ライフサイエンスコーパス: excitotoxicity

1 rning tasks) and pathologic processes (e.g., excitotoxicity).

2 ns in vitro in response to glutamate-induced excitotoxicity.

3 on, maintained field potentials, and blocked excitotoxicity.

4 ate (NMDA) receptors to protect neurons from excitotoxicity.

5 ycosides, contrasting with current models of excitotoxicity.

6 osis (MS), as well as in kainic acid-induced excitotoxicity.

7 tochondrial depolarization and resistance to excitotoxicity.

8 ce to oxidative stress and glutamate-induced excitotoxicity.

9 d, thus, to regulate synaptic plasticity and excitotoxicity.

10 e in the brain may cause neuronal damage via excitotoxicity.

11 rs neuroprotection from in vitro and in vivo excitotoxicity.

12 ng protein ADARB2, and (4) susceptibility to excitotoxicity.

13 cells (RGCs) and their axons after inducing excitotoxicity.

14 ebral perfusion preventing glutamate-induced excitotoxicity.

15 of mitochondrial Ca(2+) uptake, in neuronal excitotoxicity.

16 survival to a mediator of neuronal death in excitotoxicity.

17 hyl-D-aspartate (NMDA) receptor and inducing excitotoxicity.

18 ing susceptibility to NMDA receptor-mediated excitotoxicity.

19 agent in diseases involving calcium-related excitotoxicity.

20 lecular target for clinical intervention for excitotoxicity.

21 t (18Q), and increased vulnerability to NMDA excitotoxicity.

22 protected cortical neurons from NMDA-induced excitotoxicity.

23 hearii and found to protect CNS neurons from excitotoxicity.

24 neurodegenerative diseases characterized by excitotoxicity.

25 receptors participate prominently in hypoxic excitotoxicity.

26 eath following transient global ischemia and excitotoxicity.

27 urons against oxygen-glucose deprivation and excitotoxicity.

28 proach to preventing neuronal AMPAR-mediated excitotoxicity.

29 uN2 subtype influences NMDA receptor (NMDAR) excitotoxicity.

30 es in synaptic transmission, plasticity, and excitotoxicity.

31 mpal glutamatergic terminals defends against excitotoxicity.

32 icotinamide also protected against glutamate excitotoxicity.

33 ptor subunits also contributes critically to excitotoxicity.

34 nd much more so during neuroinflammation and excitotoxicity.

35 mate transporter EAAT2, leading to glutamate excitotoxicity.

36 pine formation and neuronal vulnerability to excitotoxicity.

37 ing in glomeruli and from mediating neuronal excitotoxicity.

38 ts, may increase the risk of dopamine neuron excitotoxicity.

39 number in response to sublethal NMDA-induced excitotoxicity.

40 he earliest indications of glutamate-induced excitotoxicity.

41 hronic neurodegenerative insults mediated by excitotoxicity.

42 y be involved in neuronal survival following excitotoxicity.

43 rons, such as burst firing and resistance to excitotoxicity.

44 mechanism may render DA cells vulnerable to excitotoxicity.

45 fects of NAD(+) and NR in protection against excitotoxicity.

46 e effect of mAChR activation on KAR-mediated excitotoxicity.

47 ng retinal neurons against glutamate-induced excitotoxicity.

48 acrine and ganglion cells to kainate-induced excitotoxicity.

49 ium influence NMDAR expression/signaling and excitotoxicity.

50 One potential mechanism is excitotoxicity.

51 ion and increases neuronal susceptibility to excitotoxicity.

52 abolism, glial cell pathology, and glutamate excitotoxicity.

53 not Prkdc(-/-) neurons from kainate-induced excitotoxicity.

54 ning is effective primarily against necrotic excitotoxicity.

55 ne its efficacy for reversal of experimental excitotoxicity.

56 activity does increase and may contribute to excitotoxicity.

57 ruling out the SR as a source of increasing excitotoxicity.

58 ion, growth factor deficiency, and glutamate excitotoxicity.

59 and lithium will alter NMDAR expression and excitotoxicity.

60 regulation diminishes neuronal resistance to excitotoxicity.

61 cker, is effective in reversing experimental excitotoxicity.

62 ted with increased vulnerability to synaptic excitotoxicity.

63 s resulted in complete blockade of glutamate excitotoxicity.

64 ocyte precursor cells are more vulnerable to excitotoxicity.

65 ing of GluR2-lacking receptors which enhance excitotoxicity.

66 licated in both normal neurotransmission and excitotoxicity.

67 important roles in synaptic transmission and excitotoxicity.

68 to neurodegeneration previously ascribed to excitotoxicity.

69 its enzymatic activity protects neurons from excitotoxicity.

70 ular processes that underlie NMDAR-dependent excitotoxicity.

71 n of the inflammatory response and glutamate excitotoxicity.

72 d-mediated neuroprotection and NMDA-mediated excitotoxicity.

73 t cortical neurons against glutamate-induced excitotoxicity.

74 synaptic hyperactivity and direct glutamate excitotoxicity.

75 ct synaptic responses and glutamate-mediated excitotoxicity.

76 ry occlusion (MCAO) and an in vitro model of excitotoxicity.

77 erapeutic strategies to protect neurons from excitotoxicity.

78 f cortical neurons to proteotoxic stress and excitotoxicity.

79 al neurons (L5-PNs) and contributed to their excitotoxicity.

80 Akt-1 activation and neuroprotection against excitotoxicity.

81 signalling and preventing glutamate-mediated excitotoxicity.

82 tervention in NOS1AP-dependent signaling and excitotoxicity.

83 tribute to this susceptibility by increasing excitotoxicity.

84 is in the brain as a result of glutamatergic excitotoxicity.

85 tes neuronal survival following NMDA-induced excitotoxicity.

86 ase-3 activation and NMDA receptor-dependent excitotoxicity.

87 n excitatory amino-acid transporter to cause excitotoxicity.

88 nduced increases in glutamate and subsequent excitotoxicity.

89 S), in the developing brain, consistent with excitotoxicity; (2) decreased protective capacity agains

90 Sustained elevated calcium levels trigger excitotoxicity, a characteristic event in Alzheimer's di

91 Excitotoxicity, a critical process in neurodegeneration,

92 Glutamate excitotoxicity, a major component of many neurodegenerat

93 nNOS) and p38MAPK are strongly implicated in excitotoxicity, a mechanism common to many neurodegenera

94 a NMDAR, and excess calcium influx increases excitotoxicity--a pathological characteristic of neurolo

95 tic manipulations that exacerbate or prevent excitotoxicity also exacerbated or prevented the enkepha

96 Interestingly, excitotoxicity also induced an accumulation of intracell

97 otection against stresses such as stroke and excitotoxicity, although the underlying mechanisms are n

98 ane, thereby rendering neurons vulnerable to excitotoxicity and apoptosis.

99 In excitotoxicity and axotomy models retinal ganglion cell

100 this sense NCX3 plays a key role in neuronal excitotoxicity and Ca(2+) extrusion during skeletal musc

101 aracterize cellular and molecular aspects of excitotoxicity and conduct therapeutic screening for pha

102 activation of glutamate receptors results in excitotoxicity and delayed cell death in vulnerable neur

103 ive activation of glutamate receptors causes excitotoxicity and delayed cell death in vulnerable neur

104 Moreover, excitotoxicity and down-regulation of CREB were exaggera

105 ng that was neuroprotective against CA1 area excitotoxicity and followed a U-shaped or hormetic dose-

106 these disorders, glutamate receptor-mediated excitotoxicity and free radical formation have been corr

107 lue-epinephrine association avoided neuronal excitotoxicity and had an additive effect both on hemody

108 ling technologies cannot distinguish between excitotoxicity and hypoxia, however, because they share

109 es improved cellular responses to oxidative, excitotoxicity and inflammatory injuries and this attenu

110 ograde degeneration following axonal damage, excitotoxicity and inflammatory/autoimmune mechanisms.

111 to necrotic propagation in mammals--e.g., in excitotoxicity and ischemia-induced neurodegeneration.

112 he protection from pharmacologically induced excitotoxicity and middle cerebral artery occlusion-indu

113 a is protective in vivo against NMDA-induced excitotoxicity and middle cerebral artery occlusion-indu

114 y controlled synaptic activity that leads to excitotoxicity and neurodegeneration.SIGNIFICANCE STATEM

115 ar milieu, which is strongly associated with excitotoxicity and neuronal degeneration.

116 ceptors (P2X7Rs) are closely associated with excitotoxicity and nociception.

117 Furthermore, the reduced seizure and excitotoxicity and normal spatial learning exhibited in

118 In particular, E2 is neuroprotective against excitotoxicity and other forms of brain injuries, a prop

119 y; (2) decreased protective capacity against excitotoxicity and oxidative stress including reduced ta

120 also for Parkinson's disease, which involves excitotoxicity and oxidative stress.

121 neuronal loss, the latter caused in part by excitotoxicity and oxidative stress.

122 llowing OGD that has the potential to reduce excitotoxicity and promote neuroprotection.

123 phyrin subsequently exacerbated SSC-mediated excitotoxicity and promoted loss of GABAergic synapses.

124 echanism by which neurons are protected from excitotoxicity and provide a possible explanation for ne

125 te molecular mechanisms of glutamate-induced excitotoxicity and screen for candidate therapeutics.

126 spinal cords to examine interactions between excitotoxicity and the presence of mutant SOD1 in the in

127 ) to SGN synapse is susceptible to glutamate excitotoxicity and to acoustic trauma, with potentially

128 ression has been reported to protect against excitotoxicity and to prevent memory deficits in mice ex

129 anifest more severe brain damage after acute excitotoxicity and transient cerebral ischemia than do c

130 eurons were highly sensitive to NMDA-induced excitotoxicity and were more susceptible to developmenta

131 mall GTPases, iron transport, p38MAPK-linked excitotoxicity, and anxiety.

132 Optic nerve crush, excitotoxicity, and elevated intraocular pressure (IOP)

133 ith clinical exacerbation, leading to edema, excitotoxicity, and entry of serum proteins and inflamma

134 matinolysis, cell death induced by glutamate excitotoxicity, and focal stroke.

135 ry events, including ischemia, inflammation, excitotoxicity, and free-radical release, contribute to

136 ological disorder characterized by seizures, excitotoxicity, and inflammation.

137 lesion pathogenesis, predisposing to oedema, excitotoxicity, and ingress of plasma proteins and infla

138 is response acts against protein misfolding, excitotoxicity, and neurotoxic reactive oxygen species.

139 a new interaction between acidotoxicity and excitotoxicity, and provide insight into the role of ASI

140 eurons have higher vulnerability to in vitro excitotoxicity, and SCaMC-3 KO mice are more susceptible

141 ons are more vulnerable to glutamate-induced excitotoxicity, and that co-treatment with the mood stab

142 ished activity-dependent Ab secretion and/or excitotoxicity, and thus also promotes neuroprotection.

143 letion of bok also increased staurosporine-, excitotoxicity-, and oxygen/glucose deprivation-induced

144 genes whose overexpression protects against excitotoxicity: anti-apoptotic Bcl-2, and a calcium-acti

145 NCE STATEMENT Neuronal hyperexcitability and excitotoxicity are increasingly recognized as important

146 NMDA- and oxygen glucose deprivation-induced excitotoxicity as well as NMDAR-mediated elevation of in

147 ut excessive tonic NMDAR activation mediates excitotoxicity associated with many neurological disorde

148 y increased ambient glutamate contributes to excitotoxicity associated with various acute and chronic

149 dynorphin-mediated potentiation of glutamate excitotoxicity at cochlear Type-I auditory dendrites tha

150 as effective in reversing acute experimental excitotoxicity at concentrations that have little effect

151 d synaptic plasticity at 2 months of age and excitotoxicity at later stages.

152 ocarpine significantly enhances KAR-mediated excitotoxicity both in the presence and absence of Con A

153 ive against glutamate NMDA receptor-mediated excitotoxicity both in vitro and in vivo and against str

154 agent, not only in diseases associated with excitotoxicity, but also in those of iron overload.

155 rotected spinal cord neurons from purinergic excitotoxicity, but also reduced local inflammatory resp

156 ced survival signaling or protection against excitotoxicity, but exogenous EGFR rescues both function

157 M kainate suppressed cellular GSH and caused excitotoxicity, but GSH levels and cell viability were c

158 h prevents the protective role of lactate on excitotoxicity, but not glutamate excitotoxicity itself.

159 ceptors and are essential for plasticity and excitotoxicity, but their functions are incompletely def

160 o early changes in membrane potential during excitotoxicity, but their precise role in these events i

161 Here the authors show that tau promotes excitotoxicity by a post-synaptic mechanism, involving s

162 TRPC5 and TRPC1/4 contribute to seizure and excitotoxicity by distinct cellular mechanisms.

163 We next asked whether we could decrease excitotoxicity by overexpressing NR3A.

164 leus; [3] sodium salicylate induces an acute excitotoxicity by potentiating glutamate neurotransmitte

165 Contrary to this model, we find that excitotoxicity can proceed without increased Ser-1303 ph

166 this protein can lead to cell damage through excitotoxicity, consistent with the observed Purkinje ce

167 ar glutamate accumulation and the subsequent excitotoxicity contribute significantly to ischemic brai

168 ost-synaptic compartmentalization of SynGAP1.Excitotoxicity contributes to neuronal injury following

169 AMPA-kainate receptor induced excitotoxicity contributes to oligodendrocyte precursor

170 Glutamate excitotoxicity contributes to the neuronal injury and de

171 neurotransmitter glutamate, termed glutamate excitotoxicity, contributes to the damage and degenerati

172 type glutamate receptors (NMDARs) results in excitotoxicity, contributing to damage in stroke and neu

173 I therefore examined whether glutamate excitotoxicity damages hair cells in zebrafish larvae ex

174 While genes related to excitotoxicity, dopamine signaling and trophic support w

175 may contribute to cortical vulnerability to excitotoxicity during the critical period for perinatal

176 synaptic toxicity through hyperactivity, and excitotoxicity following the accumulation of extracellul

177 Experimental excitotoxicity had little or no effect on ERG responses.

178 Glutamate excitotoxicity has been characterized in cochlear nerve

179 cular pathways, including glutamate-mediated excitotoxicity, has been identified in sporadic and fami

180 disease oxidative stress and calcium-induced excitotoxicity have been considered important mechanisms

181 non-neuronal cells results in cell death by excitotoxicity, hindering the development of cell-based

182 nerve fibers and helps control noise-induced excitotoxicity; however, the literature on cochlear expr

183 n, (ii) early vulnerability to NMDA-mediated excitotoxicity, (iii) impairments in motor coordination,

184 Our findings link inflammation and excitotoxicity in a potential vicious circle and indicat

185 ibly responsible for the exacerbated in vivo excitotoxicity in aralar(+/-)mice.

186 nhancing glutamate-mediated transmission and excitotoxicity in central neurons.

187 ed neuronal inhibition and may contribute to excitotoxicity in cerebral ischemia.

188 alyzed in two paradigms of glutamate-induced excitotoxicity in cortical neurons: glucose deprivation

189 A and prevented protection against glutamate excitotoxicity in glial primary cultures.

190 ticularly important for preventing glutamate excitotoxicity in HD.

191 tional interaction between acidotoxicity and excitotoxicity in hippocampal CA1 cells, and provide ins

192 to multiple insults, including glutamatergic excitotoxicity in hippocampal neurons, chemotherapy-indu

193 argeting mitochondrial energy regulation and excitotoxicity in ischemic WM injury.

194 flammation-induced sensitization to neuronal excitotoxicity in neonatal and adult neurons across spec

195 er, PRR7 knockdown attenuates NMDAR-mediated excitotoxicity in neuronal cultures in a c-Jun-dependent

196 e receptors (NMDARs), which are critical for excitotoxicity in neurons.

197 rations in neuronal excitability and enhance excitotoxicity in part by potentiating KAR function.

198 s been no in vivo demonstration of glutamate excitotoxicity in preterm infants.

199 lts demonstrate a role for glutamate-induced excitotoxicity in PrP-mediated neurodegeneration.

200 ound that TNF-alpha exacerbated AMPA-induced excitotoxicity in Purkinje neurons in a dose-dependent m

201 characterized bioenergetics during transient excitotoxicity in rat and mouse primary neurons at the s

202 The effects may reduce the risk of excitotoxicity in SNc DA neurons and may also counteract

203 nsures crisp excitatory signaling and limits excitotoxicity in the CNS.

204 rect in vivo evidence of NR2B-NMDAR-mediated excitotoxicity in the context of HD.

205 ng of the nervous system and for suppressing excitotoxicity in the developing hippocampus.

206 urrent studies suggest the role of glutamate excitotoxicity in the development and progression of mul

207 Findings from this study support glutamate excitotoxicity in the pathogenesis of punctate white mat

208 duce secondary alterations via NMDA-mediated excitotoxicity in these other pathways that prevents the

209 When challenged with excitotoxicity in vitro (via the glutamate agonist NMDA)

210 a demonstrate that IQACRG protects RGCs from excitotoxicity in vitro and in vivo.

211 th respect to control animals, in a model of excitotoxicity in which increased L-lactate levels and L

212 Neuronal excitotoxicity induced by aberrant excitation of glutama

213 Excitotoxicity induced by kainic acid (KA) caused GSK-3b

214 r staurosporine-, proteasome inhibition-, or excitotoxicity-induced apoptosis of cultured cortical ne

215 better neuroprotective agent than NAD(+) in excitotoxicity-induced AxD and that axonal protection in

216 side, a form of vitamin B3, protects against excitotoxicity-induced axonal degeneration.

217 leucine zipper kinase (DLK) is essential for excitotoxicity-induced degeneration of neurons in vivo.

218 additional source of energy during and after excitotoxicity-induced energy depletion.

219 n was up-regulated in microglia activated by excitotoxicity-induced hippocampal neuroinflammation.

220 or protecting neurons from inflammation- and excitotoxicity-induced neurodegeneration.

221 ts indicate that PKD1 inactivation underlies excitotoxicity-induced neuronal death and suggest that P

222 tional consequence, glycine protects against excitotoxicity-induced neuronal death through the non-io

223 neonatal HI-induced CNS injury by inhibiting excitotoxicity-induced, caspase-independent injury to ne

224 y during glutamate receptor overactivation ("excitotoxicity") induces acute or delayed neuronal death

225 These mechanisms involve oxidative stress, excitotoxicity, inflammation, and the activation of seve

226 Thus, NMDA-induced excitotoxicity involves a mechanism that requires the pe

227 Excitotoxicity is a condition occurring during cerebral

228 arget for the treatment of indications where excitotoxicity is a primary driver of neuronal loss.

229 Excitotoxicity is believed to be the main cause for isch

230 Glutamate excitotoxicity is caused by sustained activation of neur

231 Excitotoxicity is caused mainly by overactivation of the

232 Glutamate excitotoxicity is hypothesized to be a key mechanism in

233 methyl-D-aspartate receptor (NMDAR)-mediated excitotoxicity is implicated as a proximate cause of neu

234 To examine whether glutamate excitotoxicity is involved in establishing these deficit

235 The key GluN2B CTD-centred event in excitotoxicity is proposed to involve its phosphorylatio

236 Excitotoxicity is the prevalent model to explain ictal n

237 Cerebral ischemia leading to excitotoxicity is thought to be important in the pathoge

238 ediated damage, in addition to inhibition of excitotoxicity, is a mechanism by which these drugs prot

239 (PARP-1) is a key mediator of cell death in excitotoxicity, ischemia, and oxidative stress.

240 While NMDA receptors play a major role in excitotoxicity, it is thought to be exacerbated in this

241 lactate on excitotoxicity, but not glutamate excitotoxicity itself.

242 To induce excitotoxicity, kainic acid (KA) was injected into the v

243 Excitotoxicity led to the NMDAR-dependent degradation of

244 effect on the extent of TAI, suggesting that excitotoxicity may not be a primary mechanism underlying

245 c injury, which include therapeutics against excitotoxicity, may be successful against the progressiv

246 lling and neuronal cell death, suggestive of excitotoxicity mediated by NMDAR over-activation.

247 Glutamate-induced excitotoxicity, mediated by overstimulation of N-methyl-

248 cytes in particular are highly vulnerable to excitotoxicity, mediated through activation of AMPA/kain

249 Glutamate excitotoxicity might contribute to the pathophysiology o

250 receptor function and a rabbit retinal NMDA excitotoxicity model to verify in vitro findings under i

251 Brimonidine protects RGCs in the rabbit excitotoxicity model.

252 and showed substantial neuroprotection in an excitotoxicity model.

253 tors and rat glaucoma or rabbit retinal NMDA excitotoxicity models to verify in vitro findings under

254 entails an ischemic period that can lead to excitotoxicity, neuroinflammation, and subsequent neurol

255 Excitotoxicity occurs in multiple neurologic disorders a

256 Excitotoxicity of the retina was induced by intravitreal

257 n tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity.

258 Dependence of NMDAR excitotoxicity on the GluN2 CTD subtype can be overcome

259 the "traditional" inhibitor KN93 attenuated excitotoxicity only when present during the insult.

260 utic strategy in SCS and other conditions of excitotoxicity or Ca(2+) overload.

261 uroprotective when neurons were subjected to excitotoxicity or cortical slices were exposed to ischem

262 ot protect primary neurons against glutamate excitotoxicity or hydrogen peroxide, but decreased ICAM-

263 ing damage to SGN peripheral axons caused by excitotoxicity or noise in vivo.

264 itions and did not protect against glutamate excitotoxicity or oxygen-glucose deprivation.

265 on known canonical pathways associated with excitotoxicity, oxidative stress, mitochondrial dysfunct

266 lts suggest that synaptic NMDARs can mediate excitotoxicity, particularly when the glutamate source i

267 Glutamate excitotoxicity plays a role in white matter injury in ma

268 NMDA receptor (NMDAR)-mediated excitotoxicity plays an important role in several CNS di

269 th caused by excessive excitatory signaling, excitotoxicity, plays a central role in neurodegenerativ

270 Unexpectedly, we find that excitotoxicity provokes an early inactivation of PKD1 th

271 Excitotoxicity, reactive oxygen species-producing stimul

272 Glutamate excitotoxicity represents a major cellular component of

273 Excitotoxicity resulting from excessive Ca(2+) influx th

274 Excitotoxicity resulting from overstimulation of glutama

275 neuronal synapses and dendrites against the excitotoxicity seen in apoE-deficient mice.

276 ynaptic locations and play opposing roles in excitotoxicity, such as neurodegeneration triggered by i

277 ble iron chelator substantially reduces NMDA excitotoxicity, suggesting that Dexras1-mediated iron in

278 ure, offering a moderate-throughput model of excitotoxicity that combines the verisimilitude of prima

279 may partly reflect stress-induced glutamate excitotoxicity that culminates in neuron injury and mani

280 iated with metabolic failure of the axon and excitotoxicity that leads to chronic neurodegeneration.

281 To determine if ammonia contributed to excitotoxicity, the effect of METH and lactulose treatme

282 the striatal neurons supports the glutamate excitotoxicity theory for HD pathogenesis.

283 reas at high concentration, the AAbs promote excitotoxicity through enhanced mitochondrial permeabili

284 to confer neuroprotection against KA-induced excitotoxicity to be severely diminished in Syt10 knock-

285 Excessive NMDA receptor activation and excitotoxicity underlies pathology in many neuropsychiat

286 ysregulation of MEF2D by calpain may mediate excitotoxicity via an extrasynaptic NMDAR-dependent mann

287 uroinflammation and is thought to exacerbate excitotoxicity via overproduction of prostaglandins.

288 duced immediate protection against glutamate excitotoxicity (viability 24 h after glutamate exposure:

289 ampal NP proliferation induced by HU-308 and excitotoxicity was blocked by the mTORC1 inhibitor rapam

290 Furthermore, this strategy for alleviating excitotoxicity was found to be beneficial in mouse model

291 Excitotoxicity was measured using fluorescein diacetate/

292 2+ influx into neurons is a crucial step for excitotoxicity, we asked whether NR3A subunits are neuro

293 In a second assay of excitotoxicity, we measured tissue water content as an i

294 n on NMDAR(EX) activity and vulnerability to excitotoxicity were nonadditive and occluded each other,

295 ll bodies and processes against NMDA-induced excitotoxicity, whereas caspase inhibition or B-cell lym

296 However, its abundance can lead to excitotoxicity which necessitates the proper function of

297 AT2 expression have potential for preventing excitotoxicity, which contributes to neuronal injury and

298 its expression as important determinants of excitotoxicity, which may represent therapeutic targets

299 of MEF2D sensitized neurons to NMDA-induced excitotoxicity, which was not protected by calpain inhib

300 s its overexpression prevents NMDA-glutamate excitotoxicity while its depletion enhances death in pri