ライフサイエンスコーパス: SNL

1 SNL also significantly increased HVACC currents in small

2 SNL decreases total I(K(Ca)) in axotomized (L5) neurons,

3 SNL induced a slow (>3 d) and persistent (>21 d) activat

4 SNL led to increased immunoreactivity for met-enkephalin

5 SNL was followed by bilateral upregulation of mGluR1 in

6 SNL-enhanced kalirin immunofluorescence was coincident w

7 SNL-evoked mechanical hypersensitivity was attenuated, a

8 SNL-induced neuropathic pain was assessed behaviorally u

9 Thus it is expected that DNA-mediated 2D SNL structures open new avenues for designing miniaturiz

10 on: the carboxyl-terminal three amino acids (SNL) and the cyclic nucleotide-binding domain, respectiv

11 In addition, SNL did not alter the density of serotonergic fibers or

12 Additionally, SNL L4 neurons developed shoulders following transients

13 nced Ca(2+) buffering by neurons in adjacent SNL L4 neurons.

14 rily induced in spinal cord astrocytes after SNL.

15 en cisternae in the dorsal spinal cord after SNL.

16 persensitivity was induced in rats 2 d after SNL and lasted for >14 d.

17 p38 was activated between 5 hr and 3 d after SNL and returned to baseline within 5 d.

18 Treatment starting 1 or 7 d after SNL was ineffective.

19 y if it was started before but not 7 d after SNL.

20 er SNL and returned to baseline by 1 d after SNL.

21 nsetron in rats between 14 and 30 days after SNL and assessed effects on thermal and mechanical hyper

22 es from neuropathic rats 3 and 10 days after SNL displayed smaller EPSCs with prolonged latency, less

23 uced in injured L5 DRG neurons 14 days after SNL.

24 ized with CXCL13 and was downregulated after SNL.

25 dose (10 microg) now became effective after SNL.

26 drug effect was significantly enhanced after SNL (p<0.05).

27 ated p38 was transiently elevated 5 hr after SNL and returned to baseline by 1 d after SNL.

28 tile allodynia or thermal hyperalgesia after SNL, but it increases cold allodynia 6h after applicatio

29 Adjacent neurons (L4 after SNL) exhibit increased I(K(Ca)) current.

30 tivation was found in spinal microglia after SNL, which had fallen to near basal level by 21 d.

31 g patterns in uninjured L4 DRG neurons after SNL, in the presence or absence of TTX, were not affecte

32 tly upregulated in spinal cord neurons after SNL, resulting in spinal astrocyte activation via CXCR5

33 s are increased in adjacent L4 neurons after SNL.

34 e identified in injured L5 DRG neurons after SNL.

35 pregulated in uninjured L4 DRG neurons after SNL.

36 lyzed for total and phosphorylated p38 after SNL alone or SNL combined with etanercept pretreatment.

37 C-fiber-evoked dorsal horn potentials after SNL, which was prevented by mGluR1 antagonist AIDA [(RS)

38 SNL, showing that upregulation of SOCE after SNL is driven by store depletion.

39 These data indicate that after SNL treatment, phosphorylated p38 levels in spinal cord

40 ured DRG neurons are sensitized to TNF after SNL.

41 was resistant (>40%) to 100 microm TTX after SNL, whereas both A- and C-fiber components of sciatic n

42 tective effect of dermorphin-saporin against SNL-induced pain was blocked by beta-funaltrexamine, a s

43 RVM dermorphin or saporin did not alter SNL-induced experimental pain, and no pretreatment affec

44 In nerve injury models, AXO, PSNL, CCI, and SNL caused changes to the largest number of gait indices

45 ecreased by 5-HT2CR knockdown in control and SNL conditions to a similar degree.

46 chondrial Ca(2+) release in most Control and SNL L4 neurons, this usually failed to release mitochond

47 neuregulins blocked the effects of GDNF and SNL-CM, suggesting that both neuregulin and GDNF are req

48 t significantly different in non-injured and SNL-injured DRG neurons.

49 lectrophysiology in naive, sham-operated and SNL rats demonstrated that application of ice to recepti

50 increased both innocuous (sham-operated and SNL rats) and noxious (SNL rats) receptive field sizes o

51 els of endocannabinoids in sham-operated and SNL rats.

52 ile and thermal hypersensitivity, as well as SNL-induced upregulation of spinal dynorphin.

53 3 in the spinal cord persistently attenuated SNL-induced neuropathic pain.

54 Autochthonous SNL meat showed a higher nutraceutical quality compared

55 mitochondrial Ca(2+) buffering in axotomized SNL L5 neurons but enhanced Ca(2+) buffering by neurons

56 Because SNL-CM and GDNF-like molecules stimulated the formation

57 Treatment starting 2 d before SNL with the TNF antagonist etanercept (1 mg, i.p., ever

58 Comparisons were made between SNL rats and a sham-operated group.

59 RVM lidocaine blocked SNL-induced tactile and thermal hypersensitivity on post

60 aments 1-75 g) were markedly reduced in both SNL and control groups.

61 sis that the rescued penumbra is affected by SNL.

62 d STIM1 and Orai1 levels were not altered by SNL, showing that upregulation of SOCE after SNL is driv

63 hyperalgesia and tactile allodynia caused by SNL but had no significant effect on the normal nocicept

64 mized neurons from rats made hyperalgesic by SNL lost sensitivity to the myristoylated form of autoca

65 y with the degree of hyperalgesia induced by SNL in the rats from which the neurons were isolated.

66 CXCR5 expression induced by SNL was required for the SNL-induced activation of spina

67 d the mechanical hypersensitivity induced by SNL.

68 control of mGluR1 upregulation triggered by SNL.

69 between WT and KO mice and were unchanged by SNL injury.

70 In contrast, SNL induces a delayed (>3 d) activation of p38 in the L5

71 leukemia inhibitory factor (LIF)-expressing SNL feeders, frequently had two Xas.

72 In fact, SNL cells were found to express 100-fold higher levels o

73 al and mechanical hypersensitivity following SNL.

74 mal and mechanical pain thresholds following SNL were increasingly reversed over the days after injur

75 failed to release mitochondrial Ca(2+) from SNL L5 neurons.

76 r of CaMKII, whereas axotomized neurons from SNL animals that failed to develop hyperalgesia showed n

77 d ectopic in an ex vivo DRG preparation from SNL rats.

78 Enhanced, evoked CGRP release from SNL rats was blocked by anti-dynorphin A(1-13) antiserum

79 rom BLA to CeA recorded in brain slices from SNL rats using whole-cell patch-clamp conditions.

80 rkedly enhanced in lumbar spinal tissue from SNL rats when compared with sham-operated controls.

81 Furthermore, SNL induced a rapid (<12 h) but transient activation of

82 Furthermore, SNL induced CXCR5 expression in spinal astrocytes, and n

83 es with the rank order being AXO>PSNL=CCI >> SNL.

84 However, SNL-induced upregulation of GFAP was not attenuated by s

85 In SNL rats, subthreshold doses of TNF synergized with nerv

86 oads, the releasable mitochondrial Ca(2+) in SNL L5 neurons was less than Control while it was increa

87 ike firing, and increased burst activity) in SNL rats.

88 lus oligomycin elevated resting [Ca(2+)]c in SNL L4 neurons more than in Control neurons.

89 s the subsequent RIM1alpha/CaV2.2 cascade in SNL-induced neuropathic pain.

90 ion of 5-HT2CR in non-GABAergic BLA cells in SNL rats.

91 neurones, which was significantly greater in SNL rats than naive and sham-operated rats.

92 tor (GDNF)-like molecules were identified in SNL-CM and recombinant forms of GDNF, neurturin, and art

93 ays of metabolism have greater importance in SNL rats.

94 less than Control while it was increased in SNL L4 neurons.

95 nuated evoked responses of spinal neurons in SNL rats but did not alter hindpaw levels of endocannabi

96 tsynaptic currents of dorsal horn neurons in SNL rats.

97 acilitating mechanically-evoked responses in SNL rats.

98 Due to the collective plasmonic responses in SNL, these ultrathin 2D films display rapid and reversib

99 resulted in a 72% reduction of GLU uptake in SNL rats compared to sham controls in the ipsilateral L5

100 t is tempting to speculate that peri-infarct SNL could represent a new therapeutic target.

101 L5 SNL induced BIP upregulation in the neuron of superficia

102 arkedly altered on days 3, 7, or 14 after L5 SNL in L5 spinal cord or DRG.

103 neurons from hyperalgesic rats following L5 SNL.

104 in the SNR, substantia nigra pars lateralis (SNL), and VTA.

105 ates, a series of single-nanoparticle-layer (SNL) plasmonic films is fabricated.

106 s of spinal neurons in spinal nerve ligated (SNL) rats or hindpaw levels of endocannabinoids.

107 0.02) more neurones of spinal nerve-ligated (SNL) rats responded to brush compared with the sham cont

108 thic pain produced by spinal nerve ligation (SNL) (L5).

109 sts in rats following spinal nerve ligation (SNL) but not sham operation.

110 Axonal injury by spinal nerve ligation (SNL) elevated SOCE and I(CRAC).

111 ad received L5 and L6 spinal nerve ligation (SNL) immediately before injection.

112 perexcitability after spinal nerve ligation (SNL) in rat.

113 Spinal nerve ligation (SNL) in rats significantly increased mRNA and protein le

114 following unilateral spinal nerve ligation (SNL) in rats.

115 Furthermore, spinal nerve ligation (SNL) induced persistent neuropathic pain and MCP-1 upreg

116 Spinal nerve ligation (SNL) injury in rats pretreated with RVM dermorphin-sapor

117 al consequences of L5 spinal nerve ligation (SNL) injury.

118 Using the spinal nerve ligation (SNL) model of neuropathic pain, we found that CXCL13 was

119 ceral pain, and a rat spinal nerve ligation (SNL) model of neuropathic pain.

120 behaviors in the rat spinal nerve ligation (SNL) model.

121 the rat hot plate and spinal nerve ligation (SNL) models of acute and neuropathic pain, respectively,

122 as the hot plate and spinal nerve ligation (SNL) models of acute and neuropathic pain.

123 amined the effects of spinal nerve ligation (SNL) on the number of neurons in the rostral ventromedia

124 Spinal nerve ligation (SNL) produced expected tactile and thermal hyperesthesia

125 rats induced by L5/L6 spinal nerve ligation (SNL) via electrophysiological and neurochemical approach

126 ve transection (SNT), spinal nerve ligation (SNL), and chronic constriction injury (CCI).

127 made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP) channel activity was decreased, and s

128 After spinal nerve ligation (SNL), both wild-type (WT) and KO mice demonstrated decre

129 als in rats receiving spinal nerve ligation (SNL), but not in uninjured rats.

130 behavior after L5/L6 spinal nerve ligation (SNL), implicating a critical functional role of Na(V)1.8

131 ats, we reported that spinal nerve ligation (SNL), in addition to causing allodynia, enhances the Rab

132 hy, unilateral lumbar spinal nerve ligation (SNL), to characterize the distribution of alpha(2)delta-

133 lammatory pain and L5 spinal nerve ligation (SNL)-induced neuropathic pain in rats.

134 R) activation in a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain model.

135 ) neurons after L5/L6 spinal nerve ligation (SNL).

136 r pain behavior after spinal nerve ligation (SNL).

137 re induced in rats by spinal nerve ligation (SNL).

138 tested in rats after spinal nerve ligation (SNL).

139 root ganglia after L5 spinal nerve ligation (SNL).

140 wnregulated following spinal nerve ligation (SNL).

141 y in rats after L5-L6 spinal nerve ligation (SNL).

142 We observed that spinal nerve ligation (SNL, L5) in male Sprague Dawley rats resulted in behavio

143 ated and neuropathic (spinal nerve ligation, SNL) rats using in vivo electrophysiology to elucidate t

144 nerve ligation; PSNL, spinal nerve ligation; SNL or chronic constriction injury; CCI).

145 dium conditioned by the SNL fibroblast line (SNL-CM) is able to stimulate primary cultures of rat typ

146 s DRGs with injured spinal nerves) of living SNL rats.

147 WNS, FNW, HNA, FNS, SNK, GNV, HNH, SNY, LNW, SNL, NNF, DNA, GNS, and FNR showed no deamidation.

148 Selective neuronal loss (SNL) in the rescued penumbra could account for suboptima

149 issimus dorsi muscle from Suino Nero Lucano (SNL) and a modern crossbred (CG) pigs, before and after

150 antitative (11)C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tissue and assess its relations

151 In WT mice, SNL upregulated lumbar dynorphin content on day 10, but

152 so includes a C-terminal PDZ-binding motif (-SNL).

153 the electrophysiological responses of naive, SNL-injured, or adjacent uninjured DRG to TNF (0.1-1000

154 Ligation of the L5 spinal nerve (SNL) on one side in adult rats produces an early onset a

155 r tight ligation of L5 and L6 spinal nerves (SNL).

156 hrough tight ligation of L5/6 spinal nerves (SNL).

157 oscintigraphy (LSG) for sentinel lymph node (SNL) mapping in a woman with a breast mass presents an u

158 y passage Xa/Xi hiPSC lines generated on non-SNL feeders were converted into Xa/Xa hiPSC lines after

159 us (sham-operated and SNL rats) and noxious (SNL rats) receptive field sizes of WDR neurones.

160 In the absence of SNL, pharmacological stimulation of 5-HT(2A)R with TCB-2

161 ength differently, we purified components of SNL-CM to identify the additional contributing factor(s)

162 ior similar to that seen on feeder layers of SNL fibroblasts.

163 d rats or the contralateral sciatic nerve of SNL rats.

164 ater PO period the proportion of neurones of SNL rats responsive to prod was significantly (P = 0.007

165 morphin-saporin did not prevent the onset of SNL-induced tactile and thermal hypersensitivity, but th

166 funiculus (DLF) did not prevent the onset of SNL-induced tactile and thermal hypersensitivity, but th

167 magnitude of the evoked neuronal response of SNL rats at PO days 7-10 was comparable to that of the s

168 In addition, neuronal responses of SNL rats to mechanical punctate stimuli and the C fibre-

169 brush- and prod-evoked neuronal responses of SNL rats were significantly smaller (P = 0.05 and P = 0.

170 Previous studies of SNL used single-photon emission tomography (SPECT), did

171 ehaviors and increased sensory thresholds of SNL rats, but had no effect in sham controls.

172 Chronic PGB treatment of SNL animals, at a dose that alleviated allodynia, marked

173 Xa/Xa hiPSC lines after several passages on SNL feeders, and supplementation with recombinant LIF ca

174 al and phosphorylated p38 after SNL alone or SNL combined with etanercept pretreatment.

175 III, or IV of the dorsal horn in the CCI or SNL models.

176 g of WDR neurones in naive, sham-operated or SNL rats but inhibited mechanically-evoked responses of

177 reversed neuropathic pain in WT mice at post-SNL day 10 (when dynorphin was upregulated) but not on p

178 KO mice showed a return to baselines by post-SNL day 10.

179 n dynorphin was upregulated) but not on post-SNL day 2; intrathecal MK-801 reversed SNL-pain at both

180 tivity on post-SNL days 6-12 but not on post-SNL day 3.

181 eversed to baseline levels beginning on post-SNL day 4.

182 eversed to baseline levels beginning on post-SNL day 4.

183 tactile and thermal hypersensitivity on post-SNL days 6-12 but not on post-SNL day 3.

184 he pathogenesis of cold allodynia in the rat SNL model, but it is a potential mechanism for the analg

185 In rats receiving SNL, we found that the number of RVM neurons decreased b

186 t with the TNF antagonist etanercept reduced SNL-induced allodynia by almost 50%.

187 NA expression (10 mug, 10 mul; i.t.) reduced SNL-induced allodynia, kalirin and pNR2B expression, as

188 te, starting before the SNL surgery, reduces SNL-induced mechanical allodynia from day 1 to day 10, w

189 nto the L5 DRG prevented but did not reverse SNL-induced mechanical allodynia.

190 post-SNL day 2; intrathecal MK-801 reversed SNL-pain at both times.

191 esponses but potently prevented and reversed SNL-induced mechanical allodynia, a major symptom of neu

192 -1/CB neurons were also detected in the SNC, SNL, and VTA.

193 CR neurons were distributed in the SNC, SNR, SNL, and VTA.

194 Intrathecal D-JNKI-1 also suppressed SNL-induced phosphorylation of the JNK substrate, c-Jun,

195 ; and a downstream site where the C-terminal SNL (Ser-Asn-Leu) tripeptide of the channel interacts wi

196 These results suggest that SNL leads to hypoglutamatergic neurotransmission in the

197 The SNL L4 neurons showed decreased transient peak and area

198 a the intrathecal route, starting before the SNL surgery, reduces SNL-induced mechanical allodynia fr

199 Lesions of the DLF also blocked the SNL-induced increase in spinal dynorphin content, which

200 of somatic cells, medium conditioned by the SNL fibroblast line (SNL-CM) is able to stimulate primar

201 pression induced by SNL was required for the SNL-induced activation of spinal astrocytes and microgli

202 ith a significantly higher proportion in the SNL and CCI models, compared with SNT.

203 tric field distribution between AuNPs in the SNL film, based on which responsive surface-enhanced Ram

204 In the SNL model, mechanical allodynia failed to develop 1 and

205 astrocytes of the spinal dorsal horn in the SNL model.

206 ng SNL showed a time-related reversal of the SNL-induced experimental pain to preinjury baseline leve

207 scending influences can underlie some of the SNL-induced plasticity at the spinal level.

208 of spinal RIM1alpha expression reversed the SNL-induced allodynia and increased spontaneous EPSC (sE

209 area compared to control neurons, while the SNL L5 neurons showed increased shoulder level.

210 spinal cord was 15-30% lower, ipsilateral to SNL.

211 -HT) neurons decreased by 35% ipsilateral to SNL.

212 e DLF-lesioned or dermorphin-saporin-treated SNL rats did not exhibit enhanced capsaicin-evoked CGRP-

213 targeting signal, the C-terminal tripeptide 'SNL'.

214 or saporin, in animals previously undergoing SNL showed a time-related reversal of the SNL-induced ex