ライフサイエンスコーパス: excitotoxic

1 ed serine protease, is also proepileptic and excitotoxic.

2 ted lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons.

3 benefit may perhaps instead involve the anti-excitotoxic action of mGluR2/3 receptor agonists.

4 ceptor, and that has anti-apoptotic and anti-excitotoxic actions, reducing brain damage in adult anim

5 NR2B-containing NMDARs, but, in contrast to excitotoxic activation of extrasynaptic NMDARs, produced

6 Excitotoxic activation of p38MAPK and subsequent neurona

7 uggest that the kidney may be susceptible to excitotoxic agonists, and renal effects should be consid

8 effects within the IT cortex in monkeys with excitotoxic amygdala lesions (n = 3) with those in intac

9 ive lesion techniques, monkeys with complete excitotoxic amygdala lesions performed object reversal l

10 lopmental neuroscience also suggest that the excitotoxic and inflammatory processes that probably con

11 synthetic pathway, previously linked to both excitotoxic and neurotrophic effects.

12 nduced by neurotrophic factor withdrawal and excitotoxic and oxidative insults.

13 njuries and rescues hippocampal neurons from excitotoxic and oxidative insults.

14 ampal neurons against free radical-mediated, excitotoxic, and ischemic insults.

15 eurons to the kinds of metabolic, oxidative, excitotoxic, and proteotoxic stresses involved in the pa

16 lencing of calpain protected neurons against excitotoxic apoptosis but did not influence excitotoxic

17 sitivity to bax-gene deletion, (2) underwent excitotoxic apoptosis, characterized by recovery of NMDA

18 entify when calpains became activated during excitotoxic apoptosis, we monitored calpain activation d

19 esence of compact myelin is not required for excitotoxic axon damage, and its absence may increase vu

20 tau(-/-)) mice are profoundly protected from excitotoxic brain damage and neurological deficits follo

21 methyl-D-aspartate receptor (NMDAR)-mediated excitotoxic brain injury.

22 n and is an alternative energy source during excitotoxic brain injury.

23 we found evidence for early contributions of excitotoxic Ca(2+) and Zn(2+) accumulation in both CA1 a

24 results--showing that the various routes of excitotoxic Ca(2+) entry converge on a common pathway in

25 hereas most studies address contributions of excitotoxic Ca(2+) entry, it is apparent that Zn(2+) als

26 teracted by SCaMC-3, is an early step in the excitotoxic cascade.

27 er, the overactivation of NMDARs can lead to excitotoxic cell damage/death, and as such, they play a

28 unique role for copper in axonal extension, excitotoxic cell death and synaptic plasticity in the ce

29 ipping following rtACS protects neurons from excitotoxic cell death by silencing them.

30 of the primary causes of secondary injury is excitotoxic cell death due to dysregulation of extracell

31 and cell death, a phenotype consistent with excitotoxic cell death in anoxic mammalian brain.

32 age, Ku70-Bax interaction, and Bax-dependent excitotoxic cell death in kainic acid-treated primary co

33 Glutamate is a central tenant in provoking excitotoxic cell death in striatal neurons already weake

34 matrix (ECM) protein laminin contributes to excitotoxic cell death in the hippocampus, but the mecha

35 Excitotoxic cell death is one of the precipitating event

36 We also demonstrate that Slap reduces excitotoxic cell death triggered by activation of NMDARs

37 (2+) level is thought to be a major cause of excitotoxic cell death, but the mechanisms that control

38 t DNA-PKcs links DNA damage to Bax-dependent excitotoxic cell death, by phosphorylating Ku70 on serin

39 ich renders neurons transiently resistant to excitotoxic cell death, can also induce Zn(2+)-dependent

40 tive disease and increased susceptibility to excitotoxic cell death, suggesting a critical but undefi

41 led to a dramatic reduction in the extent of excitotoxic cell death, with slightly greater effects ob

42 ed mitochondrial membrane depolarization and excitotoxic cell death.

43 R(EX) activity and protected neurons against excitotoxic cell death.

44 otection, while extrasynaptic NMDARs promote excitotoxic cell death.

45 nge, indicating that neuronal apoE4 promotes excitotoxic cell death.

46 KAR over-activation has been implicated in excitotoxic cell death.

47 their importance in synaptic plasticity and excitotoxic cell death.

48 R2B contributions to synaptic plasticity and excitotoxic cell death.

49 NPAS4 to protect hippocampal neurons against excitotoxic cell death.

50 n ALS and is suggested to be a precursor for excitotoxic cell death.

51 intracellular Ca(2+) has been implicated in excitotoxic cell death.

52 cyclin E1 in neurons is sufficient to reduce excitotoxic cell death.

53 d resulted in loss of cortical neurons after excitotoxic challenge, indicating that neuronal apoE4 pr

54 underlie afferent terminal damage following excitotoxic challenge, suggesting that limiting Ca(2+) l

55 In response to excitotoxic challenge, the apoE-I3 mRNA was markedly inc

56 play a central role in the inflammatory and excitotoxic component of various acute and chronic neuro

57 and other neurodegenerative diseases with an excitotoxic component.

58 ell survivability by approximately 50% under excitotoxic condition, cell loss in Cx45 knock-out mouse

59 feedback to dampen neuronal excitability in excitotoxic conditions like ischaemia and epilepsy.

60 been proposed to be excessively activated in excitotoxic conditions such as HIE.

61 The upregulation of TrkB.T under excitotoxic conditions was correlated with an increase i

62 Under excitotoxic conditions, the activities of CDK5 and beta-

63 protein levels and signaling activity under excitotoxic conditions, which are characteristic of brai

64 feedback to dampen neuronal excitability in excitotoxic conditions.

65 These findings support a noncell autonomous, excitotoxic contribution from proprioceptive sensory neu

66 port capacity in ALS spinal cord supports an excitotoxic contribution to motor neuron (MN) damage in

67 the CNS, and induce neuroprotection against excitotoxic damage due to excessive glutamate (Glu) expo

68 ed synaptic dysfunction, possibly leading to excitotoxic damage in both EAE and MS diseases.

69 excitatory postsynaptic currents (EPSCs) and excitotoxic damage in rodent brain slices.

70 ents a key chemical reaction contributing to excitotoxic damage in stroke and potentially other neuro

71 Here, we first induced excitotoxic damage in the mouse brain by (i) administeri

72 fl/f) mice, which were more resistant to the excitotoxic damage induced by intraventricular injection

73 ng portion of spiral ganglion to investigate excitotoxic damage to IHC-SGN synapses in vitro.

74 her hair-cell loss was a secondary effect of excitotoxic damage to innervating neurons, I exposed neu

75 neration is to identify the cause of initial excitotoxic damage to the postsynaptic neuron.

76 However, during excitotoxic damage-a hallmark of neurological disorders-

77 peatable indicating that this was not due to excitotoxic damage.

78 (2+) channel contributing to kainate-induced excitotoxic death of amacrine and ganglion cells.

79 lucose deprivation (OGD) that causes delayed excitotoxic death of CA1 pyramidal neurons.

80 Finally, at 5-10 muM, ZIP-induced excitotoxic death of the cultured neurons.

81 o an episode of NMDA receptor activity, with excitotoxic death pathways requiring higher levels than

82 te via the system Xc(-) transporter, causing excitotoxic death to mature myelin-producing oligodendro

83 ory neurotransmitters causes them to undergo excitotoxic death via multiple synergistic injury mechan

84 composition seem to govern glutamate-induced excitotoxic death, but there is much uncertainty concern

85 d mitochondrial Ca(2+) uptake and preventing excitotoxic death.

86 ess leading from NMDA receptor activation to excitotoxic death.

87 d and N-methyl D-aspartate receptor-mediated excitotoxic death.

88 (MPC) protects primary cortical neurons from excitotoxic death.

89 cultures increased neuronal vulnerability to excitotoxic dendritic damage following a burst of synapt

90 which may represent therapeutic targets for excitotoxic disorders.

91 itional therapeutic benefit in SCS and other excitotoxic disorders.

92 22 years after the FDA approval of the anti-excitotoxic drug Riluzole before another drug was found

93 cytes to adequately protect neurons from the excitotoxic effects of glutamate, and increases intracel

94 nhibitory effect on glutamate release, block excitotoxic effects of glutamate, and potentiate postsyn

95 nto the cochlea could potentiate the already excitotoxic effects of glutamate, producing: [1] hyperac

96 The excitotoxic effects of kainic acid (KA) in the mouse hip

97 ions of interstitial glutamate exert further excitotoxic effects on healthy tissue surrounding the in

98 very of IL-1beta was associated with several excitotoxic effects, including NMDA receptor-dependent n

99 ersely, over-expression of SynGAP1 prevented excitotoxic ERK activation in wild-type neurons.

100 We also show that excitotoxic events only drive induction of COX-2 express

101 In rats subjected to excitotoxic fiber-sparing NMDA lesions circumscribed to

102 We found that excitotoxic, fiber-sparing lesions confined to OFC in mo

103 In contrast, excitotoxic global activation of synaptic and extrasynap

104 N exerted comparable efficacy in attenuating excitotoxic glutamate (200 microM)-induced intracellular

105 duced promotion of neuronal survival against excitotoxic glutamate (200 microM)-induced neurotoxicity

106 logical stimuli such as hypoxia-ischemia and excitotoxic glutamate and identify PK2 as a deleterious

107 ing metabolic challenge, where the source of excitotoxic glutamate buildup may be largely synaptic.

108 ong body of research has defined the role of excitotoxic glutamate in animal models of brain ischemia

109 lutamate exchanger is an important source of excitotoxic glutamate in response to ischemia induced by

110 g AD and may lose their capacity to regulate excitotoxic glutamate levels.

111 etrimental to neuronal viability by inducing excitotoxic glutamate release.

112 nsitizing vulnerable neuronal populations to excitotoxic glutamate signaling and inducing an excitoto

113 luding hypoxia, reactive oxygen species, and excitotoxic glutamate.

114 ells towards the oxidizer, arsenite, and the excitotoxic glutamate/glycine is demonstrated by the dos

115 been presented "where" and "when." Rats with excitotoxic hippocampal lesions showed the familiarity-d

116 To test the excitotoxic hypothesis, we crossed a well validated muri

117 Excitotoxic ibotenic acid (IBA) causes PVWMI-like lesion

118 Excitotoxic IL but not PL lesions in adult control mice

119 EN) is a delayed step causatively leading to excitotoxic (in vitro) and ischemic (in vivo) neuronal i

120 e transporter-1 (GLT-1), which would prevent excitotoxic-induced neuronal death, we proposed that GPR

121 articipate in central NMDA-receptor-mediated excitotoxic inflammation; and [5] kappa-opioid receptor

122 ntly developed in the rat where a unilateral excitotoxic injection into the globus pallidus leads to

123 ted cultured neurons from glutamate-mediated excitotoxic injury and death via EAAT2 activation.

124 in bax exerted broad neuroprotection against excitotoxic injury and oxygen/glucose deprivation in mou

125 To address this issue, we induced excitotoxic injury by systemic kainic acid injection in

126 le of calpain activation during NMDA-induced excitotoxic injury in embryonic (E16-E18) murine cortica

127 nd, by doing so, promotes the progression of excitotoxic injury in the central nervous system in path

128 em, and protected cortical neurons from slow excitotoxic injury in vitro, without influencing NMDA-in

129 is a critical early step in glutamate-evoked excitotoxic injury of CNS neurons.

130 prisingly rapid and plastic responses in two excitotoxic injury paradigms.

131 ow that increased synaptic activity prior to excitotoxic injury protects, in a transcription-dependen

132 ical conditions and that kainic acid-induced excitotoxic injury results in a profound increase in neu

133 mbrane potential (Deltapsim) analysis during excitotoxic injury revealed that bax-deficient neurons s

134 development of oligodendrocytes (OLs) or in excitotoxic injury to OLs.

135 Effects of excitotoxic injury to the thoracic gray matter on sensit

136 with activated microglia, which can promote excitotoxic injury via activation of receptors for plate

137 e metabolic profile of the mouse brain after excitotoxic injury, a mechanism of neurodegeneration imp

138 osing mouse hippocampal slices to NMDA as an excitotoxic injury, in combination with simultaneous pat

139 ia-mediated protection includes reduction of excitotoxic injury, since an absence of microglia leads

140 ) deregulation, or (3) that were tolerant to excitotoxic injury.

141 eath following transient global ischemia and excitotoxic injury.

142 necrosis or in neurons that were tolerant to excitotoxic injury.

143 the adult hippocampus at least shortly after excitotoxic injury.

144 lations that mimic features of glutamatergic excitotoxic insult and also to determine whether memanti

145 icity can be effectively stimulated after an excitotoxic insult has been delivered, and may identify

146 itotoxic glutamate signaling and inducing an excitotoxic insult itself.

147 s in a state of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effec

148 Neuron death elicited in vitro by excitotoxic insult or the expression of mutant SOD1, mut

149 Excitotoxic insult was induced by either (1) application

150 idic devices in order to deliver a localized excitotoxic insult, we replicate secondary spreading tox

151 rotected hippocampal neuronal cells from the excitotoxic insult, while efavirenz (EFV) did not contra

152 r" effects on neuronal survival following an excitotoxic insult.

153 genetically lacking NR3A to various forms of excitotoxic insult.

154 ntially compensatory neuroprotection against excitotoxic insult.

155 containing NMDA receptors (GluN2B-NMDARs) in excitotoxic-insult-induced neurodegeneration and amyloid

156 ased NMDAR(EX) activity and vulnerability to excitotoxic insults in rat cortical neurons.

157 e (NMDA) offers good neuroprotection against excitotoxic insults, but is potentially limited by the r

158 compromise neuronal survival after ischemic/excitotoxic insults.

159 s in NMDAR(EX) activity and vulnerability to excitotoxic insults.

160 g of NMDA receptor (NMDAR) activation during excitotoxic insults.

161 tects rat retinal ganglion cells (RGCs) from excitotoxic insults.

162 strong synaptic activity as a consequence of excitotoxic insults.

163 se hippocampal neurons highly susceptible to excitotoxic insults.

164 on and prevent neuronal cell death following excitotoxic insults.

165 recovery of neuronal network functions after excitotoxic insults.

166 nderlying learning and memory, as well as in excitotoxic/ischemic neuronal cell death.

167 in reversal learning, marmosets received an excitotoxic lesion of the VLPFC, OFC, or a sham control

168 he posteriodorsal medial amygdala (MePD) via excitotoxic lesion studies as a necessary nucleus in Met

169 te early gene imaging (c-Fos), fiber-sparing excitotoxic lesion, and reversible inactivation in rats,

170 Following ischemic and excitotoxic lesion, reactive, hypertrophic microglia rap

171 mpared the effects of selective LPFC and OFC excitotoxic lesions and 5,7-DHT-induced PFC serotonin de

172 with dorsal anterior cingulate cortex (dACC) excitotoxic lesions and pharmacological disinhibition; h

173 sconnected these structures via asymmetrical excitotoxic lesions before training.

174 vioral paradigms to determine the effects of excitotoxic lesions in the anterior cingulate cortex on

175 uestion was addressed by combining localized excitotoxic lesions in the PFC of a nonhuman primate and

176 In an in vivo model of NMDA-induced excitotoxic lesions in the striatum, PS dose-dependently

177 Excitotoxic lesions of analogous regions in marmosets ha

178 social threat was induced, independently, by excitotoxic lesions of either the anterior orbitofrontal

179 We investigated the effects of selective excitotoxic lesions of either the vlPFC or anterior orbi

180 Excitotoxic lesions of medial prefrontal cortex resulted

181 We examined whether bilateral excitotoxic lesions of PRh or PPRh (perirhinal plus post

182 herefore evaluated the effects of selective, excitotoxic lesions of the amygdala in rhesus monkeys on

183 We then found that bilateral, excitotoxic lesions of the amygdala markedly reduced cat

184 Large bilateral excitotoxic lesions of the auditory cortex were made in

185 sham-lesioned controls, rats with bilateral excitotoxic lesions of the basolateral amygdala (BLA) fa

186 e behavior of rats that received pretraining excitotoxic lesions of the bed nucleus of the stria term

187 After excitotoxic lesions of the BLA were created, animals und

188 Conversely, excitotoxic lesions of the dorsal hippocampus disrupted

189 The current study assessed the influence of excitotoxic lesions of the insular cortex (IC) on taste-

190 Previously, we have shown that large excitotoxic lesions of the lateral PFC (LPFC) and orbito

191 d, the present study compared the effects of excitotoxic lesions of the medial striatum (MS), amygdal

192 study investigated the effects of selective excitotoxic lesions of the nucleus accumbens shell or co

193 In 3 habituation experiments, rats with excitotoxic lesions of the perirhinal cortex were found

194 in several cost-benefit decision tasks after excitotoxic lesions of the RMTg or temporally specific o

195 scending control was also observed following excitotoxic lesions of the RVM in adult and P21 rats.

196 Excitotoxic lesions of the sensorimotor (dorsolateral) s

197 We then compared the effects of excitotoxic lesions of the Sub or the OFC on the ability

198 ment of dorsal striatal function with either excitotoxic lesions or transgenic inhibition of the tran

199 sus monkeys (Macaca mulatta) with restricted excitotoxic lesions targeting either Walker's areas 11/1

200 We then used local drug infusions and excitotoxic lesions to localize the effects of ketamine

201 objects), we examined the effects of crossed excitotoxic lesions to the POR and the contralateral PER

202 (NMDA) receptor (NMDAR) subtype and reduces excitotoxic lesions.

203 thophysiologic setting of cerebral ischemia, excitotoxic levels of glutamate contribute to neuronal c

204 ons of metabolic stress it can accumulate to excitotoxic levels.

205 The excitotoxic loss of neurons following TBI occurs largely

206 Monkeys with excitotoxic MDmc damage were tested on probabilistic thr

207 This excitotoxic mechanism may be specific to ankyrin G-bound

208 ls, to neurons and was partially mediated by excitotoxic mechanisms and soluble proteins.

209 Excitotoxic mechanisms contribute to the degeneration of

210 y to diverse neurological diseases involving excitotoxic mechanisms.

211 of inflammatory cytokines and production of excitotoxic metabolites.

212 astrocytic glutamate transport, resulting in excitotoxic motor neuron death.

213 t detect significant calpain activity during excitotoxic necrosis or in neurons that were tolerant to

214 ) murine cortical neurons that (1) underwent excitotoxic necrosis, characterized by immediate deregul

215 excitotoxic apoptosis but did not influence excitotoxic necrosis.

216 These findings demonstrate that SSC drives excitotoxic neurodegeneration in MoCD and introduce NMDA

217 synaptic mechanism linking inflammation and excitotoxic neurodegeneration in MS.

218 a neuropathological process contributing to excitotoxic neurodegeneration in MS/EAE.

219 eonatal and adult rodent cortical neurons to excitotoxic neurodegeneration with in vitro IL-1beta sen

220 ed the sensitizing effect of inflammation on excitotoxic neurodegeneration.

221 sensitization of human and rodent neurons to excitotoxic neurodegeneration.

222 creased microglial recruitment and resisting excitotoxic neurodegeneration.

223 eurotransmitter release and are resistant to excitotoxic neurodegeneration.

224 es examining AMPAR-dependent potentiation of excitotoxic neuron death and dysfunction caused by TNFal

225 We propose that this activity contributes to excitotoxic neuron death because TNFalpha potentiation o

226 -apoptotic role analogous to the response to excitotoxic neuron injury.

227 he essential NMDAR subunit NR1 protects from excitotoxic neuronal cell death in vivo and from traumat

228 Moreover, excitotoxic neuronal cell death, an underlying process f

229 enger system and indicate its involvement in excitotoxic neuronal cell death.

230 oinhibitory function may result in unopposed excitotoxic neuronal damage in amyotrophic lateral scler

231 2+) loading is central to most hypotheses of excitotoxic neuronal damage.

232 d glutamate clearance, a major transducer of excitotoxic neuronal damage.

233 ompanied by neurotoxicity, and Abeta induces excitotoxic neuronal death by increasing calcium influx

234 ebellar granule cells; 2) protection against excitotoxic neuronal death in mixed cultures of cortical

235 te (NMDA) -type glutamate receptors leads to excitotoxic neuronal death in stroke, brain trauma, and

236 f Cytokine Signaling-3 (SOCS3) in regulating excitotoxic neuronal death in vitro.

237 Excitotoxic neuronal death is mediated in part by NMDA r

238 cleaving Src in neurons and protects against excitotoxic neuronal death.

239 vation in neurons in vivo, strongly enhances excitotoxic neuronal death.

240 NF-induced inhibition of RhoA, a mediator of excitotoxic neuronal death.

241 tion are both required for glutamate-induced excitotoxic neuronal death.

242 ctivation constitute a unified mechanism for excitotoxic neuronal death.

243 ss glutamate from synaptic clefts to prevent excitotoxic neuronal death.

244 apeutic role for miR-223 in stroke and other excitotoxic neuronal disorders.

245 ctivation in the inferior olive resulting in excitotoxic neuronal injury in the cerebellum is the und

246 GABAergic drugs on neonatal seizures and on excitotoxic neuronal injury in the immature brain.

247 o be explored for developing therapeutics of excitotoxic neuronal injury.

248 urn, limits the positive-feedback cascade of excitotoxic neuronal injury.

249 a) has been implicated in the progression of excitotoxic neuronal injury.

250 g traumatic brain injury (TBI) may be due to excitotoxic neuronal loss.

251 xogenous glutamate analogs, like the classic excitotoxic neurotoxins kainic acid, domoic acid, and NM

252 on signaling, purinergic receptor signaling, excitotoxic neurotransmitter signaling, perturbations in

253 nizes the GABA(A) receptor and behaves as an excitotoxic neurotransmitter that causes blood brain bar

254 bosis via the Rose Bengal method, as well as excitotoxic NMDA lesions, we show that dnSNARE animals e

255 dose-dependently mouse cortical neurons from excitotoxic NMDA-mediated neuritic bead formation and ap

256 disconnected from each other with unilateral excitotoxic (NMDA) lesions on either the same or opposit

257 veractivation of these receptors can mediate excitotoxic OL injury.

258 approximately 70% after induction of either excitotoxic or ischemic insult conditions.

259 s exhibit increased apoptosis in response to excitotoxic or oxidative stress in vitro.

260 ors as a valuable therapeutic target against excitotoxic pathologies including acute and chronic neur

261 fy MCP-1 as a key downstream effector in the excitotoxic pathway triggered by plasmin and identify pl

262 We demonstrate that excitotoxic pathways can be regulated, in cortical neuro

263 Mice with excitotoxic PRH/LEC lesions exhibit deficits in pattern

264 ith apparent recruitment of L-VGCCs into the excitotoxic process.

265 lpha (TNF-alpha), may directly interact with excitotoxic processes.

266 agonist, which combines antioxidant and anti-excitotoxic properties, to block axonal damage and reduc

267 Our findings suggest that tau mediates excitotoxic Ras/ERK signaling by controlling post-synapt

268 siological and pathological roles, including excitotoxic release of glutamate in stroke.

269 TNFalpha-induced AMPAR trafficking to early excitotoxic secondary injury after CNS trauma in vivo, a

270 d the protective effect of adenosine against excitotoxic seizure and neuronal death in mice.

271 gs, such as kainate and domoate, which cause excitotoxic shellfish poisoning, induce nondesensitizing

272 Thus, GluN2B-driven excitotoxic signaling can proceed independently of Dapk1

273 e nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities f

274 is a component of the NMDA-receptor-mediated excitotoxic signaling pathway, which plays a key role in

275 tive therapeutic target since it potentiates excitotoxic signaling.

276 rkB.T receptors coupled to inhibition of the excitotoxic signaling.

277 iched phosphatase (STEP), a component of the excitotoxic-signaling pathway that plays a role in neuro

278 t likely represents an early response during excitotoxic states.

279 Excitotoxic stimulation of cultured rat hippocampal or s

280 We found that excitotoxic stimulation of N-methyl-d-aspartate (NMDA) r

281 s transduced with TrkB.T when present during excitotoxic stimulation with glutamate, in contrast with

282 protection against neuronal death caused by excitotoxic stimulation.

283 xpression in response to proinflammatory and excitotoxic stimuli.

284 Notably, an excitotoxic stimulus (150 microM glutamate) induced S141

285 Conversely, exposure of neurons to an excitotoxic stimulus (i.e. NMDA) inhibits alpha-secretas

286 Here, we show that an excitotoxic stimulus in rat cortical neurons in primary

287 Excitotoxic stimulus induces recruitment of NOS1AP to nN

288 neuronal Ca(2+)homeostasis in response to an excitotoxic stimulus; this was accompanied by a prolonge

289 ynaptic responses, sensitivity to mechanical/excitotoxic stress and neuroprotection.

290 phic support and increased mitochondrial and excitotoxic stress have been reported in HD striatal and

291 significantly resistant to injury induced by excitotoxic stress or mitochondrial toxicity.

292 s, thus protecting against glutamate-induced excitotoxic stress.

293 res are reminiscent of those associated with excitotoxic stress.

294 n increased vulnerability to AMPAR-dependent excitotoxic stress.

295 /H(+) exchange are thus potent regulators of excitotoxic superoxide production.

296 s blocking CP-AMPARs protects terminals from excitotoxic swelling.

297 g via mu-opioid receptors, exacerbates these excitotoxic Tat effects at the same subcellular location

298 ignals are able to induce the release of the excitotoxic transmitter glutamate from these glia, we as

299 zebrafish larvae exposed to drugs that mimic excitotoxic trauma.

300 Our results indicate that enhanced excitotoxic vulnerability with age in culture was associ