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1 n a rat model of neuropathic pain induced by spinal nerve ligation.
2 development of mechanical allodynia after L5 spinal nerve ligation.
3 n the absence of injury and 2 weeks after L5 spinal nerve ligation.
4 tions such as peripheral inflammation and L5 spinal nerve ligation.
5 ute to mechanical hypersensitivity following spinal nerve ligation.
6 on in the sciatic nerve of the rat following spinal nerve ligation.
7 Sprague-Dawley rats underwent left L5 and L6 spinal nerve ligation.
8 ared nerve injury, chronic constriction, and spinal nerve ligation.
9 gesia and allodynia in the hind paw after L5 spinal nerve ligation.
10  discharges of injured sensory neurons after spinal nerve ligation.
11 lmost all ectopic discharges originate after spinal nerve ligation.
12 cally characterized neurons in the RVM after spinal nerve ligation, a model of neuropathic pain that
13        RVM neurons were studied 7-14 d after spinal nerve ligation, and classified as "on-cells," "of
14 G was extensive as early as 2 days after the spinal nerve ligation, and the sprouted fibers were almo
15 dorsal horn was dramatically increased after spinal nerve ligation, and this was abolished by saporin
16                                        After spinal nerve ligation, axotomized neurons had less I(h)
17 vity was lost in the hind paw ipsilateral to spinal nerve ligation, but maintained in the contralater
18                                           L5 spinal nerve ligation did not alter the number of GABA(B
19                                              Spinal nerve ligation did not significantly alter alpha-
20 a in a variety of rat pain models including: spinal nerve ligation (ED(50) = 47 mg/kg, i.p.), sciatic
21                                              Spinal nerve ligation in rats significantly increased th
22 e not been thoroughly investigated following spinal nerve ligation in the rat.
23 ot (DR) and the spinal nerve 7-14 days after spinal nerve ligation in the rat.
24 in-43 (GAP-43) in the L5 DRG 1 week after L5 spinal nerve ligation, indicated sprouting of sympatheti
25           AM1241 was also active in blocking spinal nerve ligation-induced tactile and thermal hypers
26 -4 (TSP4), using a neuropathic pain model of spinal nerve ligation injury.
27        Sustained neuropathic pain induced by spinal nerve ligation is accompanied by D1R and met-enke
28                                   A modified spinal nerve ligation method was used to induce the dege
29                                        After spinal nerve ligation, MMP-9 shows a rapid and transient
30 ing, and attenuated tactile allodynia in the spinal nerve ligation model of neuropathic pain (ED(50)=
31  reverse thermal hyperalgesia in vivo in the spinal nerve ligation model of neuropathic pain with exc
32 anical and thermal stimuli in vivo using the spinal nerve ligation model of neuropathic pain.
33 ciceptive responses of spinal neurons in the spinal nerve ligation model of neuropathic pain.
34 D50 of 8 and 5.1 mg/kg, respectively, in rat spinal nerve ligation neuropathic pain model.
35      Peripheral nerve injury in a rat model (spinal nerve ligation) of neuropathic pain triggers spro
36                                The effect of spinal nerve ligation on alpha-CTX MII-induced mechanica
37            This study examined the effect of spinal nerve ligation on different populations of immuno
38 logical studies were performed 14-18 d after spinal nerve ligation or sham surgery, and the effects o
39 as 1, but with much lower doses, in a rodent spinal nerve ligation pain model.
40                        The data suggest that spinal nerve ligation produced attenuated glutamate upta
41                                              Spinal nerve ligation produces a unilateral loss of alph
42 nd thermal hyperalgesia in a standard Chung (spinal nerve ligation) rat neuropathic pain model.
43 utely isolated from normal rats (no previous spinal nerve ligation) responded to either mATP or ATP.
44 e (vector QHGAD67) 7 days after selective L5 spinal nerve ligation reversed mechanical allodynia and
45 kinase (JNK) in neuropathic pain produced by spinal nerve ligation (SNL) (L5).
46 5-HT3 receptor antagonists in rats following spinal nerve ligation (SNL) but not sham operation.
47                             Axonal injury by spinal nerve ligation (SNL) elevated SOCE and I(CRAC).
48 rats and in rats that had received L5 and L6 spinal nerve ligation (SNL) immediately before injection
49 in 5-HT(2A)R-induced hyperexcitability after spinal nerve ligation (SNL) in rat.
50                                              Spinal nerve ligation (SNL) in rats significantly increa
51 on mechanical allodynia following unilateral spinal nerve ligation (SNL) in rats.
52                                 Furthermore, spinal nerve ligation (SNL) induced persistent neuropath
53                                              Spinal nerve ligation (SNL) injury in rats pretreated wi
54 ioral and neuroanatomical consequences of L5 spinal nerve ligation (SNL) injury.
55                                    Using the spinal nerve ligation (SNL) model of neuropathic pain, w
56 PPQ) model of acute visceral pain, and a rat spinal nerve ligation (SNL) model of neuropathic pain.
57 ty and neuropathic pain behaviors in the rat spinal nerve ligation (SNL) model.
58 dependent flush as well as the hot plate and spinal nerve ligation (SNL) models of acute and neuropat
59 20 was also studied in the rat hot plate and spinal nerve ligation (SNL) models of acute and neuropat
60 ur present study, we examined the effects of spinal nerve ligation (SNL) on the number of neurons in
61                                              Spinal nerve ligation (SNL) produced expected tactile an
62 lated from neuropathic rats induced by L5/L6 spinal nerve ligation (SNL) via electrophysiological and
63 ury models: sciatic nerve transection (SNT), spinal nerve ligation (SNL), and chronic constriction in
64 mized neurons from rats made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP) channel activi
65                                        After spinal nerve ligation (SNL), both wild-type (WT) and KO
66  C-fiber-evoked potentials in rats receiving spinal nerve ligation (SNL), but not in uninjured rats.
67 verses neuropathic pain behavior after L5/L6 spinal nerve ligation (SNL), implicating a critical func
68 olving Sprague Dawley rats, we reported that spinal nerve ligation (SNL), in addition to causing allo
69 o rat model of neuropathy, unilateral lumbar spinal nerve ligation (SNL), to characterize the distrib
70 FA)-induced chronic inflammatory pain and L5 spinal nerve ligation (SNL)-induced neuropathic pain in
71 ed protein response (UPR) activation in a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain
72 ts in DRG neurons is downregulated following spinal nerve ligation (SNL).
73 5th lumbar (L5) dorsal root ganglia after L5 spinal nerve ligation (SNL).
74 reduced hypersensitivity in rats after L5-L6 spinal nerve ligation (SNL).
75 rsal root ganglion (DRG) neurons after L5/L6 spinal nerve ligation (SNL).
76 scade in vivo to trigger pain behavior after spinal nerve ligation (SNL).
77 mal hypersensitivity were induced in rats by spinal nerve ligation (SNL).
78 ws or intrathecally was tested in rats after spinal nerve ligation (SNL).
79                             We observed that spinal nerve ligation (SNL, L5) in male Sprague Dawley r
80 ion in naive, sham-operated and neuropathic (spinal nerve ligation, SNL) rats using in vivo electroph
81 ; AXO, partial sciatic nerve ligation; PSNL, spinal nerve ligation; SNL or chronic constriction injur
82            Following either sham surgery, or spinal nerve ligation, spinal muscimol inhibited Abeta-,
83 nglionic neurons was greatly increased after spinal nerve ligation, suggesting the increased number o

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