ライフサイエンスコーパス: thermal hyperalgesia

1 etection of noxious heat and in inflammatory thermal hyperalgesia.

2 the TRPV1 channel, and contributes to acute thermal hyperalgesia.

3 rawal to radiant heat in mice, indicative of thermal hyperalgesia.

4 urons, and thereby sensitizes TRPV1 to cause thermal hyperalgesia.

5 V1 receptors may play a role in inflammatory thermal hyperalgesia.

6 cation channel required for certain types of thermal hyperalgesia.

7 gion in spinal lamina II, leading to reduced thermal hyperalgesia.

8 dly exhibit deficits in inflammation-induced thermal hyperalgesia.

9 l allodynia but no significant reductions in thermal hyperalgesia.

10 TRPV1, or PKC may abrogate protease-induced thermal hyperalgesia.

11 M-1 also blocked neutrophil accumulation and thermal hyperalgesia.

12 th the development of morphine tolerance and thermal hyperalgesia.

13 e development of both morphine tolerance and thermal hyperalgesia.

14 but blocked prostaglandin E2 (PGE2)-induced thermal hyperalgesia.

15 Freund's Adjuvant)-induced inflammation and thermal hyperalgesia.

16 nt of both morphine tolerance and associated thermal hyperalgesia.

17 ical allodynia and inflammatory pain but not thermal hyperalgesia.

18 the endogenous amino acid L-cysteine, induce thermal hyperalgesia.

19 itivity to noxious heat, a phenomenon termed thermal hyperalgesia.

20 atic nerve produces mechanical allodynia and thermal hyperalgesia.

21 ein structure of gp120 blocked gp120-induced thermal hyperalgesia.

22 (48 nmol) completely blocked the SP-induced thermal hyperalgesia.

23 pain sensation and for tissue injury-induced thermal hyperalgesia.

24 to highly noxious stimuli and mechanical and thermal hyperalgesia.

25 Trk inhibitor GNF-5837 prevented C5a-induced thermal hyperalgesia.

26 and thus provides a mechanism for peripheral thermal hyperalgesia.

27 1 receptors (CRFR1s) reduces stress-induced thermal hyperalgesia.

28 duced apoptosis mice abolished C5a-dependent thermal hyperalgesia.

29 s and may be critical in the pathogenesis of thermal hyperalgesia.

30 ay an impaired sensation of noxious heat and thermal hyperalgesia.

31 P causes sensitization of TRPV1 and produces thermal hyperalgesia.

32 (FeTMPyP(5+)) dose-dependently reversed this thermal hyperalgesia.

33 as indicated by nerve conduction slowing and thermal hyperalgesia.

34 gesia and allodynia as well as taxol-induced thermal hyperalgesia.

35 exhibited symptoms of tactile allodynia and thermal hyperalgesia.

36 blocked CFA-induced mechanical allodynia and thermal hyperalgesia 1 day post-CFA injection.

37 und's adjuvant model of chronic inflammatory thermal hyperalgesia ( 32, 15).

38 (ED(50) approximately 100 mg/kg, i.p.), and thermal hyperalgesia after intraplantar complete Freund'

39 The laser treatment significantly diminished thermal hyperalgesia after SCI as measured by the Planta

40 ons, and attenuated mechanical allodynia and thermal hyperalgesia after SCI.

41 nM to 1microM) affected tactile allodynia or thermal hyperalgesia after SNL, but it increases cold al

42 econdary, but not primary, mechanical and/or thermal hyperalgesia after topical mustard oil applicati

43 f C5a into the mouse hindpaw produced strong thermal hyperalgesia, an effect that was absent in TRPV1

44 show that epinephrine-induced mechanical and thermal hyperalgesia and acetic acid-associated hyperalg

45 hronic pain states, including mechanical and thermal hyperalgesia and allodynia.

46 ose-dependent inhibition of mGluR-1-mediated thermal hyperalgesia and by colocalization of the antibo

47 ced complete Freund's adjuvant (CFA)-induced thermal hyperalgesia and chronic constriction injury (CC

48 The development of mechanical and thermal hyperalgesia and increased production of PGE(2)

49 significantly inhibited carrageenan-induced thermal hyperalgesia and indomethicin inhibited paw infl

50 Mrgprb2 mediates inflammatory mechanical and thermal hyperalgesia and is required for recruitment of

51 The development of thermal hyperalgesia and mechanical allodynia after CCI

52 = 10-15 micromolkg s.c.) in attenuating both thermal hyperalgesia and mechanical allodynia after chro

53 and DM (15 mg/kg) effectively reversed both thermal hyperalgesia and mechanical allodynia although e

54 of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated

55 sation through TRPV1, and enduringly reduced thermal hyperalgesia and mechanical allodynia caused by

56 -/-) mice, and this correlated with enhanced thermal hyperalgesia and mechanical allodynia in Pap(-/-

57 ganglion (DRG) neurons and the responses to thermal hyperalgesia and mechanical allodynia in strepto

58 compounds crizotinib or lorlatinib reversed thermal hyperalgesia and mechanical allodynia induced by

59 Thermal hyperalgesia and mechanical allodynia occurred i

60 egulation by PD98059 resulted in exacerbated thermal hyperalgesia and mechanical allodynia reversible

61 eloped a rat model of NGF-induced persistent thermal hyperalgesia and mechanical allodynia to determi

62 Lastly, both thermal hyperalgesia and mechanical allodynia to i.t. gp

63 Thermal hyperalgesia and mechanical allodynia were also

64 Additionally, thermal hyperalgesia and mechanical allodynia were endur

65 e development of neuropathic pain behaviors (thermal hyperalgesia and mechanical allodynia) induced b

66 Pain behaviors (thermal hyperalgesia and mechanical allodynia) were esta

67 he same substances that are known to mediate thermal hyperalgesia and mechanical allodynia.

68 degrees C stimulation, thereby demonstrating thermal hyperalgesia and mechanical allodynia.

69 n, while silencing these neurons resulted in thermal hyperalgesia and mechanical allodynia.

70 normal motor performance but have increased thermal hyperalgesia and mechanical allodynia.

71 (i.th.) administration of ligand 14 reversed thermal hyperalgesia and mechanical hypersensitivity in

72 l group II mGluRs inhibits forskolin-induced thermal hyperalgesia and nociceptor heat sensitization,

73 n and morphine were able to block or reverse thermal hyperalgesia and normalize gait in the CARR mode

74 Behavioral analysis revealed thermal hyperalgesia and perturbation of accurate paw pl

75 , but it significantly prevented progressive thermal hyperalgesia and prevented C-fiber atrophy, dege

76 ing behavior, as well as carrageenan-induced thermal hyperalgesia and tactile allodynia.

77 MHC-II in myelinating Schwann cells reduces thermal hyperalgesia and, to a lesser extent, also dimin

78 in response thresholds to both heat stimuli (thermal hyperalgesia) and light tactile stimuli (mechani

79 Both lowering of thermal pain threshold (thermal hyperalgesia) and lowering of response threshold

80 of PGE(2) in DRGs, decreased mechanical and thermal hyperalgesia, and decreased sensitization of noc

81 erated nitroglycerine-induced mechanical and thermal hyperalgesia, and furthermore, show that cloxyqu

82 oTx elicits nonneurogenic inflammatory pain, thermal hyperalgesia, and mechanical allodynia, of which

83 uction, PEA-m was able to reduce mechanical, thermal hyperalgesia, and motor alterations as well as r

84 d in the development of analgesic tolerance, thermal hyperalgesia, and tactile allodynia in response

85 P acting at the NK1 receptor causes chronic thermal hyperalgesia, and that the reduced opioid effica

86 Tests of tactile and thermal hyperalgesia are additional markers of neural hy

87 c nerve developed significant mechanical and thermal hyperalgesia as tested by the withdrawal respons

88 (2)(*-) (1 microM) led to the development of thermal hyperalgesia associated with a profound localize

89 fibre nociceptors and is responsible for the thermal hyperalgesia associated with inflammatory pain.

90 Animals exhibited moderate thermal hyperalgesia at this time.

91 While DM alone was effective in reducing thermal hyperalgesia at three tested doses (15, 30 or 60

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

93 but not spinally, reduced carrageenan-evoked thermal hyperalgesia but had no effect by any route with

94 MAPK signaling pathway in the production of thermal hyperalgesia, but not inflammation, in the mouse

95 geenan) produced a significant inhibition of thermal hyperalgesia, but not inflammation.

96 also plays a critical role in development of thermal hyperalgesia, but the underlying mechanism remai

97 eby phosphoinositide turnover contributes to thermal hyperalgesia by disinhibiting the channel.

98 suggest that complement fragment C5a induces thermal hyperalgesia by triggering macrophage-dependent

99 The thermal hyperalgesia caused by UVB irradiation was inhib

100 vivo, 52 fully reversed carrageenan-induced thermal hyperalgesia (CITH) in rats and dose-dependently

101 IkappaBalpha-dn mice had less mechanical and thermal hyperalgesia compared to WT mice post-CCI.

102 PAR2-induced thermal hyperalgesia depends on sensitization of transie

103 opment of permanent mechanical allodynia and thermal hyperalgesia due to interruption and subsequent

104 Intradermal NADA also induces VR1-mediated thermal hyperalgesia (EC(50) = 1.5 +/- 0.3 microg).

105 omol/kg, mouse) and efficacy in pain models (thermal hyperalgesia, ED 50 = 72 micromol/kg, rat).

106 c indwelling intrathecal catheters the acute thermal hyperalgesia evoked by the spinal delivery of su

107 ndent effects: the persistent mechanical and thermal hyperalgesia following reincision in adulthood w

108 uration reversal of mechanical allodynia and thermal hyperalgesia for at least 4 weeks.

109 nociceptive hypersensitivity, we found that thermal hyperalgesia (for OIH) and cold allodynia (for C

110 ures of static allodynia (von Frey test) and thermal hyperalgesia (Hargreaves test).

111 displayed time-related tactile allodynia and thermal hyperalgesia (i.e., opioid-induced "pain"); plac

112 uction and increased formation of PGE(2) and thermal hyperalgesia in a dose-dependent manner.

113 Compound 46ad also reversed thermal hyperalgesia in a model of inflammatory pain, wh

114 ption, and reversed mechanical allodynia and thermal hyperalgesia in a model of neuropathic pain.

115 as effective at reversing both allodynia and thermal hyperalgesia in a standard Chung (spinal nerve l

116 silocybin on mechanical hypersensitivity and thermal hyperalgesia in a well-established rat model of

117 inhibitors blocked mechanical allodynia and thermal hyperalgesia in all three pain models although t

118 CFA-induced inflammatory pain produced thermal hyperalgesia in both males and females that was

119 Wild-type mice exhibited mechanical but not thermal hyperalgesia in both paws 1 d after acid injecti

120 ignificantly increased tactile allodynia and thermal hyperalgesia in both the early (first week) and

121 eletion of the P2X3 receptor causes enhanced thermal hyperalgesia in chronic inflammation.

122 EAE and attenuated mechanical allodynia and thermal hyperalgesia in EAE.

123 ype V1) plays a key role in the induction of thermal hyperalgesia in inflammatory pain models, we eva

124 Mechanical and thermal hyperalgesia in mice is correlated with live bac

125 ts BD-1063 and S1RA abolished mechanical and thermal hyperalgesia in mice with carrageenan-induced ac

126 nd currents in HEK 293 cells, and suppressed thermal hyperalgesia in mice.

127 tral sensitisation to produce mechanical and thermal hyperalgesia in rats and humans.

128 development of taxol-induced mechanical and thermal hyperalgesia in rats.

129 Cdk5 activity is associated with attenuated thermal hyperalgesia in TGF-beta1 receptor conditional k

130 ed sensitivity to light touch, pinprick, and thermal hyperalgesia in the absence of injury, without a

131 V)1.7 in lumbar dorsal root ganglia, reduced thermal hyperalgesia in the inflammatory state, decrease

132 ehaviorally result in chronic persistence of thermal hyperalgesia in the ipsilateral forepaw.

133 ) reduced complete Freund's adjuvant-induced thermal hyperalgesia in the rat.

134 the TRPV1 antagonist decreased inflammatory thermal hyperalgesia in transgenic but not wild-type ani

135 intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the

136 eral inflammation, mechanical allodynia, and thermal hyperalgesia in vector control animals that pers

137 cation of cis-45, which was shown to reverse thermal hyperalgesia in vivo in the spinal nerve ligatio

138 hecal administration of bradykinin induces a thermal hyperalgesia in vivo, which is reduced by inhibi

139 2-f-LIGRLO-NH(2) stimulated PAR(2)-dependent thermal hyperalgesia in vivo.

140 hermore, activin administration caused acute thermal hyperalgesia in wild-type mice, but not in TRPV1

141 NGF negated both neutrophil accumulation and thermal hyperalgesia, indicating the dependence of NGF o

142 s displayed enhanced scratching behavior and thermal hyperalgesia indicative of peripheral neuroinfla

143 s; however, it was ineffective at preventing thermal hyperalgesia induced by complete Freund's adjuva

144 in rats) and was also effective at reducing thermal hyperalgesia induced by complete Freund's adjuva

145 sevanol (1-10 mg/kg) significantly reversed thermal hyperalgesia induced by complete Freund's adjuva

146 sensitization of capsaicin receptors and the thermal hyperalgesia induced by PGE2, and suggest that p

147 Thermal hyperalgesia induced by PMA or burn injury in KI

148 nce P (SP; 20 nmol) or NMDA (2 nmol) and the thermal hyperalgesia induced by the injection of carrage

149 Thermal hyperalgesia is dramatically reduced after ablat

150 of hairy hind foot skin in rats, a transient thermal hyperalgesia lasting <2 h, and longlasting prima

151 hibitor, rolipram (1 mug/kg), rapidly evokes thermal hyperalgesia (lasting >5 h).

152 We find that UV-treated larvae develop both thermal hyperalgesia, manifested as an exaggerated respo

153 lantation (TCI) produces bone cancer-related thermal hyperalgesia, mechanical allodynia, spontaneous

154 in a model of inflammatory pain (CFA-induced thermal hyperalgesia, MED = 0.83 mg/kg, p.o.).

155 These findings suggest that inflammatory thermal hyperalgesia mediated by TRPV1 may be further ag

156 f 42 mumol/kg (ip) in a rat post-carrageenan thermal hyperalgesia model of inflammatory pain.

157 t saline, demonstrated tactile allodynia and thermal hyperalgesia of the hindpaws (during the DAMGO i

158 of melatonin alone was effective in reducing thermal hyperalgesia only at the highest dose (120 mg/kg

159 ith the development of tactile allodynia and thermal hyperalgesia, spinal CaMKIIalpha activity was si

160 us opioid enkephalin (ENK) in the RVM during thermal hyperalgesia, suggesting potential in situ inter

161 ministration of A-784168 blocked CFA-induced thermal hyperalgesia, suggesting that both peripheral an

162 Robust thermal hyperalgesia (tail-flick, TF, and Hargreaves tes

163 ation into four sensory phenotypes (healthy, thermal hyperalgesia [TH], mechanical hyperalgesia [MH],

164 lower-extremity sensory phenotypes (healthy, thermal hyperalgesia [TH], mechanical hyperalgesia [MH],

165 are involved in the mechanical allodynia and thermal hyperalgesia that develop following cold injury

166 (intrathecal, IT) application of SP produces thermal hyperalgesia that is mediated by activation of t

167 inducing but not maintaining mechanical and thermal hyperalgesia that is mediated by CaMKIIalpha sig

168 emin, neurturin, GDNF, or NGF produced acute thermal hyperalgesia that lasted up to 4 h; combined inj

169 on of spinal neurons, and the mechanical and thermal hyperalgesia that normally occurs after peripher

170 Each peptide evoked dose-dependent thermal hyperalgesia that required activation of the mit

171 into mouse hindpaw led to the development of thermal hyperalgesia that was attenuated by administrati

172 ceramide (10 mug) led to the development of thermal hyperalgesia that was dependent on induction of

173 njection of a PAR2 agonist caused persistent thermal hyperalgesia that was prevented by antagonism or

174 n of an OSCC cell line caused mechanical and thermal hyperalgesia that was reversed by LI-1.

175 Avoiders exhibited thermal hyperalgesia that was reversed by systemic or in

176 t MK-801 blocked both morphine tolerance and thermal hyperalgesia that were potentiated by PDC.

177 e ligation reversed mechanical allodynia and thermal hyperalgesia; the antiallodynic effect lasted 6

178 ng the initiation of mechanical allodynia or thermal hyperalgesia, these cells may not be as importan

179 als from developing mechanical allodynia and thermal hyperalgesia throughout the 96 h after CFA.

180 serum blocked tactile allodynia and reversed thermal hyperalgesia to above baseline levels (i.e., ant

181 d similar levels of mechanical allodynia and thermal hyperalgesia to wild-type mice but reduced mecha

182 F-kappaB expression and nerve injury-induced thermal hyperalgesia using a rat model of constriction s

183 lthough local administration of NGF mediates thermal hyperalgesia via mechanisms involving concomitan

184 Much longer lasting thermal hyperalgesia was apparent in glabrous skin (1 h

185 Carrageenan-induced thermal hyperalgesia was associated with increased 3-nit

186 their ability to develop carrageenan-induced thermal hyperalgesia was completely absent.

187 In these studies, carrageenan-induced thermal hyperalgesia was evaluated in the mouse and the

188 Thermal hyperalgesia was examined on day 0 and postopera

189 Accordingly, leukotriene B4-induced thermal hyperalgesia was mediated through BLT1 and TRPV1

190 Inflammatory thermal hyperalgesia was only marginally attenuated in K

191 In behavioral testing, PGE(2)-induced thermal hyperalgesia was significantly diminished in Del

192 Notably, NGF-induced thermal hyperalgesia was unaffected by macrophage deplet

193 By focusing on the mechanisms of C5a-induced thermal hyperalgesia, we show that this process requires

194 sponses assessed by mechanical allodynia and thermal hyperalgesia were almost identical in the two mo

195 Swelling and mechanical and thermal hyperalgesia were assessed before and for 28 day

196 Mechanical and thermal hyperalgesia were reduced significantly with enr

197 of TRPA1 in vitro but did not cause pain or thermal hyperalgesia when injected into the hind paw of

198 nical hyperalgesia, mechanical allodynia and thermal hyperalgesia, which are blocked following co-inj

199 pression and the behavioral manifestation of thermal hyperalgesia, which is likely to be mediated thr

200 an induced a time-dependent inflammation and thermal hyperalgesia, which was maximal 4 h post adminis

201 SR 141716A evoked thermal hyperalgesia with an ED50 of 0.0012 fmol.

202 al administration of either compound blocked thermal hyperalgesia with similar potency.

203 GF either systemically or in the skin causes thermal hyperalgesia within minutes.