ライフサイエンスコーパス: hyperalgesic

1 melanoma tumor-implanted mice, which are not hyperalgesic.

2 ogy in mice, eliciting either an anti-opioid/hyperalgesic action or analgesia depending upon the dose

3 Hyperalgesic actions of these compounds following i.t. a

4 nimals did not develop tolerance to the anti-hyperalgesic activity of NM0127 and NM0127 was active in

5 infusion of the highest morphine dose (i.e., hyperalgesic adaptation), hyperalgesia was restored afte

6 sensation in vivo, Iheat is enhanced by the hyperalgesic agent prostaglandin E2 and only partially a

7 ore but not after injection of direct-acting hyperalgesic agents (prostaglandin E2 and purine and ser

8 gnitude to that induced by the direct-acting hyperalgesic agents but much longer in duration (>48 vs

9 in-1 (ET-1) is unique among a broad range of hyperalgesic agents in that it induces hyperalgesia in r

10 PKA) inhibitors either before or after these hyperalgesic agents resulted in reduced hyperalgesia, su

11 h properties of nociceptors, is a target for hyperalgesic agents.

12 ission within the spinal cord contributes to hyperalgesic and allodynic responses following nerve inj

13 ation of nicotinic agonists can produce both hyperalgesic and analgesic effects in vivo.

14 There was no difference in the anti-hyperalgesic and anti-inflammatory actions of SzV-1287 a

15 model as suitable for the assessment of anti-hyperalgesic and anti-inflammatory agents.

16 ings suggest a mechanism for integrating the hyperalgesic and proinflammatory roles of TRPV1 and lino

17 may facilitate the development of novel anti-hyperalgesic approaches aimed at attenuating activation

18 These results confirm that mice are hyperalgesic at late time points after formalin or adjuv

19 Both alkaloids were hyperalgesic at the site of injection.

20 eshold and enhancement of bradykinin-induced hyperalgesic behavior after vagotomy are dependent on a

21 agmatic vagotomy enhances bradykinin-induced hyperalgesic behavior and decreases baseline paw withdra

22 r may exist in diabetic rats, as exaggerated hyperalgesic behavior coexists with reduced peripheral n

23 Hyperalgesic behavior in diabetic rats is associated wit

24 Diabetic rats display exaggerated hyperalgesic behavior in response to noxious stimuli tha

25 enhancement of bradykinin-induced mechanical hyperalgesic behavior, both of which were maintained ove

26 prostaglandin production to this exaggerated hyperalgesic behavior.

27 Axotomized neurons from rats made hyperalgesic by SNL lost sensitivity to the myristoylate

28 In axotomized neurons from rats made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP

29 ts were no longer significantly mechanically hyperalgesic compared to the sham animals (P > or = 0.09

30 CCI animals were hyperalgesic compared to the sham operated animals at 14

31 l stimuli, both in the basal state and under hyperalgesic conditions such as peripheral inflammation

32 Furthermore, the lack of hyperalgesic cross-adaptation between high and low morph

33 Importantly, intrathecal wortmannin at anti-hyperalgesic doses reversed the evoked increase not only

34 pamycin (an mTORC1 inhibitor) displayed anti-hyperalgesic effect in both inflammatory pain models.

35 mor-bearing limbs may contribute to the anti-hyperalgesic effect of elevated AEA levels.

36 genous NO precursor or donor could mimic the hyperalgesic effect of endogenous NO.

37 This attenuation was not due to a hyperalgesic effect of NRM inactivation.

38 esia in unstressed rats and blocked the anti-hyperalgesic effect of systemic CRFR1 antagonist in stre

39 This anti-hyperalgesic effect was mimicked by SFLLRN, the natural

40 served uncertainty had a specific and potent hyperalgesic effect.

41 ad ligand 14 blocked Dyn A-(2-13) 10-induced hyperalgesic effects and motor impairment in in vivo ass

42 ent of pain may become effective when opioid hyperalgesic effects are blocked by coadministration of

43 se inhibitor, oseltamivir, blocks morphine's hyperalgesic effects by decreasing neuronal levels of GM

44 of CTX-B (10 ng/kg, s.c.) selectively blocks hyperalgesic effects elicited by morphine or by a kappa

45 Importantly, the anti-hyperalgesic effects of AEA and URB597 were blocked by a

46 /kg, i.p.) for 7 d, we investigated the anti-hyperalgesic effects of anandamide (AEA) and cyclohexylc

47 1 is one of the key mechanisms mediating the hyperalgesic effects of inflammatory mediators, such as

48 This signaling pathway may contribute to the hyperalgesic effects of opioids that can be efficiently

49 a. 0.1 microg/kg) can, in fact, elicit acute hyperalgesic effects, manifested by rapid onset of decre

50 naltrexone (NTX) which blocks opioid-induced hyperalgesic effects, unmasking potent opioid analgesia.

51 tively antagonizes high-efficacy excitatory (hyperalgesic) Gs-coupled opioid receptor-mediated signal

52 of the living animal, Go-deficient mice are hyperalgesic (hot-plate test) and display a severe motor

53 it is not beneficial to the animal to become hyperalgesic (i.e., to alter its behavior in order to pr

54 coeruleus (LC) in a rat model of unilateral hyperalgesic inflammation.

55 d 54% of C-fibers, an effect enhanced by the hyperalgesic inflammatory mediator prostaglandin E2.

56 Because hyperalgesic mechanisms may be important in establishing

57 perfusates collected from the tumor sites of hyperalgesic mice between PID 7 and 12.

58 DRG of STZ-injected diabetic and nondiabetic hyperalgesic mice compared with control mice.

59 from primary afferent fibers in control and hyperalgesic mice with tumor revealed the development of

60 fMRI analysis of hyperalgesic nocebo responses to identical calibrated no

61 ed hyperalgesia, and revealed differences in hyperalgesic onset between morphine infusion doses.

62 Hyperalgesic onset was preceded by dose-dependent analge

63 We report that when an inducer of hyperalgesic priming (monocyte chemotactic protein 1) is

64 cted lesion of dopaminergic neurons reverses hyperalgesic priming in both sexes and that a D1/D5 anta

65 fective pain behaviors, and strongly reduced hyperalgesic priming in mice lacking eIF4E phosphorylati

66 We used 2 mouse models of hyperalgesic priming in which the transition from acute

67 These studies demonstrate a novel form of hyperalgesic priming induced by repeated administration

68 neurons engaged by dopamine signaling in the hyperalgesic priming model, we used c-fos labeling.

69 Furthermore, hyperalgesic priming of mechanical hypersensitivity requ

70 he inhibitor of protein translation reversed hyperalgesic priming only when injected at the site wher

71 Hyperalgesic priming with carrageenan induced a sustaine

72 Hyperalgesic priming, a form of neuroplasticity in nocic

73 Hyperalgesic priming, a model of pain chronification in

74 Acute insults produce hyperalgesic priming, a neuroplastic change in nocicepto

75 contribution of alphaCaMKII to induction of hyperalgesic priming, a phenomenon implicated in the tra

76 Hyperalgesic priming, an estrogen dependent model of the

77 ing serotonergic neurons were ablated before hyperalgesic priming, IL-6- and carrageenan-induced mech

78 ium signaling is present in the induction of hyperalgesic priming, in females.

79 This neuroplastic change, hyperalgesic priming, is dependent on activation of cyto

80 This phenomenon, "hyperalgesic priming," depends on the epsilon isoform of

81 n a model of the transition to chronic pain, hyperalgesic priming.

82 din E2 (PGE2) hyperalgesia, a key feature of hyperalgesic priming.

83 g the presence of a chronic pain state using hyperalgesic priming.

84 glandin E(2) (PGE(2)), a phenomenon known as hyperalgesic priming.

85 he transition of from acute to chronic pain, hyperalgesic priming.

86 n E(2) hyperalgesia, simultaneously produced hyperalgesic priming.

87 plasticity in a model of chronic pain called hyperalgesic priming.

88 ptors that contributes to sex differences in hyperalgesic priming.SIGNIFICANCE STATEMENT The present

89 xotomized L5 or adjacent L4 DRG neurons from hyperalgesic rats following L5 SNL.

90 microinfusion of rrTNF alpha exacerbates the hyperalgesic response by ligatured animals, and induces

91 GE(2) do not show the enhanced and prolonged hyperalgesic response by which primed IB(4)(+)-nocicepto

92 ligature placement completely abolishes the hyperalgesic response characteristic of this model, as a

93 epsilon inhibitor antagonized this prolonged hyperalgesic response equally.

94 response by ligatured animals, and induces a hyperalgesic response in animals not receiving ligatures

95 The hyperalgesic response returned to baseline by approximat

96 develop a PKCepsilon-dependent long-lasting hyperalgesic response to a subsequent challenge by the p

97 homeostasis at the spinal level, because the hyperalgesic response to exogenous glutamate was enhance

98 ed neuropeptides, has been shown to induce a hyperalgesic response when injected subcutaneously into

99 hat this latter effect was consistent with a hyperalgesic response.

100 Results showed significant analgesic and hyperalgesic responses (P < 0.001), and responses were i

101 establish whether conditioned analgesic and hyperalgesic responses could be acquired by unseen (subl

102 mpletely blocked both the lesser and greater hyperalgesic responses observed in spinal transected and

103 oltage-gated sodium channels may underly the hyperalgesic responses of mammalian sensory neurones.

104 ccumbens, an area previously associated with hyperalgesic responses to the blockade of opioid recepto

105 nses to chemical stimulation of the face and hyperalgesic responses to thermal stimulation of the hin

106 sity radiant heat assay capable of detecting hyperalgesic responses, each of the OFQ/N fragments in t

107 ch as psychologically mediated analgesic and hyperalgesic responses.

108 ns, and amygdala, which were associated with hyperalgesic responses.

109 which the aging process affects the thermal hyperalgesic responsiveness of these animals was investi

110 ce compared with TRPV1-/- mice, with thermal hyperalgesic sensitivity observed at 24 hours and at 1 w

111 out how the aging process alters the thermal hyperalgesic sensitivity to peripheral nerve injury.

112 rents within the capsaicin-induced secondary hyperalgesic skin induced SEFs at identical latencies an

113 evealed hyperthermia confined to painful and hyperalgesic skin of distal extremities, in absence of s

114 trical stimulus applied within the secondary hyperalgesic skin were analyzed.

115 receptor-mediated suppression of a sustained hyperalgesic state.

116 utes to the development and maintenance of a hyperalgesic state.

117 ceptor-induced effects in both analgesic and hyperalgesic states, and suggest inhibition of glutamate

118 so suggests distinct morphine dose-dependent hyperalgesic systems.

119 The effect was significantly larger for hyperalgesic than analgesic responses (P < 0.001).

120 hold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their a

121 datives, en route to avoiding emetogenic and hyperalgesic volatile anesthetics.