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1 e PGE2-induced increase in pain sensitivity (hyperalgesia).
2 tra-CeA CRF infusion mimicked stress-induced hyperalgesia.
3 iezo2 contributes to inflammatory mechanical hyperalgesia.
4 assessed by measuring thermal and mechanical hyperalgesia.
5 tors (CRFR1s) reduces stress-induced thermal hyperalgesia.
6 peralgesia during remission from CFA-induced hyperalgesia.
7 optosis mice abolished C5a-dependent thermal hyperalgesia.
8 ked prolongation of prostaglandin E2-induced hyperalgesia.
9 itaxel-induced mechanical allodynia and heat hyperalgesia.
10 tal role in inflammatory pain and mechanical hyperalgesia.
11 s a potent inflammatory mediator that causes hyperalgesia.
12 icated in mediating enhanced translation and hyperalgesia.
13 der basal conditions and during inflammatory hyperalgesia.
14 kedly prolongs inflammatory mediator-induced hyperalgesia.
15 on or extinction of conditioned analgesia or hyperalgesia.
16 t mechanisms modulating comorbid anxiety and hyperalgesia.
17 a pivotal role in stress-induced anxiety and hyperalgesia.
18 mportant role in the peripheral inflammatory hyperalgesia.
19 ical role in the development of inflammatory hyperalgesia.
20 iceptive sensitivities and developed similar hyperalgesia.
21 ct centrally mediated referred allodynia and hyperalgesia.
22 hanges and associated morphine tolerance and hyperalgesia.
23 sitivity in two mouse models of inflammatory hyperalgesia.
24 pretreatment with 46 prevented NPFF-induced hyperalgesia.
25 ensor and integrator of inflammation-induced hyperalgesia.
26 esting their importance for the PGE2-induced hyperalgesia.
27 effect on an equivalent thermal inflammatory hyperalgesia.
28 the degeneration of these fibers that drives hyperalgesia.
29 on, attenuating inflammatory and neuropathic hyperalgesia.
30 ortex mediated the effect of value on nocebo hyperalgesia.
31 eased by spinal glial cells for both LTP and hyperalgesia.
32 g GRK2 or decreasing EPAC1 inhibited chronic hyperalgesia.
33 dynamic mechanical allodynia and mechanical hyperalgesia.
34 nociceptive pathways is a cellular model of hyperalgesia.
35 f, and intraoperative use and opioid-induced hyperalgesia.
36 y be critical in the pathogenesis of thermal hyperalgesia.
37 proalgesic agents capable of promoting heat hyperalgesia.
38 nhibited sound stress-induced enhancement of hyperalgesia.
39 useful strategy for inhibiting inflammatory hyperalgesia.
40 paired sensation of noxious heat and thermal hyperalgesia.
41 lgesic in three mouse models of inflammatory hyperalgesia.
42 ators produces markedly prolonged mechanical hyperalgesia.
43 ure eliminated SIEH without attenuating ET-1 hyperalgesia.
44 inflammation and development of inflammatory hyperalgesia.
45 nduce cold pain, whereas they did evoke heat hyperalgesia.
46 IL-1beta and TNF-alpha and for some forms of hyperalgesia.
47 layed the development of mechanical and heat hyperalgesia.
48 B(3) at doses that attenuated the associated hyperalgesia.
49 sensitization of TRPV1 and produces thermal hyperalgesia.
50 verse effects including weight loss and cold hyperalgesia.
51 (5+)) dose-dependently reversed this thermal hyperalgesia.
52 in spinal nociceptive processing leading to hyperalgesia.
53 ut a significant correlation with behavioral hyperalgesia.
54 but could also be correlated with behavioral hyperalgesia.
55 velopment of chemotherapy-induced mechanical hyperalgesia.
56 o baseline but partially recovered from peak hyperalgesia.
57 attenuated neuronal coupling and mechanical hyperalgesia.
58 decoy receptor) markedly reduced CCI-induced hyperalgesia.
59 CRF-CRFR1 signaling in CeA in stress-induced hyperalgesia.
60 IFN-alpha by a neutralizing antibody induced hyperalgesia.
61 bitor GNF-5837 prevented C5a-induced thermal hyperalgesia.
62 provides a mechanism for peripheral thermal hyperalgesia.
63 s Adjuvant)-induced inflammation and thermal hyperalgesia.
65 xant and ataxic effects, reversed mechanical hyperalgesia 24h after injury, while it was devoid of cl
66 In adults, acute physiological stress causes hyperalgesia [5-7], and increased background stress incr
67 rked prolongation of prostaglandin E2 (PGE2) hyperalgesia, a key feature of hyperalgesic priming.
68 ristine cause pronounced mechanical and heat hyperalgesia, a significant decrease in tail compound ne
69 repeat restraint stress each led to visceral hyperalgesia, accompanied by mucosal inflammation and im
74 icroM) affected tactile allodynia or thermal hyperalgesia after SNL, but it increases cold allodynia
76 to the mouse hindpaw produced strong thermal hyperalgesia, an effect that was absent in TRPV1 knock-o
84 antigen induced arthritis as well as in the hyperalgesia and angiogenesis model at a well-tolerated
85 Guanethidine completely suppressed the heat hyperalgesia and attenuated mechanical and cold hypersen
86 ndent inhibition of mGluR-1-mediated thermal hyperalgesia and by colocalization of the antibody with
87 onal anaesthesia might impact the acute pain/hyperalgesia and chronic postsurgical pain, the controve
89 adult injury selectively prevented both the hyperalgesia and early microglial reactivity associated
92 06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthri
93 thesia is able to reduce postoperative acute hyperalgesia and long-term chronic pain by decreasing pa
94 eptor (MOR) agonist DAMGO induced mechanical hyperalgesia and marked prolongation of prostaglandin E2
95 rat model of NGF-induced persistent thermal hyperalgesia and mechanical allodynia to determine the r
97 administration of ligand 14 reversed thermal hyperalgesia and mechanical hypersensitivity in a dose-d
98 ficacy in preclinical models of inflammatory hyperalgesia and neuropathic allodynia and is devoid of
99 opriate for treating pain disorders in which hyperalgesia and not allodynia is the primary symptom.
101 ies will have to specifically evaluate acute hyperalgesia and postoperative chronic pain and not only
102 c inhibition with imatinib ameliorates tonic hyperalgesia and prevents hypoxia/reoxygenation-induced
103 enan, interleukin 6, as well as BDNF-induced hyperalgesia and priming are reduced specifically in mal
104 the dorsal root ganglion induced mechanical hyperalgesia and priming with an onset more rapid than w
105 d pro-dynorphin KO mice showed recovery from hyperalgesia and reinstatement by NTX; (3) there was no
106 beta(3)-specific siRNA normalized mechanical hyperalgesia and tactile allodynia caused by SNL but had
107 show a reduction in inflammatory mechanical hyperalgesia and TRPA1- but not TRPV1-mediated pain.
108 st to show that the maintenance of secondary hyperalgesia and underlying central sensitization associ
109 in myelinating Schwann cells reduces thermal hyperalgesia and, to a lesser extent, also diminishes me
115 its nonneurogenic inflammatory pain, thermal hyperalgesia, and mechanical allodynia, of which the lat
116 ese changes probably underlie the allodynia, hyperalgesia, and spontaneous pain seen in patients.
117 ress induces a persistent elevation of IL-6, hyperalgesia, and susceptibility to chronic muscle pain,
120 estigated to what extent behavioral signs of hyperalgesia are correlated with immunohistochemical cha
122 developed significant mechanical and thermal hyperalgesia as tested by the withdrawal responses of th
124 is essential for the development of the heat hyperalgesia associated with persistent inflammation.
125 hic pain conditions characterized by primary hyperalgesia at the site of injury and secondary hyperal
126 an important role in the development of heat hyperalgesia at the spinal cord level after L5 nerve inj
127 or expression on nociceptors attenuated ET-1 hyperalgesia but had no effect on SIEH, suggesting that
129 ) axons abolishes heat, mechanical, and cold hyperalgesia but tactile and cold allodynia remain follo
130 model, we were able to study not only evoked hyperalgesia, but also for the first time to demonstrate
131 ys a critical role in development of thermal hyperalgesia, but the underlying mechanism remains uncer
133 e most efficient analgesic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%.
134 such as prostaglandin-E2 or bradykinin cause hyperalgesia by activating cellular kinases that phospho
136 We further demonstrated that suppression of hyperalgesia by MORs was due to their constitutive activ
137 elastase to mice caused edema and mechanical hyperalgesia by PAR(2)- and TRPV4-mediated mechanisms.
138 that complement fragment C5a induces thermal hyperalgesia by triggering macrophage-dependent signalin
139 provides evidence that spontaneous pain and hyperalgesia can have distinct underlying mechanisms wit
141 ical threshold), and decreases in mechanical hyperalgesia, cold allodynia, and sciatic nerve conducti
143 that the induction of primary and secondary hyperalgesia depended on peripheral input from the injur
145 oligodeoxynucleotides, chronic PGE2-induced hyperalgesia development was prevented in the 2 priming
148 elta-, and kappa-opioid receptors reinstated hyperalgesia during remission from CFA-induced hyperalge
149 low pH and noxious heat, is a key factor in hyperalgesia during tissue injury as well as pathologica
150 e induction of synaptic facilitation and the hyperalgesia elicited by ultra-low-dose buprenorphine.
151 opathic pain symptoms, such as allodynia and hyperalgesia, for several weeks in murine chronic constr
153 are thought to promote opioid tolerance and hyperalgesia; however, how opioids drive such changes re
154 lly related conditions such as allodynia and hyperalgesia in a comparative setting that offers unique
155 e demonstrate that GRK2 inhibits CFA-induced hyperalgesia in a kinase activity-dependent manner.
157 tive at reversing both allodynia and thermal hyperalgesia in a standard Chung (spinal nerve ligation)
159 kg(-1)), which caused thermal and mechanical hyperalgesia in behaving animals, induced an enhancement
160 These results suggest that pruritus and hyperalgesia in chronic cholestatic BDL rats are associa
161 so doing completely and selectively reverses hyperalgesia in diabetic ob/ob mice without altering bas
165 implicated in environmental thermosensation, hyperalgesia in inflamed tissues, skin sensitization, an
170 r injection of Cat-S caused inflammation and hyperalgesia in mice that was attenuated by PAR2 or TRPV
171 63 and S1RA abolished mechanical and thermal hyperalgesia in mice with carrageenan-induced acute (3 h
181 of this study suggest that the inflammatory hyperalgesia in peripheral tissue depends on activation
183 ge of hyperalgesic agents in that it induces hyperalgesia in rats that is markedly enhanced by repeat
188 revent intestinal abnormalities and visceral hyperalgesia in response to chronic psychological stress
192 on of DF2593A effectively reduced mechanical hyperalgesia in several models of acute and chronic infl
194 peralgesia in the V2 territory and secondary hyperalgesia in territories innervated by the mandibular
195 -/-) mice are protected against inflammatory hyperalgesia in the complete Freund's adjuvant (CFA) mod
196 uding joint inflammation, primary mechanical hyperalgesia in the ipsilateral ankle, and secondary mec
199 ents we observed attenuation of PGE2-induced hyperalgesia in the paw by the knockdown of NMDAR subuni
200 -2,3-dione had no effect in the PGE2-induced hyperalgesia in the paw, showing specific involvement of
201 NMDA into the fifth lumbar (L5)-DRG induced hyperalgesia in the rat hind paw with a profile similar
202 tory primary afferent inputs, and mechanical hyperalgesia in the territories of injured and uninjured
203 to produce constant and long-lasting primary hyperalgesia in the V2 territory and secondary hyperalge
205 cal injection of ARN077 decreased mechanical hyperalgesia in tumor-bearing mice, and the effect was b
206 he endothelium also appears to contribute to hyperalgesia in two ergonomic pain models (eccentric exe
207 eA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyp
209 ibution to OIH by comparing morphine-induced hyperalgesia in wild type (WT) and MOR knockout (KO) mic
210 romedial medulla injection of AM 404 reduced hyperalgesia in wild-type mice but not in CB1(-/-) mice.
211 peptide, psiepsilonRACK, produced mechanical hyperalgesia in wild-type mice but not in Scn10a-/- mice
212 morphine-3beta-D-glucuronide (M3G) elicited hyperalgesia in WT but not in MOR KO animals, as well as
213 nergic and delta-opioid receptors reinstated hyperalgesia in WT mice and abolished the partial recove
216 lerance (diminished pain-relieving effects), hyperalgesia (increased pain sensitivity), and drug depe
217 yed enhanced scratching behavior and thermal hyperalgesia indicative of peripheral neuroinflammation.
218 antisense to CD44 mRNA, which also prevents hyperalgesia induced by a CD44 receptor agonist, A6.
220 PKCepsilon, dependence; (3) prolongation of hyperalgesia induced by an activator of PKA, 8-bromo cAM
221 ely our results show that MOR is involved in hyperalgesia induced by chronic morphine and its metabol
222 ate that inflammatory thermal and mechanical hyperalgesia induced by complete Freund's adjuvant was a
227 Although CD44 antisense has no effect on the hyperalgesia induced by inflammatory mediators or paclit
228 can be detected in spinal cord (as prolonged hyperalgesia induced by intrathecal PGE2), but only when
229 andin formation, acetaminophen also reversed hyperalgesia induced by intrathecal prostaglandin E2 To
230 containing Hnic and ina inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-in
233 , whereas the maintenance phase of secondary hyperalgesia involved central sensitization in Vc neuron
236 nt of opioid-induced analgesic tolerance and hyperalgesia is a clinical challenge for managing chroni
238 lls, supporting the idea that the peripheral hyperalgesia is an event modulated by a glutamatergic sy
241 mice, the development of mechanical and heat hyperalgesia is blocked and the loss in tail compound ne
242 e of the TRPV1 channel in the development of hyperalgesia is established, but the role of the neurotr
244 of heat, is an important contributor because hyperalgesia is reduced when TRPV1 is either genetically
245 cotic Bowel Syndrome (NBS)/Opioid-Induced GI Hyperalgesia, is characterized by the paradoxical develo
247 hind foot skin in rats, a transient thermal hyperalgesia lasting <2 h, and longlasting primary mecha
248 Tonic MOR(CA) suppression of withdrawal hyperalgesia may prevent the transition from acute to ch
250 pain neuraxis, associated with allodynia and hyperalgesia observed in patients with chronic pain.
252 that prostaglandin plays in the inflammatory hyperalgesia of peripheral tissue has not been establish
254 ith opioid tolerance (OT) and opioid-induced hyperalgesia (OIH), which limit efficacy and compromise
257 e for PKCepsilon did not inhibit either ET-1 hyperalgesia or SIEH, suggesting no role for neuronal PK
260 1 receptor antagonists produces long-lasting hyperalgesia rather than the transient hyperalgesia seen
261 ovide evidence for a novel form of cognitive hyperalgesia relating to perceptual uncertainty, induced
262 e specific GFRalpha3 ligand that evokes heat hyperalgesia, robustly sensitized cold responses in a TR
265 nfluence of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is common
266 R55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR5
267 d enkephalin (ENK) in the RVM during thermal hyperalgesia, suggesting potential in situ interactions.
269 g but not maintaining mechanical and thermal hyperalgesia that is mediated by CaMKIIalpha signaling i
270 hat rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in
271 peptidergic nociceptors to induce mechanical hyperalgesia that is prevented by intrathecal oligodeoxy
272 se hindpaw led to the development of thermal hyperalgesia that was attenuated by administration of sp
273 showed significant dose-dependent mechanical hyperalgesia that was fully established at 30 days after
275 adenosine 3',5'-monophosphate overshoot and hyperalgesia) that required N-methyl-D-aspartate recepto
276 ction of peripheral inflammation, a model of hyperalgesia, there was a switch in the current-voltage
277 nitiation of mechanical allodynia or thermal hyperalgesia, these cells may not be as important for th
279 eceptors (BRs) in the spinal cord to promote hyperalgesia through an excitatory effect, which is oppo
281 n processing and the development of referred hyperalgesia using a conditional nociceptor-specific NaV
288 Accordingly, leukotriene B4-induced thermal hyperalgesia was mediated through BLT1 and TRPV1 as show
291 ty because of the following: (1) CFA-induced hyperalgesia was reinstated by the MOR inverse agonist n
293 ing on the mechanisms of C5a-induced thermal hyperalgesia, we show that this process requires recruit
294 1 in vitro but did not cause pain or thermal hyperalgesia when injected into the hind paw of mice.
295 d in temperature perception and inflammatory hyperalgesia, whereas in pancreatic beta-cells the chann
296 ed both acute pain and persistent mechanical hyperalgesia which were almost completely abolished by T
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
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