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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 , corresponding anatomical localization, and hyperalgesic behavioral alterations in the surgical inci
28 in a rat model of a surgical incision, using hyperalgesic behavioral tests, histological analyses, an
29            Axotomized neurons from rats made hyperalgesic by SNL lost sensitivity to the myristoylate
30         In axotomized neurons from rats made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP
31 ts were no longer significantly mechanically hyperalgesic compared to the sham animals (P > or = 0.09
32                             CCI animals were hyperalgesic compared to the sham operated animals at 14
33 l stimuli, both in the basal state and under hyperalgesic conditions such as peripheral inflammation
34                     Furthermore, the lack of hyperalgesic cross-adaptation between high and low morph
35  Importantly, intrathecal wortmannin at anti-hyperalgesic doses reversed the evoked increase not only
36 pamycin (an mTORC1 inhibitor) displayed anti-hyperalgesic effect in both inflammatory pain models.
37 mor-bearing limbs may contribute to the anti-hyperalgesic effect of elevated AEA levels.
38 genous NO precursor or donor could mimic the hyperalgesic effect of endogenous NO.
39 gh p-chlorophenylalanine attenuated the anti-hyperalgesic effect of enriched diet and companionship.
40            This attenuation was not due to a hyperalgesic effect of NRM inactivation.
41 esia in unstressed rats and blocked the anti-hyperalgesic effect of systemic CRFR1 antagonist in stre
42                                    This anti-hyperalgesic effect was mimicked by SFLLRN, the natural
43 served uncertainty had a specific and potent hyperalgesic effect.
44 ad ligand 14 blocked Dyn A-(2-13) 10-induced hyperalgesic effects and motor impairment in in vivo ass
45 ent of pain may become effective when opioid hyperalgesic effects are blocked by coadministration of
46 se inhibitor, oseltamivir, blocks morphine's hyperalgesic effects by decreasing neuronal levels of GM
47 of CTX-B (10 ng/kg, s.c.) selectively blocks hyperalgesic effects elicited by morphine or by a kappa
48                        Importantly, the anti-hyperalgesic effects of AEA and URB597 were blocked by a
49 /kg, i.p.) for 7 d, we investigated the anti-hyperalgesic effects of anandamide (AEA) and cyclohexylc
50 1 is one of the key mechanisms mediating the hyperalgesic effects of inflammatory mediators, such as
51 This signaling pathway may contribute to the hyperalgesic effects of opioids that can be efficiently
52 ripheral afferent neurons prevented the anti-hyperalgesic effects of the intrathecal Y1 agonist.
53 primary sensory neurons in the analgesic and hyperalgesic effects produced by systemic opioid adminis
54 a. 0.1 microg/kg) can, in fact, elicit acute hyperalgesic effects, manifested by rapid onset of decre
55 naltrexone (NTX) which blocks opioid-induced hyperalgesic effects, unmasking potent opioid analgesia.
56 tively antagonizes high-efficacy excitatory (hyperalgesic) Gs-coupled opioid receptor-mediated signal
57  of the living animal, Go-deficient mice are hyperalgesic (hot-plate test) and display a severe motor
58 it is not beneficial to the animal to become hyperalgesic (i.e., to alter its behavior in order to pr
59 d treatment for osteoarthritis pain, is anti-hyperalgesic in preclinical models of inflammatory and n
60  coeruleus (LC) in a rat model of unilateral hyperalgesic inflammation.
61 d 54% of C-fibers, an effect enhanced by the hyperalgesic inflammatory mediator prostaglandin E2.
62                                      Because hyperalgesic mechanisms may be important in establishing
63 perfusates collected from the tumor sites of hyperalgesic mice between PID 7 and 12.
64 DRG of STZ-injected diabetic and nondiabetic hyperalgesic mice compared with control mice.
65  from primary afferent fibers in control and hyperalgesic mice with tumor revealed the development of
66                             fMRI analysis of hyperalgesic nocebo responses to identical calibrated no
67 ed hyperalgesia, and revealed differences in hyperalgesic onset between morphine infusion doses.
68                                              Hyperalgesic onset was preceded by dose-dependent analge
69                       Using a mouse model of hyperalgesic priming (HP), we show that monocytes enable
70            We report that when an inducer of hyperalgesic priming (monocyte chemotactic protein 1) is
71 ciceptor population mediating opioid-induced hyperalgesic priming (OIHP), a model of pain chronificat
72 ablished an in vitro model of opioid-induced hyperalgesic priming (OIHP), in male rats, to identify n
73 r systemic fentanyl, rats had also developed hyperalgesic priming (opioid-primed rats), long-lasting
74 MORs), and that MOR and TLR4 agonists induce hyperalgesic priming (priming), which also occurs in CIP
75                        To test this, we used hyperalgesic priming and the spared nerve injury neuropa
76              Furthermore, HCQ acutely abated hyperalgesic priming behavior in mice exposed to CIH.
77 nhibition of hypusine biosynthesis prevented hyperalgesic priming by inflammatory mediators in vivo a
78 cted lesion of dopaminergic neurons reverses hyperalgesic priming in both sexes and that a D1/D5 anta
79 ssion in Nav1.8(+) neurons was necessary for hyperalgesic priming in female, but not male, mice.
80  neurons is necessary for the development of hyperalgesic priming in female, but not male, mice.
81 vity in both sexes because CLP257 alleviated hyperalgesic priming in male and female mice.
82 fective pain behaviors, and strongly reduced hyperalgesic priming in mice lacking eIF4E phosphorylati
83 urther studies are needed to clarify whether hyperalgesic priming in nonpeptidergic afferents or repe
84                    We used 2 mouse models of hyperalgesic priming in which the transition from acute
85                                           In hyperalgesic priming induced by activation of interleuki
86    These studies demonstrate a novel form of hyperalgesic priming induced by repeated administration
87                                    Using the hyperalgesic priming model in male mice, we demonstrate
88 nsible for a decrease in the duration of the hyperalgesic priming model of chronic pain.
89                              A mouse two-hit hyperalgesic priming model of migraine was used.
90 neurons engaged by dopamine signaling in the hyperalgesic priming model, we used c-fos labeling.
91 ynia in both acute and chronic phases of the hyperalgesic priming model.
92                                 Furthermore, hyperalgesic priming of mechanical hypersensitivity requ
93 use model of chronic widespread pain through hyperalgesic priming of muscle, we show that neutrophils
94 h given intrathecally, blocked, and reversed hyperalgesic priming only in females.
95 he inhibitor of protein translation reversed hyperalgesic priming only when injected at the site wher
96 /o) subunits in analgesia, hyperalgesia, and hyperalgesic priming produced by fentanyl and morphine,
97 /o) subunits in analgesia, hyperalgesia, and hyperalgesic priming produced by fentanyl and morphine,
98 ically activating proprioceptors resulted in hyperalgesic priming that favored chronic pain induced b
99 ehavioral responses, animals were tested for hyperalgesic priming using a normally non-noxious dose o
100                                              Hyperalgesic priming with carrageenan induced a sustaine
101                                      We used hyperalgesic priming with interleukin 6 (IL-6) priming a
102  inflammatory-mediator-induced hyperalgesia (hyperalgesic priming).
103 cal u-opioid receptor (MOR) agonists produce hyperalgesic priming, a form of maladaptive nociceptor n
104                                              Hyperalgesic priming, a form of neuroplasticity in nocic
105                                              Hyperalgesic priming, a model of pain chronification in
106                        Acute insults produce hyperalgesic priming, a neuroplastic change in nocicepto
107  contribution of alphaCaMKII to induction of hyperalgesic priming, a phenomenon implicated in the tra
108                                              Hyperalgesic priming, an estrogen dependent model of the
109                                              Hyperalgesic priming, assessed by prolongation of prosta
110                                              Hyperalgesic priming, assessed by prolongation of prosta
111 ing serotonergic neurons were ablated before hyperalgesic priming, IL-6- and carrageenan-induced mech
112 ium signaling is present in the induction of hyperalgesic priming, in females.
113                    This neuroplastic change, hyperalgesic priming, is dependent on activation of cyto
114 e ability of a HFD to stimulate diet-induced hyperalgesic priming, or diet sensitization in male and
115                            This phenomenon, "hyperalgesic priming," depends on the epsilon isoform of
116 uch as fentanyl can produce hyperalgesia and hyperalgesic priming.
117 s of the dorsal root ganglia consistent with hyperalgesic priming.
118 n a model of the transition to chronic pain, hyperalgesic priming.
119 eral macrophage ablation blocked CIH-induced hyperalgesic priming.
120 second dural injection of pH 7.0 to test for hyperalgesic priming.
121 plasticity in a model of chronic pain called hyperalgesic priming.
122 din E2 (PGE2) hyperalgesia, a key feature of hyperalgesic priming.
123 g the presence of a chronic pain state using hyperalgesic priming.
124 luated whether Prlr signaling contributes to hyperalgesic priming.
125 glandin E(2) (PGE(2)), a phenomenon known as hyperalgesic priming.
126 he transition of from acute to chronic pain, hyperalgesic priming.
127 n E(2) hyperalgesia, simultaneously produced hyperalgesic priming.
128 ptors that contributes to sex differences in hyperalgesic priming.SIGNIFICANCE STATEMENT The present
129 xotomized L5 or adjacent L4 DRG neurons from hyperalgesic rats following L5 SNL.
130 microinfusion of rrTNF alpha exacerbates the hyperalgesic response by ligatured animals, and induces
131 GE(2) do not show the enhanced and prolonged hyperalgesic response by which primed IB(4)(+)-nocicepto
132  ligature placement completely abolishes the hyperalgesic response characteristic of this model, as a
133 epsilon inhibitor antagonized this prolonged hyperalgesic response equally.
134 response by ligatured animals, and induces a hyperalgesic response in animals not receiving ligatures
135                                          The hyperalgesic response returned to baseline by approximat
136  develop a PKCepsilon-dependent long-lasting hyperalgesic response to a subsequent challenge by the p
137 homeostasis at the spinal level, because the hyperalgesic response to exogenous glutamate was enhance
138 ed neuropeptides, has been shown to induce a hyperalgesic response when injected subcutaneously into
139 hat this latter effect was consistent with a hyperalgesic response.
140     Results showed significant analgesic and hyperalgesic responses (P < 0.001), and responses were i
141  establish whether conditioned analgesic and hyperalgesic responses could be acquired by unseen (subl
142 mpletely blocked both the lesser and greater hyperalgesic responses observed in spinal transected and
143 oltage-gated sodium channels may underly the hyperalgesic responses of mammalian sensory neurones.
144 ccumbens, an area previously associated with hyperalgesic responses to the blockade of opioid recepto
145 nses to chemical stimulation of the face and hyperalgesic responses to thermal stimulation of the hin
146 sity radiant heat assay capable of detecting hyperalgesic responses, each of the OFQ/N fragments in t
147 ch as psychologically mediated analgesic and hyperalgesic responses.
148 ns, and amygdala, which were associated with hyperalgesic responses.
149  which the aging process affects the thermal hyperalgesic responsiveness of these animals was investi
150 ce compared with TRPV1-/- mice, with thermal hyperalgesic sensitivity observed at 24 hours and at 1 w
151 out how the aging process alters the thermal hyperalgesic sensitivity to peripheral nerve injury.
152 rents within the capsaicin-induced secondary hyperalgesic skin induced SEFs at identical latencies an
153 evealed hyperthermia confined to painful and hyperalgesic skin of distal extremities, in absence of s
154 trical stimulus applied within the secondary hyperalgesic skin were analyzed.
155 s by 90%, from 30 to 3 seconds, indicating a hyperalgesic state.
156 receptor-mediated suppression of a sustained hyperalgesic state.
157 utes to the development and maintenance of a hyperalgesic state.
158 ceptor-induced effects in both analgesic and hyperalgesic states, and suggest inhibition of glutamate
159 so suggests distinct morphine dose-dependent hyperalgesic systems.
160      The effect was significantly larger for hyperalgesic than analgesic responses (P < 0.001).
161 hold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their a
162 datives, en route to avoiding emetogenic and hyperalgesic volatile anesthetics.

 
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