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1 S in descending RVM 5-HT neurons that drives pronociceptive 5-HT(3)R signaling in the dorsal horn, an
2 nus of the NK(1)R are necessary for the full pronociceptive actions of SP.
3 litatory systems and enhanced expression and pronociceptive actions of spinal dynorphin.
4                                          The pronociceptive actions of these opioids were blocked by
5 ins (PGs) are mediators of inflammation with pronociceptive actions within the PAG under normal condi
6 ciated with the DRGs and involving increased pronociceptive activity of SGCs, which in turn act on se
7                Medication-induced persistent pronociceptive adaptations might be responsible for lowe
8 in" intensity as a consequence of persistent pronociceptive adaptive changes.
9          Thus, endogenous dynorphin had both pronociceptive and antinociceptive actions after nerve i
10 ive pathways is still controversial, as both pronociceptive and antinociceptive actions have been rep
11                                         Both pronociceptive and antinociceptive effects of HA are med
12 ipheral pain signaling reflects a balance of pronociceptive and antinociceptive influences; the contr
13 tentional load; specific RVM regions showing pronociceptive and antinociceptive processes (in line wi
14                                 We show that pronociceptive and inflammatory factors, such as nerve g
15  a molecular exchange of bioactive contents (pronociceptive and protumorigenic) via paracrine and aut
16 ge, (2) that upregulated spinal dynorphin is pronociceptive and required for the maintenance of persi
17  peripheral and central 5-HT(3) receptors is pronociceptive and that the contribution of peripheral 5
18 of the delta opioid receptor and the MOR are pronociceptive, and that drugs that spare such heteromer
19 -6) signaling, immune system activation, and pronociceptive autoantibodies are characteristic of comp
20 ther, injection of L-368899 per se induces a pronociceptive behavioral effect, suggesting a tonic end
21  of the rostral ventromedial medulla induces pronociceptive behaviors in rats.
22                                          The pronociceptive effect of alpha-CTX MII was partially blo
23                                          The pronociceptive effect of HXA(3) correlated with enhanced
24 ivation of these channels contributes to the pronociceptive effects of ATP.
25                                          The pronociceptive effects of GAs combined with surgical tis
26                                          The pronociceptive effects of IgG are likely mediated throug
27                            Consistently, the pronociceptive effects of IgG passive transfer were lost
28 causes generalized hyperalgesia by enhancing pronociceptive effects of immune mediators.
29 of protein kinase Cepsilon (PKCepsilon), the pronociceptive effects of PGE2 in DAMGO-treated rats dem
30 counteract the EP2 and EP4 receptor-mediated pronociceptive effects of PGE2.
31  that such modulation cannot account for the pronociceptive effects of this gasotransmitter.
32 a and hyperalgesia, and at least part of the pronociceptive effects of TNFalpha have been suggested a
33 olecystokinin (CCK) has been identified as a pronociceptive endogenous peptide which also possesses a
34 us, a point mutation allows neurotrophic and pronociceptive functions of NGF to be split, with intere
35 ciception without activating the concomitant pronociceptive functions that monomeric KOR also subserv
36 and female mice results in the production of pronociceptive IgG, which accumulates around the lumbar
37 uces IgG accumulation after CCI, attenuating pronociceptive IgG-FcgammaR signaling around the lumbar
38 ventrolateral periaqueductal gray (vlPAG) is pronociceptive in naive and acutely inflamed animals, bu
39          Here, we tested the hypothesis that pronociceptive individuals have an enhanced TSP response
40 sensitization induced by both a prototypical pronociceptive inflammatory mediator PGE(2) and paclitax
41 he rostral ventral medulla (RVM) that convey pronociceptive input to the spinal cord.
42                      Redirecting the flow of pronociceptive intracellular cAMP toward up-regulation o
43  We report that surgical incision recruits a pronociceptive latent pain sensitization that persisted
44 n-coupled receptor (GPCR), C5aR, is a potent pronociceptive mediator in several models of inflammator
45                      The altered response to pronociceptive mediators involved a switch in coupling o
46 , mechanical hyperalgesia induced by diverse pronociceptive mediators involved in inflammatory and ne
47                                   Oncogenic, pronociceptive mediators packaged in cancer cell-derived
48       In addition to increased production of pronociceptive mediators, HNC is accompanied by a dampen
49 reverses the hyperalgesia induced by diverse pronociceptive mediators, prostaglandin E2, epinephrine,
50  states via secretion of proinflammatory and pronociceptive mediators, such as tumor necrosis factor
51                                              Pronociceptive mediators, together with nerve injury, ca
52 monooxygenase-expressing astrocytes into the pronociceptive metabolite 3-hydroxykynurenine.
53 nt sensitization characterized by persistent pronociceptive neural adaptations in dural afferents and
54                                   Late-phase pronociceptive neurochemical changes in the DRG were blo
55                When subjects were grouped as pronociceptive or antinociceptive based on whether they
56              Surprisingly, inhibition of the pronociceptive P2X2/3 receptor did not affect the activa
57 he possibility that cholecystokinin (CCK), a pronociceptive peptide, may drive such descending facili
58 ia caused by inflammation, nerve injury, and pronociceptive receptor activation.
59 tionally, Pip5k1c haploinsufficiency reduces pronociceptive receptor signaling and TRPV1 sensitizatio
60  (DRG) neurons and if these kinases regulate pronociceptive receptor signaling.
61  levels were elevated coincident with injury/pronociceptive receptor stimulation.
62 vels were elevated in the absence of ongoing pronociceptive receptor stimulation.
63                     Numerous pain-producing (pronociceptive) receptors signal via phosphatidylinosito
64              Our data, therefore, supports a pronociceptive role for 5-HT2 receptors, most likely thr
65 nisms by which Substance P (Sub P) assumes a pronociceptive role in the rostral ventromedial medulla
66                        5HT3 receptors play a pronociceptive role in the spinal cord and ondansetron h
67  following noxious stimulation, underlie the pronociceptive role of Sub P under conditions of persist
68 ng paclitaxel-induced pain-like behavior and pronociceptive signaling in DRGs and spinal cord dorsal
69 e behavior in males and females and prevents pronociceptive signaling in DRGs and spinal cord dorsal
70    Latent sensitization (LS) of pain engages pronociceptive signaling pathways in the dorsal horn tha
71 ter thal-BA 3a or RVM-sgACC FC respectively, pronociceptive subjects showed greater TSP responses.
72 ing the anti-opioid peptide cholecystokinin, pronociceptive Substance P (SP), Neurokinin B, and a lat
73 e that GPR55 activation at central levels is pronociceptive, suggesting that interfering with GPR55 s
74 ptors eliminated morphine tolerance, OIH and pronociceptive synaptic long-term potentiation without a
75 of KOR and thereby endogenous dynorphin from pronociceptive to antinociceptive.
76 pain-modulatory capabilities are regarded as pronociceptive, whereas individuals with reduced pain pr