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1 increase in pain-like responses (mechanical allodynia).
2 of peripheral nerves to light touch (tactile allodynia).
3 (C-fibers) has limited effects on mechanical allodynia.
4 e elusive dorsal horn circuit for mechanical allodynia.
5 tely reversed oxaliplatin-induced mechanical allodynia.
6 ain without affecting the sensory mechanical allodynia.
7 genesis that are associated with neuropathic allodynia.
8 critical for expression of hyperalgesia and allodynia.
9 ritical role in the expression of mechanical allodynia.
10 l cord dorsal horn only in mice with ongoing allodynia.
11 ncreased thermal hyperalgesia and mechanical allodynia.
12 been implicated in the expression of tactile allodynia.
13 produced long-lasting generalized cutaneous allodynia.
14 , but also alleviated SNI-induced mechanical allodynia.
15 echanotransduction contributes to mechanical allodynia.
16 neuron hyperactivity and reversed mechanical allodynia.
17 selective antibody attenuated the associated allodynia.
18 butes to centrally mediated hyperalgesia and allodynia.
19 tration in rodent models of hyperalgesia and allodynia.
20 e to peripheral inflammation-induced tactile allodynia.
21 810 or HC030031 reduced spinal HXA(3)-evoked allodynia.
22 ous and long-lasting pain, hyperalgesia, and allodynia.
23 ons and in a rat behavioral model of thermal allodynia.
24 f SNC80 to inhibit PGE(2)-stimulated thermal allodynia.
25 ileuton) dose-dependently attenuated tactile allodynia.
26 resence of pain was confirmed by testing for allodynia.
27 natomical source of the influence of CGIC on allodynia.
28 ly frequency of migraine attacks, as well as allodynia.
29 nan-induced thermal hyperalgesia and tactile allodynia.
30 the expression of subsequent PGE(2)-induced allodynia.
31 g to abnormally elevated pain states such as allodynia.
32 jection after the resolution of IL-6-induced allodynia.
33 or cingulate compared to migraineurs without allodynia.
34 ve neuronal type recruited during mechanical allodynia.
35 vided an 11.2-fold attenuation of mechanical allodynia.
36 thresholds were measured to detect cutaneous allodynia.
37 heat hyperalgesia and neuropathic mechanical allodynia.
38 pinal dorsal horn of rats displaying tactile allodynia.
39 ding mechanical and thermal hyperalgesia and allodynia.
40 V1, leading to the development of mechanical allodynia.
41 s, depression, sleep disorders and cutaneous allodynia.
42 E by antibodies blocks CFA-evoked mechanical allodynia.
43 of diabetes, and protects against mechanical allodynia.
44 ented or significantly attenuated IM-induced allodynia.
45 c acid metabolites rapidly evokes mechanical allodynia.
46 ensheathed nociceptors to sustain mechanical allodynia.
47 anisms underlying cephalic and extracephalic allodynia.
48 acrophage infiltration, oxidative stress and allodynia.
49 sts attenuated cortical theta and mechanical allodynia.
50 g siRNA against C/EBPbeta reduced mechanical allodynia.
51 hannels without producing heat or mechanical allodynia.
52 emporally coincident with the alleviation of allodynia.
53 lization or PD-1 blockade induced mechanical allodynia.
54 phosphorylation leading to hyperalgesia and allodynia.
55 in severity of paclitaxel-induced mechanical allodynia.
56 xogenous IL-10 attenuated paclitaxel-induced allodynia.
57 tassium current IKD in damage-triggered cold allodynia.
58 t this contributes to neuropathic mechanical allodynia.
59 heral injury induced long-lasting (>1 month) allodynia.
60 recovery from paclitaxel-induced mechanical allodynia.
61 in WT mice attenuated neuropathic mechanical allodynia.
62 mPFC of SNI rats induced a decrease in cold allodynia.
63 eurons, which we show also convey mechanical allodynia.
64 1, which has been frequently associated with allodynia.
67 nerve injury, effectively reduced mechanical allodynia, a cardinal feature of late-phase neuropathic
68 horn, has been implicated in injury-induced allodynia, a condition wherein pain is produced by innoc
69 nsitized response to a painful stimulus, and allodynia, a pain-like response to an innocuous stimulus
70 onse to noxious thermal stimuli, and thermal allodynia, a responsiveness to subthreshold thermal stim
73 hdrawal-like behavioral signs and mechanical allodynia, activates NR1 and NR2 receptors, and downregu
75 -314) dose-dependently suppresses mechanical allodynia after chemotherapy, nerve injury, and diabetic
78 Disruption of this inhibition results in allodynia, allowing low-threshold drive onto pain and te
79 sed both thermal hyperalgesia and mechanical allodynia although each individual dose alone did not re
80 ave previously been implicated in mechanical allodynia, an A-fiber-selective pharmacological blocker
84 ver several days prevented the expression of allodynia and enhanced sensitivity to stress observed fo
85 s time, BAMBI-KO mice were protected against allodynia and exhibited increased expression and functio
87 nt receptor potential (TRP) channels mediate allodynia and hyperalgesia downstream of these pathways.
88 (Hh) signaling is required for both thermal allodynia and hyperalgesia following ultraviolet irradia
89 n and potentially related conditions such as allodynia and hyperalgesia in a comparative setting that
92 zation in the pain neuraxis, associated with allodynia and hyperalgesia observed in patients with chr
93 Spinal application of TNFalpha induces both allodynia and hyperalgesia, and at least part of the pro
94 ate-phase neuropathic pain symptoms, such as allodynia and hyperalgesia, for several weeks in murine
95 ld relieve the paclitaxel-induced mechanical allodynia and hyperalgesia, which was assessed 30 min af
101 eline levels, rats showed enhanced cutaneous allodynia and increased CGRP in the blood following chal
102 IM1alpha expression reversed the SNL-induced allodynia and increased spontaneous EPSC (sEPSC) frequen
103 of inflammatory hyperalgesia and neuropathic allodynia and is devoid of ancillary cardiovascular or C
104 RPV1) plays a major role in hyperalgesia and allodynia and is expressed both in the peripheral and ce
107 is critical for the expression of cutaneous allodynia and may mask the expression of diffuse noxious
111 e-specific trkB.T1 KO mice; using mechanical allodynia and pain-related measurements on the CatWalk,
115 r necrosis factor (TNF) signaling to mediate allodynia and that distinct transient receptor potential
116 ter SNI, wild-type mice developed mechanical allodynia and the functionality of mu-opioid receptors w
117 inished in cKO mice, but both the mechanical allodynia and the microgliosis generated by nerve injury
118 significantly blocked CFA-induced mechanical allodynia and thermal hyperalgesia 1 day post-CFA inject
119 duced a long-duration reversal of mechanical allodynia and thermal hyperalgesia for at least 4 weeks.
120 ute pain perception, and reversed mechanical allodynia and thermal hyperalgesia in a model of neuropa
121 , cis-(+)-37 was effective at reversing both allodynia and thermal hyperalgesia in a standard Chung (
123 Correlating with the development of tactile allodynia and thermal hyperalgesia, spinal CaMKIIalpha a
124 t tibial fracture with pinning triggers cold allodynia and up-regulates nerve injury and inflammatory
126 pain threshold, mechanical pain sensitivity, allodynia and/or windup), yielded four phenotypes of fib
128 ession of cranial and extracranial cutaneous allodynia, and are consistent with a brainstem generator
129 ynucleotide against TNFRI reduced mechanical allodynia, and decreased mtO2(.-), pCREB and pC/EBPbeta.
132 s sufficient to induce persistent mechanical allodynia, and this allodynia was suppressed by CXCL1 ne
134 Therefore, NGF-evoked thermal and mechanical allodynia are mediated by spatially distinct mechanisms.
136 rsed oxaliplatin-induced cold and mechanical allodynia as well as social interaction impairment.
141 on of ATL313 in rats with neuropathy-induced allodynia but had no effect on allodynia in the absence
142 r HXB(3) evoked profound, persistent tactile allodynia, but 12(S)-HpETE and HXA(3) produced relativel
143 ice that lack Ccr2 also developed mechanical allodynia, but this started to resolve from 8 wk onwards
146 n suggested that they play a crucial role in allodynia by modulating voltage-gated calcium channel cu
147 contribute more to the maintenance phase of allodynia by redirecting tactile information to the cort
148 basal mechanical sensitivity and mechanical allodynia by regulating auxiliary voltage-gated calcium
151 reduced thermal hyperalgesia and mechanical allodynia caused by inflammation, nerve injury, and pron
152 rmalized mechanical hyperalgesia and tactile allodynia caused by SNL but had no significant effect on
153 sociated with the pathogenesis of mechanical allodynia, changes in cortical circuits also accompany p
157 nerve ligation (SNL), in addition to causing allodynia, enhances the Rab3-interactive molecule-1alpha
161 ects of this drug were studied on mechanical allodynia following unilateral spinal nerve ligation (SN
163 dependent attenuation of hind paw mechanical allodynia for up to 1h after administration, with no not
164 by six weeks after STZ injection, mechanical allodynia had developed (mechanical withdrawal threshold
167 nisms for the development and maintenance of allodynia have been investigated in the spinal cord, bra
168 ctivity; these changes probably underlie the allodynia, hyperalgesia, and spontaneous pain seen in pa
170 ndicate that EA at 10 Hz inhibits mechanical allodynia/hyperalgesia more potently than does EA at 100
171 EA significantly inhibits paclitaxel-induced allodynia/hyperalgesia through spinal opioid receptors,
172 ared nerve injury (SNI) developed mechanical allodynia in 1 wk; nerve blockade with a single dose of
173 of the TAT-4BB reversed M3G-induced tactile allodynia in a dose-dependent manner but did not affect
175 olecule 20 (AM-1488), which reversed tactile allodynia in a mouse spared-nerve injury (SNI) model.
176 2-mediated suppression of paclitaxel-induced allodynia in CB1KO mice; these antiallodynic effects wer
178 ompletely blocked the development of tactile allodynia in diabetic rats, whereas relatively minor eff
184 genated fatty acids (EpFAs), greatly reduces allodynia in rats caused by streptozocin-induced type I
185 ed naloxone-sensitive reversal of mechanical allodynia in rats following chronic constriction injury
186 rved marked increases in mechanical and cold allodynia in rats of both sexes that were maintained on
187 ertain whether HBO2 treatment might suppress allodynia in rats with neuropathic pain and whether this
188 inal ganglia and in development of cutaneous allodynia in response to migraine triggers, even weeks a
191 eversible enzyme inhibition, 3 reversed cold allodynia in the chronic constriction injury model of ne
194 tribute directly to the pathogenesis of cold allodynia in the rat SNL model, but it is a potential me
195 in-induced flinching, and attenuated tactile allodynia in the spinal nerve ligation model of neuropat
197 Importantly, P7C3-A20 blocked PTX-induced allodynia in tumored mice without reducing antitumoral e
202 of AM1710 also attenuated paclitaxel-induced allodynia in WT mice, but not CB2KO mice, implicating a
205 and this is causally related to the onset of allodynia, in which a non-noxious stimulus becomes painf
207 b.i.d. for 3 d, intraperitoneal) suppressed allodynia induced by chronic constriction injury of the
208 there was a significant decrease in thermal allodynia induced by CIP, but no effect on edema formati
213 ensitivity is controlled in nociceptors, and allodynia involves TrkB(+) light-touch mechanoreceptors.
219 izing other modalities after an insult, cold allodynia is mediated exclusively by a single molecular
224 n (10 mug, 10 mul; i.t.) reduced SNL-induced allodynia, kalirin and pNR2B expression, as well as kali
225 etreatment with l-THP reduced the mechanical allodynia (MA) induced by direct activation of sigma-1 r
226 nt of SNL animals, at a dose that alleviated allodynia, markedly reduced the elevation of alpha(2)del
227 iabetes-induced thermal hypoalgesia, tactile allodynia, motor and sensory nerve conduction velocity d
231 y pain, thermal hyperalgesia, and mechanical allodynia, of which the latter is completely dependent o
233 f icilin (0.1nM to 1microM) affected tactile allodynia or thermal hyperalgesia after SNL, but it incr
234 required during the initiation of mechanical allodynia or thermal hyperalgesia, these cells may not b
235 We describe the defining feature of the cold allodynia pain percept in the human brain and illustrate
239 Surprisingly, Merkel cells also mediate allodynia, providing a new cellular target for chronic p
240 , and cold hyperalgesia but tactile and cold allodynia remain following peripheral nerve injury.
242 tent thermal hypersensitivity and mechanical allodynia require de novo protein translation and are me
244 day 12, while both MAPK phosphorylation and allodynia resolved on postoperative day 7 in wild-type m
246 the loss of tactile sensitivity and tactile allodynia seen in patients who have diabetes, inflammato
247 These effects were reminiscent of cutaneous allodynia seen in patients with migraine or other primar
248 eral manifestations of the neuropathic state-allodynia, sensory loss, shooting pains, etc, that can m
249 In addition, because disinhibition-induced allodynia shares some features with the immature dorsal
250 ventromedial medulla (RVM) also reversed the allodynia, showing this brain area to be an important si
251 cer-related thermal hyperalgesia, mechanical allodynia, spontaneous and movement-evoked pain behavior
254 with either AAV-Ag50 vector or SCP1, blocked allodynia suppression, agrin upregulation, and NR1 phosp
255 pinA3N developed more neuropathic mechanical allodynia than wild-type (WT) mice, and exogenous delive
257 (EA) on paclitaxel-induced hyperalgesia and allodynia that has not been studied in an animal model.
260 e-dependent and reversible cutaneous tactile allodynia that was maintained throughout and transiently
262 ignificantly reduced the nerve crush-induced allodynia; this anti-allodynic effect of HBO2 was revers
263 rsistent thermal hyperalgesia and mechanical allodynia to determine the role of transient receptor po
264 We used CTXs as a surrogate model of cold allodynia to dissect the framework of cold allodynia-act
265 hibition completely abolished both prolonged allodynia to hindpaw PGE(2) and enhanced nocifensive beh
266 ch as respiratory suppression, constipation, allodynia, tolerance, and dependence, as well as abuse p
267 In a murine model of chemotherapy-induced allodynia, VCR treatment induced upregulation of endothe
269 ns of heat on capsaicin-sensitized skin, hot allodynia was assessed during 3 Tesla functional magneti
270 ce, chemotherapy-induced development of cold allodynia was attenuated and the milder, temporary cold
278 ce persistent mechanical allodynia, and this allodynia was suppressed by CXCL1 neutralization, CXCL1
280 Consistent with clinical observations, the allodynia was unaffected by a neurokinin-1 antagonist.
281 eful animal surrogate of headache-associated allodynia, we next showed that blocking pain-facilitatin
283 ionally, thermal hyperalgesia and mechanical allodynia were enduringly enhanced when PIP(2) levels we
284 and superoxide production in the retina and allodynia were inhibited in diabetic animals in which iN
285 istic of the early stages of retinopathy and allodynia were measured in chimeric mice lacking inducib
288 were effective in preventing PGE(2)-induced allodynia when given immediately after IL-6, but not aft
289 ons may result in the development of tactile allodynia, where non-painful stimuli gain the capacity t
290 ly-phase analgesia and late-phase mechanical allodynia which requires NMDAR; both phases are prolonge
291 persensitivity to cold or mechanical-induced allodynia, which are established tests to assess acute o
292 n sensory perception, such as photophobia or allodynia, which have in common an uncomfortable amplifi
293 of NMDA induces GluN2B-dependent mechanical allodynia, which is prolonged in Arrb2-KO mice and condi
295 e Sprague Dawley rats resulted in behavioral allodynia, which was associated with phosphorylated SGK1
296 luR5-signaling pathway suppressed mechanical allodynia, while activating this pathway in the absence
297 injury prevented exacerbation of mechanical allodynia with a concurrent improvement of depression-li
298 2 agonists for managing chemotherapy-induced allodynia with a favorable therapeutic ratio marked by s
300 lencing in nociceptors attenuated mechanical allodynia, without affecting macrophage infiltration and
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