase-mediated phosphorylation leading to hyperalgesia and allodynia.

76 ojection neurons, critical for expression of hyperalgesia and allodynia.

77 antigen induced arthritis as well as in the hyperalgesia and angiogenesis model at a well-tolerated

78 ndent inhibition of mGluR-1-mediated thermal hyperalgesia and by colocalization of the antibody with

79 lete Freund's adjuvant (CFA)-induced thermal hyperalgesia and chronic constriction injury (CCI) induc

80 , such as fentanyl and morphine, can produce hyperalgesia and chronification of pain.

81 n the potency of SNC80 to inhibit mechanical hyperalgesia and decreased acute tolerance.

82 ssion of M-channels' subunit KCNQ3, relieved hyperalgesia and decreased relapse-like alcohol consumpt

83 as nearby uninjured afferents, resulting in hyperalgesia and ectopic pain originating from adjacent

84 The role of PB itself in hyperalgesia and how it recruits descending facilitation

85 ceptor agonists such as fentanyl can produce hyperalgesia and hyperalgesic priming.

86 pain (somatic and emotional) while producing hyperalgesia and hyperkatifeia, which drive pronounced d

87 intrathecal injection of IL-33 enhanced CCI hyperalgesia and induced hyperalgesia in naive mice.

88 They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release

89 06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthri

90 mediates inflammatory mechanical and thermal hyperalgesia and is required for recruitment of innate i

91 eptor (MOR) agonist DAMGO induced mechanical hyperalgesia and marked prolongation of prostaglandin E2

92 rat model of NGF-induced persistent thermal hyperalgesia and mechanical allodynia to determine the r

93 motor performance but have increased thermal hyperalgesia and mechanical allodynia.

94 administration of ligand 14 reversed thermal hyperalgesia and mechanical hypersensitivity in a dose-d

95 opriate for treating pain disorders in which hyperalgesia and not allodynia is the primary symptom.

96 SzV-1287 significantly inhibited hyperalgesia and oedema in both models.

97 shed inflammation interfered with behavioral hyperalgesia and ON-cell and OFF-cell responses.

98 c inhibition with imatinib ameliorates tonic hyperalgesia and prevents hypoxia/reoxygenation-induced

99 enan, interleukin 6, as well as BDNF-induced hyperalgesia and priming are reduced specifically in mal

100 We evaluated the hypothesis that hyperalgesia and priming induced by opioids are mediated

101 the dorsal root ganglion induced mechanical hyperalgesia and priming with an onset more rapid than w

102 KCepsilon) AS-ODN also prevented LDM-induced hyperalgesia and priming, whereas analgesia and priming

103 d pro-dynorphin KO mice showed recovery from hyperalgesia and reinstatement by NTX; (3) there was no

104 dult male and female rats induced equivalent hyperalgesia and spinal dorsal horn expression of genes

105 nced degree and duration of incision-induced hyperalgesia and spinal microglial responses to reincisi

106 show a reduction in inflammatory mechanical hyperalgesia and TRPA1- but not TRPV1-mediated pain.

107 in myelinating Schwann cells reduces thermal hyperalgesia and, to a lesser extent, also diminishes me

108 cts (analgesic tolerance), paradoxical pain (hyperalgesia), and addiction.

109 is associated with spontaneous burning pain, hyperalgesia, and allodynia.

110 ced by prostaglandin E2, carrageenan-induced hyperalgesia, and antigen-induced arthritis.

111 tivity, persistence of heat perception, cold hyperalgesia, and cold analgesia.

112 2) in DRGs, decreased mechanical and thermal hyperalgesia, and decreased sensitization of nociceptors

113 nderstanding of tolerance and opioid-induced hyperalgesia, and discuss current and future strategies

114 itroglycerine-induced mechanical and thermal hyperalgesia, and furthermore, show that cloxyquin conve

115 C in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation.

116 its nonneurogenic inflammatory pain, thermal hyperalgesia, and mechanical allodynia, of which the lat

117 PEA-m was able to reduce mechanical, thermal hyperalgesia, and motor alterations as well as reduce ma

118 beta-arrestin-2 is implicated in tolerance, hyperalgesia, and other opioid side-effects.

119 ress induces a persistent elevation of IL-6, hyperalgesia, and susceptibility to chronic muscle pain,

120 cause several symptoms, including allodynia, hyperalgesia, anxiety, and depression.

121 The mechanisms of opioid tolerance and hyperalgesia are complex, involving mu opioid receptor s

122 estigated to what extent behavioral signs of hyperalgesia are correlated with immunohistochemical cha

123 Ongoing LMWH and A6 hyperalgesia are reversed by HMWH.

124 developed significant mechanical and thermal hyperalgesia as tested by the withdrawal responses of th

125 ciceptors and is responsible for the thermal hyperalgesia associated with inflammatory pain.

126 is essential for the development of the heat hyperalgesia associated with persistent inflammation.

127 an important role in the development of heat hyperalgesia at the spinal cord level after L5 nerve inj

128 a (at 10-30 mug sc), and CCI-induced thermal hyperalgesia (at 11.5 mg/kg ip) mice models.

129 lpha-when injected into the ganglion produce hyperalgesia but not priming.

130 ) axons abolishes heat, mechanical, and cold hyperalgesia but tactile and cold allodynia remain follo

131 model, we were able to study not only evoked hyperalgesia, but also for the first time to demonstrate

132 combination, prevented systemic LDM-induced hyperalgesia, but not priming.

133 ys a critical role in development of thermal hyperalgesia, but the underlying mechanism remains uncer

134 n channel TRPM3 alleviates inflammatory heat hyperalgesia, but the underlying mechanisms are unknown.

135 ng primary hyperalgesia by 80% and secondary hyperalgesia by 40%.

136 e most efficient analgesic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%.

137 demonstrate that attenuation of inflammatory hyperalgesia by HMWH is mediated by its action at cluste

138 We further demonstrated that suppression of hyperalgesia by MORs was due to their constitutive activ

139 elastase to mice caused edema and mechanical hyperalgesia by PAR(2)- and TRPV4-mediated mechanisms.

140 that complement fragment C5a induces thermal hyperalgesia by triggering macrophage-dependent signalin

141 re, women with GWI, CFS and FM have systemic hyperalgesia compared to sedentary controls.

142 Thermal and mechanical hyperalgesia developed in the rats with bone cancer pain

143 oligodeoxynucleotides, chronic PGE2-induced hyperalgesia development was prevented in the 2 priming

144 se data reveal a central role for the LHb in hyperalgesia during alcohol withdrawal, which may be due

145 IL-33-mediated hyperalgesia during CCI was dependent on a reciprocal re

146 tral ventromedial medulla neurons attenuates hyperalgesia during masseter inflammation.

147 elta-, and kappa-opioid receptors reinstated hyperalgesia during remission from CFA-induced hyperalge

148 The treatment with TPPU ameliorates hyperalgesia, edema, and decreases the expression of imp

149 e induction of synaptic facilitation and the hyperalgesia elicited by ultra-low-dose buprenorphine.

150 fects: the persistent mechanical and thermal hyperalgesia following reincision in adulthood was preve

151 nociceptive circuitry, resulting in enhanced hyperalgesia following reinjury in adulthood.

152 opathic pain symptoms, such as allodynia and hyperalgesia, for several weeks in murine chronic constr

153 Hyperalgesia gradually developed after sciatic nerve inj

154 ing <2 h, and longlasting primary mechanical hyperalgesia (>/=7 days).

155 are thought to promote opioid tolerance and hyperalgesia; however, how opioids drive such changes re

156 rolongation of inflammatory-mediator-induced hyperalgesia (hyperalgesic priming).

157 Allodynia was observed in 36% of patients, hyperalgesia in 22%, accelerated colonic transit in 18%,

158 lly related conditions such as allodynia and hyperalgesia in a comparative setting that offers unique

159 e demonstrate that GRK2 inhibits CFA-induced hyperalgesia in a kinase activity-dependent manner.

160 nd reversed mechanical allodynia and thermal hyperalgesia in a model of neuropathic pain.

161 emogenetic activation of LHb neurons induced hyperalgesia in alcohol-naive rats.

162 he LHb as a potential therapeutic target for hyperalgesia in alcoholics.

163 ammatory pain, 2,6-DTBP reduced inflammatory hyperalgesia in an alpha3GlyR-dependent manner.

164 kg(-1)), which caused thermal and mechanical hyperalgesia in behaving animals, induced an enhancement

165 These results suggest that pruritus and hyperalgesia in chronic cholestatic BDL rats are associa

166 attenuated mechanical allodynia and thermal hyperalgesia in EAE.

167 d that blocking its synthesis would decrease hyperalgesia in HbSS-BERK mice.

168 expressing sensory neurons also impairs heat hyperalgesia in homozygous and heterozygous mice.

169 Opioid receptor antagonists increase hyperalgesia in humans and animals, which indicates that

170 implicated in environmental thermosensation, hyperalgesia in inflamed tissues, skin sensitization, an

171 ockout (Deltae4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain.

172 Therefore, these four receptors suppress hyperalgesia in latent sensitization.

173 r injection of Cat-S caused inflammation and hyperalgesia in mice that was attenuated by PAR2 or TRPV

174 63 and S1RA abolished mechanical and thermal hyperalgesia in mice with carrageenan-induced acute (3 h

175 emonstrate reversible peripheral and central hyperalgesia in mice with induced endometriosis.

176 ent of carrageenan-induced inflammatory heat hyperalgesia in mice.

177 mice and abolished the partial recovery from hyperalgesia in MOR KO mice.

178 IL-33 enhanced CCI hyperalgesia and induced hyperalgesia in naive mice.

179 All hybrids alleviated allodynia and hyperalgesia in neuropathic pain models.

180 sitisation to produce mechanical and thermal hyperalgesia in rats and humans.

181 and morphine reversed thermal and mechanical hyperalgesia in rats with bone cancer pain.

182 ntral amygdala (CeA) mediates stress-induced hyperalgesia in rats with high stress reactivity.

183 We induced visceral hyperalgesia in rats, via chronic water avoidance or rep

184 exception of a small decrease of mechanical hyperalgesia in response to a pinprick.

185 sia to wild-type mice but reduced mechanical hyperalgesia in response to a pinprick.

186 revent intestinal abnormalities and visceral hyperalgesia in response to chronic psychological stress

187 to intestinal barrier function, and visceral hyperalgesia in response to chronic stress.

188 nergy and completely reverses opioid-induced hyperalgesia in rodent behavioral models.

189 Predator odor stress produces hyperalgesia in rodents.

190 on of DF2593A effectively reduced mechanical hyperalgesia in several models of acute and chronic infl

191 a and prevents hypoxia/reoxygenation-induced hyperalgesia in sickle mice.

192 peralgesia in the V2 territory and secondary hyperalgesia in territories innervated by the mandibular

193 tivity to light touch, pinprick, and thermal hyperalgesia in the absence of injury, without associate

194 -/-) mice are protected against inflammatory hyperalgesia in the complete Freund's adjuvant (CFA) mod

195 uding joint inflammation, primary mechanical hyperalgesia in the ipsilateral ankle, and secondary mec

196 lly result in chronic persistence of thermal hyperalgesia in the ipsilateral forepaw.

197 ral ankle, and secondary mechanical and heat hyperalgesia in the ipsilateral hindpaw.

198 ents we observed attenuation of PGE2-induced hyperalgesia in the paw by the knockdown of NMDAR subuni

199 -2,3-dione had no effect in the PGE2-induced hyperalgesia in the paw, showing specific involvement of

200 NMDA into the fifth lumbar (L5)-DRG induced hyperalgesia in the rat hind paw with a profile similar

201 tory primary afferent inputs, and mechanical hyperalgesia in the territories of injured and uninjured

202 to produce constant and long-lasting primary hyperalgesia in the V2 territory and secondary hyperalge

203 taneous pain, mechanical allodynia, and heat hyperalgesia in TOW mice.

204 eA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyp

205 ibution to OIH by comparing morphine-induced hyperalgesia in wild type (WT) and MOR knockout (KO) mic

206 romedial medulla injection of AM 404 reduced hyperalgesia in wild-type mice but not in CB1(-/-) mice.

207 morphine-3beta-D-glucuronide (M3G) elicited hyperalgesia in WT but not in MOR KO animals, as well as

208 nergic and delta-opioid receptors reinstated hyperalgesia in WT mice and abolished the partial recove

209 dministration led to analgesic tolerance and hyperalgesia in WT mice but not in MOR KO mice.

210 The putative mechanisms of hyperalgesia include activation of bimodal opioid regula

211 lerance (diminished pain-relieving effects), hyperalgesia (increased pain sensitivity), and drug depe

212 antisense to CD44 mRNA, which also prevents hyperalgesia induced by a CD44 receptor agonist, A6.

213 HMWH also reverses the hyperalgesia induced by activation of intracellular seco

214 PKCepsilon, dependence; (3) prolongation of hyperalgesia induced by an activator of PKA, 8-bromo cAM

215 ely our results show that MOR is involved in hyperalgesia induced by chronic morphine and its metabol

216 ate that inflammatory thermal and mechanical hyperalgesia induced by complete Freund's adjuvant was a

217 HMWH also reverses the hyperalgesia induced by diverse pronociceptive mediators

218 Although CD44 antisense has no effect on the hyperalgesia induced by inflammatory mediators or paclit

219 can be detected in spinal cord (as prolonged hyperalgesia induced by intrathecal PGE2), but only when

220 andin formation, acetaminophen also reversed hyperalgesia induced by intrathecal prostaglandin E2 To

221 Thermal hyperalgesia induced by PMA or burn injury in KI was ide

222 containing Hnic and ina inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-in

223 HMWH attenuated mechanical hyperalgesia induced by the inflammatory mediator prosta

224 stinal inflammation or induction of visceral hyperalgesia induced by water avoidance stress.

225 unteers followed by assessment of paw edema, hyperalgesia, inflammation, and central glial activation

226 The centralization of the secondary hyperalgesia involved descending 5-HT drive from the ros

227 nt of opioid-induced analgesic tolerance and hyperalgesia is a clinical challenge for managing chroni

228 lls, supporting the idea that the peripheral hyperalgesia is an event modulated by a glutamatergic sy

229 Hyperalgesia is an exaggerated response to noxious stimu

230 mice, the development of mechanical and heat hyperalgesia is blocked and the loss in tail compound ne

231 e of the TRPV1 channel in the development of hyperalgesia is established, but the role of the neurotr

232 mpletely understood; however, opioid-induced hyperalgesia is likely to be a central facet.

233 Hyperalgesia is particularly problematic as further opio

234 cotic Bowel Syndrome (NBS)/Opioid-Induced GI Hyperalgesia, is characterized by the paradoxical develo

235 administration of 8-bromo cAMP also produced hyperalgesia, it did not produce priming.

236 hind foot skin in rats, a transient thermal hyperalgesia lasting <2 h, and longlasting primary mecha

237 Molecular mechanisms of systemic hyperalgesia may provide new insights into the neuropath

238 SNC80 were lost in a model of opioid induced hyperalgesia/medication overuse headache in Dlx-DOR cond

239 rious side effects, such as morphine-induced hyperalgesia (MIH) and anti-nociceptive tolerance.

240 which leads to the maintenance of mechanical hyperalgesia of inflamed masseter muscle.

241 OX-2 play in the development of inflammatory hyperalgesia of peripheral tissue.

242 ed and prolonged swelling and induced stable hyperalgesia of the incised paw compared with IgG from h

243 Hyperalgesia often occurs in alcoholics, especially duri

244 to analgesia, opioids produce opioid-induced hyperalgesia (OIH) and neuroplasticity characterized by

245 cussed.SIGNIFICANCE STATEMENT Opioid-induced hyperalgesia (OIH) and priming are common side effects o

246 europlasticity mediating this opioid-induced hyperalgesia (OIH) and priming induced by fentanyl.

247 Opioid-induced hyperalgesia (OIH) is a serious adverse event produced b

248 ith opioid tolerance (OT) and opioid-induced hyperalgesia (OIH), which limit efficacy and compromise

249 uding analgesic tolerance and opioid-induced hyperalgesia (OIH).

250 uding analgesic tolerance and opioid-induced hyperalgesia (OIH).

251 nociceptor terminals, it produced mechanical hyperalgesia (OIH).

252 rsistent ongoing spontaneous pain and evoked hyperalgesia pain in EAE.

253 ose needed for analgesia) and opioid-induced hyperalgesia (paradoxical increase in pain with opioid a

254 Accompanying the behavioural hyperalgesia phenotype, voltage-clamp recordings of smal

255 eural circuits mediating craniofacial muscle hyperalgesia potentially enhances treatment of chronic m

256 d OIH and prolongation of prostaglandin E(2) hyperalgesia (priming) induced by LDM.

257 To evaluate the distribution of reincision hyperalgesia, prior neonatal incision was performed at d

258 iopaque markers); compliance, allodynia, and hyperalgesia (rectal barostat); anxiety and depression (

259 horn neurons is a critical factor in muscle hyperalgesia related to ectopic pain and emotional stres

260 le for systemic opioid-induced analgesia and hyperalgesia remain unclear.

261 nfluence of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is common

262 R55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR5

263 The physical sign of systemic hyperalgesia (tenderness) was assessed in 920 women who

264 expensive medication led to stronger nocebo hyperalgesia than labeling it as cheap medication.

265 g but not maintaining mechanical and thermal hyperalgesia that is mediated by CaMKIIalpha signaling i

266 hat rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in

267 peptidergic nociceptors to induce mechanical hyperalgesia that is prevented by intrathecal oligodeoxy

268 showed significant dose-dependent mechanical hyperalgesia that was fully established at 30 days after

269 OSCC cell line caused mechanical and thermal hyperalgesia that was reversed by LI-1.

270 Avoiders exhibited thermal hyperalgesia that was reversed by systemic or intra-CeA

271 ction of peripheral inflammation, a model of hyperalgesia, there was a switch in the current-voltage

272 nitiation of mechanical allodynia or thermal hyperalgesia, these cells may not be as important for th

273 Especially with respect to hyperalgesia, they showed to be more effective than the

274 eceptors (BRs) in the spinal cord to promote hyperalgesia through an excitatory effect, which is oppo

275 r levels of mechanical allodynia and thermal hyperalgesia to wild-type mice but reduced mechanical hy

276 ems responsible for mediating opioid-induced hyperalgesia, tolerance, and dependence.

277 n processing and the development of referred hyperalgesia using a conditional nociceptor-specific NaV

278 tionally, chronic morphine treatment-induced hyperalgesia was absent in Oprm1-cKO mice.

279 Much longer lasting thermal hyperalgesia was apparent in glabrous skin (1 h to >72 h

280 In hairy skin, transient hyperalgesia was associated with sensitization of withdr

281 The transience of the hyperalgesia was attributable to a rapidly engaged desce

282 ntermittent access paradigm for eight weeks, hyperalgesia was evident (as measured by paw withdrawal

283 IL-33-induced hyperalgesia was markedly attenuated by inhibitors of PI

284 Hyperalgesia was maximal when the same paw was reincised

285 Accordingly, leukotriene B4-induced thermal hyperalgesia was mediated through BLT1 and TRPV1 as show

286 Inflammatory thermal hyperalgesia was only marginally attenuated in KI mice.

287 Oxaliplatin-induced mechanical hyperalgesia was reduced in germ-free mice and in mice p

288 CCI-induced mechanical hyperalgesia was reduced in IL-33R (ST2)(-/ -) mice comp

289 ty because of the following: (1) CFA-induced hyperalgesia was reinstated by the MOR inverse agonist n

290 Notably, NGF-induced thermal hyperalgesia was unaffected by macrophage depletion.

291 ing on the mechanisms of C5a-induced thermal hyperalgesia, we show that this process requires recruit

292 1 in vitro but did not cause pain or thermal hyperalgesia when injected into the hind paw of mice.

293 d in temperature perception and inflammatory hyperalgesia, whereas in pancreatic beta-cells the chann

294 t model of mustard oil (MO)-induced visceral hyperalgesia whether the number and size of acupoints we

295 ed both acute pain and persistent mechanical hyperalgesia which were almost completely abolished by T

296 hat contralateral PB is required to initiate hyperalgesia, which is then maintained by ipsilateral PB

297 st day of testing, THC significantly reduced hyperalgesia, with a trend effect of CBD, and no effect

298 bution of SP or CGRP to inflammation-induced hyperalgesia, with or without the presence of vesicular

299 inhibits established CFA-induced mechanical hyperalgesia without affecting normal mechanical sensiti

300 on and maintenance of morphine tolerance and hyperalgesia, without affecting basal pain perception or