ライフサイエンスコーパス: excitotoxicity

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

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

3 Akt-1 activation and neuroprotection against excitotoxicity.

4 signalling and preventing glutamate-mediated excitotoxicity.

5 tervention in NOS1AP-dependent signaling and excitotoxicity.

6 tribute to this susceptibility by increasing excitotoxicity.

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

8 tes neuronal survival following NMDA-induced excitotoxicity.

9 n excitatory amino-acid transporter to cause excitotoxicity.

10 nduced increases in glutamate and subsequent excitotoxicity.

11 on, maintained field potentials, and blocked excitotoxicity.

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

13 ycosides, contrasting with current models of excitotoxicity.

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

15 tochondrial depolarization and resistance to excitotoxicity.

16 ce to oxidative stress and glutamate-induced excitotoxicity.

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

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

19 ility of astrocytes, which may contribute to excitotoxicity.

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

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

22 ebral perfusion preventing glutamate-induced excitotoxicity.

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

24 survival to a mediator of neuronal death in excitotoxicity.

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

26 ing susceptibility to NMDA receptor-mediated excitotoxicity.

27 agent in diseases involving calcium-related excitotoxicity.

28 lecular target for clinical intervention for excitotoxicity.

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

30 into the neuron, and protects from glutamate excitotoxicity.

31 other neurological diseases associated with excitotoxicity.

32 protected cortical neurons from NMDA-induced excitotoxicity.

33 hearii and found to protect CNS neurons from excitotoxicity.

34 receptors participate prominently in hypoxic excitotoxicity.

35 eath following transient global ischemia and excitotoxicity.

36 urons against oxygen-glucose deprivation and excitotoxicity.

37 proach to preventing neuronal AMPAR-mediated excitotoxicity.

38 uN2 subtype influences NMDA receptor (NMDAR) excitotoxicity.

39 es in synaptic transmission, plasticity, and excitotoxicity.

40 mpal glutamatergic terminals defends against excitotoxicity.

41 icotinamide also protected against glutamate excitotoxicity.

42 ptor subunits also contributes critically to excitotoxicity.

43 nd much more so during neuroinflammation and excitotoxicity.

44 mate transporter EAAT2, leading to glutamate excitotoxicity.

45 pine formation and neuronal vulnerability to excitotoxicity.

46 ing in glomeruli and from mediating neuronal excitotoxicity.

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

48 number in response to sublethal NMDA-induced excitotoxicity.

49 he earliest indications of glutamate-induced excitotoxicity.

50 hronic neurodegenerative insults mediated by excitotoxicity.

51 y be involved in neuronal survival following excitotoxicity.

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

53 mechanism may render DA cells vulnerable to excitotoxicity.

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

55 ng retinal neurons against glutamate-induced excitotoxicity.

56 acrine and ganglion cells to kainate-induced excitotoxicity.

57 ium influence NMDAR expression/signaling and excitotoxicity.

58 One potential mechanism is excitotoxicity.

59 ion and increases neuronal susceptibility to excitotoxicity.

60 abolism, glial cell pathology, and glutamate excitotoxicity.

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

62 ning is effective primarily against necrotic excitotoxicity.

63 ne its efficacy for reversal of experimental excitotoxicity.

64 activity does increase and may contribute to excitotoxicity.

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

66 ion, growth factor deficiency, and glutamate excitotoxicity.

67 and lithium will alter NMDAR expression and excitotoxicity.

68 its protection of neurons against glutamate excitotoxicity.

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

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

71 rs neuroprotection from in vitro and in vivo excitotoxicity.

72 in pathological conditions such as glutamate excitotoxicity.

73 neurodegenerative diseases characterized by excitotoxicity.

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

75 to neurodegeneration previously ascribed to excitotoxicity.

76 its enzymatic activity protects neurons from excitotoxicity.

77 ular processes that underlie NMDAR-dependent excitotoxicity.

78 n of the inflammatory response and glutamate excitotoxicity.

79 d-mediated neuroprotection and NMDA-mediated excitotoxicity.

80 t cortical neurons against glutamate-induced excitotoxicity.

81 synaptic hyperactivity and direct glutamate excitotoxicity.

82 ct synaptic responses and glutamate-mediated excitotoxicity.

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

84 erapeutic strategies to protect neurons from excitotoxicity.

85 f cortical neurons to proteotoxic stress and excitotoxicity.

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

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

88 Excitotoxicity, a critical process in neurodegeneration,

89 Glutamate excitotoxicity, a major component of many neurodegenerat

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

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

92 Interestingly, excitotoxicity also induced an accumulation of intracell

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

94 rench Polynesian isolate producing primarily excitotoxicity and a Brazilian isolate being almost excl

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

96 nificant enrichment associated with neuronal excitotoxicity and cerebral damage is detected in TBM.

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

98 This imbalance could potentiate glutamate excitotoxicity and contribute to neuronal dysfunction, e

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

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

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

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

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

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

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

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

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

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

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

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

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

112 To determine the additive effects of excitotoxicity and overnutrition on beta-cell function a

113 In addition, excitotoxicity and overnutrition, individually and toget

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 (2+) concentration (referred to hereafter as excitotoxicity), brought on by chronic metabolic stress,

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

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

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

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

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

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

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

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

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

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

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

159 s, thus protecting neurons against glutamate excitotoxicity by reduction of the calcium overload and

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

161 Excitotoxicity caused beta-cells to be more susceptible

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

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

164 AMPA-kainate receptor induced excitotoxicity contributes to oligodendrocyte precursor

165 Excitotoxicity contributes to secondary cell death in ze

166 Glutamate excitotoxicity contributes to the neuronal injury and de

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

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

169 actors in neurodegenerative diseases, namely excitotoxicity, disease-associated RBPs, and nucleocytop

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

171 ings are consistent with the hypothesis that excitotoxicity during the acute phase of illness leads t

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

173 we studied the effects of glutamate-induced excitotoxicity, external osmotic pressure, and inhibitio

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

175 Glutamate excitotoxicity has been characterized in cochlear nerve

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

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

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

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

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

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

182 ronic environmental stress and glutamatergic excitotoxicity in AD, suggesting that targeting of gluta

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

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

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

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

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

188 ticularly important for preventing glutamate excitotoxicity in HD.

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

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

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

192 in KO astrocytes limited astrocyte-dependent excitotoxicity in motor neurons.

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

194 late synaptic transmission and contribute to excitotoxicity in neurological diseases.

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

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

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

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

208 oxide production in response to ischemia and excitotoxicity in vitro and ex vivo Last, deletion of Bb

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

210 RBPs affected by excitotoxicity included TAR DNA-binding protein 43 (TDP-

211 Neuronal excitotoxicity induced by aberrant excitation of glutama

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

213 ry cortical and motor neurons, we found that excitotoxicity induced the translocation of select ALS-l

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 ey regulator Ppargc1a Overnutrition worsened excitotoxicity-induced mitochondrial dysfunction, increa

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 Glutamate excitotoxicity is a pathology in which excessive glutama

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

230 Excitotoxicity is believed to be the main cause for isch

231 Glutamate excitotoxicity is caused by sustained activation of neur

232 Excitotoxicity is caused mainly by overactivation of the

233 Glutamate excitotoxicity is hypothesized to be a key mechanism in

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 Noise-induced excitotoxicity is thought to depend on glutamate.

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

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

240 lactate on excitotoxicity, but not glutamate excitotoxicity itself.

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

242 Excitotoxicity led to the NMDAR-dependent degradation of

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

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

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

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

247 Glutamate excitotoxicity might contribute to the pathophysiology o

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

249 Brimonidine protects RGCs in the rabbit excitotoxicity model.

250 and showed substantial neuroprotection in an excitotoxicity model.

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

252 Excitotoxicity occurs in multiple neurologic disorders a

253 Excitotoxicity of the retina was induced by intravitreal

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

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

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

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

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

259 totic death as well as cell death induced by excitotoxicity or ER stress, which are GPX4 independent.

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

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

262 Excitotoxicity, overnutrition, and the combination of bo

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

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

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

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

267 However, the relationships between excitotoxicity, RBP function, and disease have not been

268 Excitotoxicity, reactive oxygen species-producing stimul

269 s and enhanced vulnerability to NMDA-induced excitotoxicity, reflecting the predominance of GluN2B-co

270 Glutamate excitotoxicity represents a major cellular component of

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

272 Excitotoxicity resulting from overstimulation of glutama

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

289 Excitotoxicity was measured using fluorescein diacetate/

290 The recovery after the glutamate-induced excitotoxicity was slow or absent because of a steady in

291 2+ influx into neurons is a crucial step for excitotoxicity, we asked whether NR3A subunits are neuro

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

293 viscoelastic properties caused by glutamate excitotoxicity were similar to those induced by the hypo

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

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

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

297 s of this neurotransmitter lead to glutamate excitotoxicity, which is accountable for neuronal death

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