ライフサイエンスコーパス: kainic acid

1 ampus affects behavioral seizures induced by kainic acid.

2 1(+/+) mice after administration of 15 mg/kg kainic acid.

3 and hippocampal c-fos expression induced by kainic acid.

4 c ketone as a key intermediate for (-)-alpha-kainic acid.

5 cumulation and lipid peroxidation induced by kainic acid.

6 hione peroxidase activity in the presence of kainic acid.

7 is demonstrated in a synthesis of (+)-alpha-kainic acid.

8 id not affect the eating response induced by kainic acid.

9 ional distribution using focal injections of kainic acid.

10 o the excitotoxic glutamate receptor agonist kainic acid.

11 age induced by intraventricular injection of kainic acid.

12 was induced by intrahippocampal injection of kainic acid.

13 al time upon extracellular administration of kainic acid.

14 y, which can further be markedly enhanced by kainic acid.

15 at were systemically injected with saline or kainic acid.

16 had no effect on lesions produced by AMPA or kainic acid.

17 nificantly protected against the excitotoxin kainic acid.

18 -methyl-4-isoxazolepropionic acid (AMPA) and kainic acid.

19 ols to focal hippocampal seizures induced by kainic acid.

20 verity and mortality) to flurothyl, PTZ, and kainic acid.

21 ified in a similar F2 population tested with kainic acid.

22 lateral intracerebroventricular injection of kainic acid.

23 owing generalized clonic seizures induced by kainic acid.

24 tivity to seizures induced by the convulsant kainic acid.

25 local injection of a glutamatergic agonist, kainic acid.

26 n an eight-step total synthesis of (-)-alpha-kainic acid.

27 ensitivity of hippocampal pyramidal cells to kainic acid.

28 administration of the excitatory amino acid kainic acid.

29 ) based on their affinity for the neurotoxin kainic acid.

30 of the potent neurochemicals domoic acid and kainic acid.

31 eal (i.p.) injection of 0, 7, 10 or 14 mg/kg kainic acid.

32 hesized in a parallel fashion from (-)-alpha-kainic acid 1.

33 Microinjections of kainic acid (100 microM, 0.2 microl) into Gi and DPGi in

34 Kainic acid (100 nm) induced coherent network oscillatio

35 )pyrrolidine-2,4-dicarboxylic acid 43, alpha-kainic acid 12, alpha-isokainic acid 14, and alpha-dihyd

36 nistration of bicuculline (0.5 mg/kg, i.v.), kainic acid (12.0 mg/kg, i.v.) or pentylenetetrazol (100

37 eceived either intraperitoneal injections of kainic acid (20 mg/kg) to induce status epilepticus or t

38 Rat pups were injected three times with kainic acid (3x KA) on P6, P9, and P13 and subsequently

39 does not block the hyperalgesia produced by kainic acid (a non-NMDA glutamate receptor agonist) prov

40 Homologues of kainic acid, a naturally occurring potent glutamate rece

41 In vivo, within 6 h of systemic kainic acid administration at postnatal day 6, mRNA leve

42 ostnatal day 21 (P21) and following systemic kainic acid administration in adults.

43 yer (DSGL) following intracerebroventricular kainic acid administration in young adult, middle-aged,

44 ompany CAST depletion after intrahippocampal kainic acid administration to mice, and are substantiall

45 ocampal dentate gyrus neurons after systemic kainic acid administration, from 21.9 to 64.4%.

46 Seven days after kainic acid administration, the [(125)I]insulin receptor

47 combined potassium and serum withdrawal, and kainic acid administration.

48 hreshold and higher lethality in response to kainic acid administration.

49 against focal cerebral ischemia and systemic kainic acid administration.

50 mpal slices in culture with the excitotoxin, kainic acid, also produced calpain-mediated truncation o

51 entified NMDA (N-methyl-d-aspartate) and KA (kainic acid)/AMPA (alpha-amino-3-hydroxy-5-methyl-4-isox

52 approach to the total syntheses of (-)-alpha-kainic acid and (+)-alpha-allokainic acid, where the ste

53 Seizures evoked by kainic acid and a variety of experimental methods induce

54 bserved using inhibitors specific for EAAT2 (kainic acid and dihydrokainic acid) and EAAT3 (cysteine)

55 In response to kainic acid and electroconvulsive shock-induced seizures

56 venting and suppressing seizures in both the kainic acid and flurothyl models of symptomatic neonatal

57 models of status epilepticus (intra-amygdala kainic acid and intraperitoneal pilocarpine).

58 eizures in response to the chemoconvulsants, kainic acid and pilocarpine.

59 show supersensitive behavioral responses to kainic acid and that a kainate receptor antagonist norma

60 morphine (approximately 5 min vs. 1 min for kainic acid), and the antinociceptive efficacy of microi

61 zygous (Dbh +/-) controls to flurothyl, PTZ, kainic acid, and audiogenic seizures and enhanced sensit

62 ether (flurothyl), pentylenetetrazol (PTZ), kainic acid, and high-decibel sound.

63 e epileptic by intrahippocampal injection of kainic acid, and in patients with mesial temporal lobe e

64 Furthermore PMNs exacerbated kainic acid- and oxygen glucose deprivation-induced neur

65 arkedly increased sensitivity to flurothyl-, kainic acid-, and hyperthermia-induced seizures measured

66 after perforant path stimulation or systemic kainic acid, as well as greater severity of pentylenetet

67 o exhibited enhanced behavioral responses to kainic acid at a dose of 15 mg/kg but no lethal seizures

68 dge of DabA and a homologous enzyme from the kainic acid biosynthetic pathway, KabA, to reengineer th

69 Kainic acid-challenged wild-type or Apoe-/- mice had a s

70 xazole-4-propionic acid (AMPA) and 20 microM kainic acid depolarized the membrane equivalently but di

71 explants, and the glutamatergic excitotoxin kainic acid disrupting metabolism only in CA3 explants,

72 exposure to diverse neurotoxicants including kainic acid, domoic acid, 3-nitropropionic acid, Fluoro-

73 gs, like the classic excitotoxic neurotoxins kainic acid, domoic acid, and NMDA; the therapeutic glut

74 l and/or bilateral injections of muscimol or kainic acid eliminated eupnoea only transiently.

75 Kainic acid evoked a completely different pattern with a

76 activity wheel running would protect against kainic acid-evoked seizures and whether galaninergic sig

77 This contrasts to kainic acid excitotoxicity and traumatic brain injury, w

78 2 potentiates the intensity and lethality of kainic acid excitotoxicity in coincidence with potentiat

79 In vivo CA1 cell damage following kainic acid exposure was greatly attenuated.

80 ricularly (i.c.v.) with 0.2 or 0.4 microg of kainic acid following either an injection of M-40 (a gal

81 ton is exemplified by the synthesis of (+/-)-kainic acid from 3-butyn-1-ol.

82 e concise two-enzyme biosynthetic pathway to kainic acid from l-glutamic acid and dimethylallyl pyrop

83 Although application of kainic acid imposed the same level of noxious stress, th

84 nization of epileptiform activity induced by kainic acid in a novel preparation of superfused rat hip

85 inolinic acid, an NMDA receptor agonist, and kainic acid in gene targeted and transgenic mice that un

86 he cerebellar cortex by local application of kainic acid in normal mice.

87 itive to excitotoxic neural damage caused by kainic acid, in the absence of tonic-clonic seizures.

88 A convulsant, kainic acid, increased bursts only in the specifically t

89 In adult rats, systemic injection of kainic acid induced c-fos expression in granule cells an

90 Results show that kainic acid induced c-fos synthesis in most of these gli

91 were no differences between the genotypes in kainic acid induced Fos in the amygdala, hippocampus, la

92 At a dose of 20 mg/kg, kainic acid induced lethal seizures in 100% of the NR1(n

93 It is also found in vivo after kainic acid induced seizures.

94 In support of this, kainic acid induced translocation of a Bax-EGFP fusion p

95 t endogenous tPA mediates the progression of kainic acid-induced (KA-induced) seizures by promoting t

96 Deleting Fgfr1/2/3 abolished kainic acid-induced bSC dendritic overgrowth.

97 nd glia in models of brain injury, including kainic acid-induced epilepsy in the hippocampus, mechani

98 SF1R under physiological conditions and that kainic acid-induced excitotoxic injury results in a prof

99 l for multiple sclerosis (MS), as well as in kainic acid-induced excitotoxicity.

100 even with different promoters, and prevented kainic acid-induced hilar cell death.

101 netic methods in multiple brain regions of a kainic acid-induced model of TLE in VGAT-ChR2 transgenic

102 Kainic acid-induced neuron loss in the hippocampal denta

103 the engrafted cells migrated toward areas of kainic acid-induced neuronal death.

104 Neuroserpin also attenuated kainic acid-induced neuronal death.

105 xerts a strong neuroprotective effect in the kainic acid-induced oxidative hippocampal neurodegenerat

106 Overexpression of TRF2-S rescues kainic acid-induced REST nuclear accumulation and its ge

107 systemic administration of C4-3 potentiates kainic acid-induced seizure development.

108 inistration of anti-NPY antibody accelerated kainic acid-induced seizure onset and increased seizure-

109 pike-wave discharges in BACE1-null mice, and kainic acid-induced seizures also occurred more frequent

110 They show that protection against kainic acid-induced seizures and cell death is conferred

111 a-dose of ARALAR in aralar(+/-)mice enhanced kainic acid-induced seizures and neuronal damage with re

112 Exercise decreased kainic acid-induced seizures at the 0.2 microg dose, and

113 Kainic acid-induced seizures elicited production of pro-

114 C1), relevant to neurodegeneration following kainic acid-induced seizures in rats.

115 d hippocampal function and responsiveness to kainic acid-induced seizures in Y5R-deficient (Y5R-/-) m

116 In adult rats, kainic acid-induced seizures increased fibronectin mRNA

117 Kainic acid-induced seizures revealed that EYFP(+) bDC r

118 Kainic acid-induced seizures, a rodent model of human te

119 ound that these mutant mice have more severe kainic acid-induced seizures, increased neuronal excitab

120 These mice resisted kainic acid-induced seizures, showing a 36% decrease in

121 n this study, we demonstrate that, following kainic acid-induced seizures, the proNGF processing enzy

122 s is induced by neuronal activity, including kainic acid-induced seizures, whether and how c-fos is i

123 ctivity; however, they are more sensitive to kainic acid-induced seizures.

124 us, class I MHC mRNA levels are increased by kainic acid-induced seizures.

125 tivity also showed diminished sensitivity to kainic acid-induced seizures.

126 ficantly reduced neuronal degeneration after kainic acid-induced seizures.

127 ersistently decreased following induction of kainic acid-induced seizures.

128 heightened susceptibility to spontaneous and kainic acid-induced seizures.

129 Three episodes of neonatal kainic acid-induced status epilepticus (3KA-SE), each el

130 imental TLE was triggered by pilocarpine- or kainic acid-induced status epilepticus (SE).

131 Experimental TLE was provoked by kainic acid-induced status epilepticus (SE).

132 Conversely, kainic acid-induced status epilepticus in chronically im

133 Three days after kainic acid-induced status epilepticus or prolonged perf

134 , which was augmented after pilocarpine- and kainic acid-induced status epilepticus.

135 3 border several weeks after pilocarpine- or kainic acid-induced status epilepticus.

136 that developed epilepsy after intra-amygdala kainic acid-induced status epilepticus.

137 mice activated TrkB in the brain, inhibited kainic acid-induced toxicity, decreased infarct volumes

138 In kainic-acid-induced mouse models of drug-resistant focal

139 nhanced seizure susceptibility to later-life kainic-acid-induced seizures.

140 However, it did not protect against OGD- or kainic-acid-induced toxicity.

141 he Homer1 protein, which could be induced by kainic acid injection and is likely homologous to the ma

142 uting do not occur until 2-3 weeks after the kainic acid injection and the specific transcription fac

143 least 6-fold on the side ipsilateral to the kainic acid injection compared to controls, but signific

144 Our laboratory has shown that a single kainic acid injection elicits acute increases of activat

145 e, we induced excitotoxic injury by systemic kainic acid injection in transgenic Apoe knockout mice e

146 in, hippocampal FGF-2 increased after either kainic acid injection or middle cerebral artery occlusio

147 other mouse model of axonal damage (that is, kainic acid injection) and detected in cultured neurons

148 ignificantly less dystonia was induced after kainic acid injection, implicating Purkinje cells and th

149 stays at an elevated level for 2 weeks after kainic acid injection.

150 show less hippocampal cell damage following kainic acid injection.

151 t areas, much less correlation was seen with kainic acid injection.

152 ng 0.2 microl of morphine was less than with kainic acid injections.

153 n of the adult rat hippocampus at early post-kainic acid injury for providing a lasting inhibition of

154 tatus epilepticus (SE) evoked by infusion of kainic acid into the amygdala of adult mice.

155 Seizures evoked by microinjection of kainic acid into the amygdala of the rat induced unilate

156 Microinjection of low doses of kainic acid into the cerebellar vermis of mice elicited

157 e dissociated by microinjecting morphine and kainic acid into various subdivisions of the caudal PAG.

158 onist bicuculline, and the glutamate agonist kainic acid, into the CA3 area of hippocampus.

159 of the selective glutamate receptor agonist, kainic acid, into the uninjured rat spinal cord.

160 The total synthesis of (-)-alpha-Kainic acid is accomplished using a linear strategy invo

161 Kainic acid is known to induce seizures, neuronal damage

162 The partial agonist, kainic acid (KA) activates a less desensitized, and more

163 nd N-terminal phosphorylated c-Jun following kainic acid (KA) administration in two strains of mice.

164 in hippocampus after intracerebroventricular kainic acid (KA) administration, a model of temporal lob

165 ult of seizure activity elicited by systemic kainic acid (KA) administration.

166 We used a rat model based on intraperitoneal kainic acid (KA) administration.

167 ures evoked by intraperitoneal injections of kainic acid (KA) and pilocarpine in mice with a conditio

168 Excitotoxicity induced by kainic acid (KA) caused GSK-3beta truncation at C-termin

169 he response to CNS injury following an acute kainic acid (KA) challenge (30 mg kg-1, i.p.) was determ

170 by pathophysiologic synaptic activity after kainic acid (KA) exposure and its absence renders mouse

171 yl-5-methylisoxazole-4-propionic acid (AMPA)/kainic acid (KA) iGluR agonists and odorants (glutamine,

172 and aged male mice treated systemically with kainic acid (KA) in a strain reported to be resistant to

173 Here, we injected low and high levels of kainic acid (KA) in the dentate gyrus to assess whether

174 The excitotoxic effects of kainic acid (KA) in the mouse hippocampus is strain depe

175 ated with the excitotoxic glutamate analogue kainic acid (KA) in vitro and in vivo.

176 campal neurons using the epileptogenic agent kainic acid (KA) increased the number of Shh(+) MCs indi

177 onic stimulation with cyclothiazide (CTZ) or kainic acid (KA) induces robust epileptiform activity in

178 Kainic acid (KA) induces status epilepticus in both adul

179 There is evidence that acute exposure to kainic acid (KA) induces the release of endogenous ligan

180 Bilateral kainic acid (KA) infusions depressed compound AN respons

181 We used systemic kainic acid (KA) injection to investigate how the develo

182 oral lobe epilepsy based on intrahippocampal kainic acid (KA) injection.

183 ministered saline, 192-IgG saporin (SAP), or kainic acid (KA) into the MSDB and then behaviorally tes

184 Conversely, depolarizing HCs by puffing kainic acid (KA) into the outer plexiform layer (OPL) ca

185 esioned with single unilateral injections of kainic acid (KA) into the septum to further characterize

186 f mice differ in their susceptibility to the kainic acid (KA) model of seizure-induced cell death, bu

187 The effects of kainic acid (KA) on neurogenesis in the developing rat h

188 egeneration caused by treatment of rats with kainic acid (KA) or ibogaine (IBO) to the neuropathology

189 otropic glutamate receptor (iGluR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contrib

190 Kainic acid (KA) produced limbic seizures at a comparabl

191 cluster of 5-7 individual seizures evoked by kainic acid (KA) rapidly (within 30 min) induced gamma-H

192 together with N-methyl-D-aspartate (NMDA) or kainic acid (KA) receptor agonists on DNA fragmentation

193 In vivo excitatory stimulation with kainic acid (KA) resulted in an increase in luciferase a

194 jury and the inflammatory reaction using the kainic acid (KA) seizure model.

195 Kainic acid (KA) selectively damages afferent synapses t

196 n this study we administered the excitotoxin kainic acid (KA) to generate reactive oxygen species (RO

197 imals received intra-amygdaloid injection of kainic acid (KA) to induce seizures for 45 min during co

198 udy examined changes in GluR1 subunits after kainic acid (KA) treatment of organotypic hippocampal cu

199 assess if this is an age-related phenomenon, kainic acid (KA) was administered to induce status epile

200 To induce excitotoxicity, kainic acid (KA) was injected into the vitreous humor of

201 city of brain areas such as the hippocampus, kainic acid (KA) was used in the current study to induce

202 Treatment with kainic acid (KA), a glutamate analog known to activate t

203 In this study, we injected kainic acid (KA), a glutamate receptor agonist that spec

204 f two mechanistically different neurotoxins, kainic acid (KA), an NMDA agonist and 3-Nitropropionic a

205 l-5-methylisoxazole-4-propionic acid (AMPA), kainic acid (KA), and N-methyl-D-aspartic acid (NMDA) ac

206 omparing to a well-known epileptogenic agent kainic acid (KA), CTZ affects neuronal activity mainly t

207 tor agonists, N-methyl-D-aspartate (NMDA) or kainic acid (KA), we quantified the increases in cGMP-li

208 ncompetent virus mutant DeltaRR and prevents kainic acid (KA)-induced epileptiform seizures and neuro

209 iment, intrastriatal DNQX was shown to block kainic acid (KA)-induced Fos expression in the striatum,

210 ury were used to evaluate the time course of kainic acid (KA)-induced hippocampal damage in adult C57

211 The effects of kainic acid (KA)-induced limbic seizures have been inves

212 ablished the involvement of free radicals in kainic acid (KA)-induced neurotoxicity.

213 Kainic acid (KA)-induced seizures elicit edema associate

214 und such animals to be highly susceptible to kainic acid (KA)-induced seizures in terms of both seizu

215 ring the cardiovascular responses to 2 mg/kg kainic acid (KA)-induced seizures in urethane anesthetiz

216 Kainic acid (KA)-induced seizures increased splanchnic s

217 8a(med) and Scn8a(med-jo), to flurothyl- and kainic acid (KA)-induced seizures.

218 Kainic acid (KA)-induced status epilepticus (SE) in adul

219 Kainic acid (KA)-induced status epilepticus in adult rat

220 te to identify changes that evolve following kainic acid (KA)-induced status epilepticus.

221 s treatment with high doses of CORT enhanced kainic acid (KA)-induced toxicity of cortical neurons.

222 susceptibility to neurologic injury using a kainic acid (KA)-induced, established 'two-hit' seizure

223 se somatosensory cortex (S1), and in a mouse kainic acid (KA)-seizure model.

224 oxic insult produced by the glutamate analog kainic acid (KA).

225 cell death induced by systemic injections of kainic acid (KA).

226 pal cultures challenged with the excitotoxin kainic acid (KA).

227 ystemic exposure to an excitotoxic stimulus, kainic acid (KA).

228 rographic and behavioral seizures induced by kainic acid (KA).

229 y injected quinolinic acid (QA, 60 nmol) and kainic acid (KA, 2.5 nmol), we compared the effects of a

230 eurons, we examined the effect of unilateral kainic acid (KA; PBS vehicle, 1.25, 2.5 and 5.0 nmol) ad

231 oreactivity in extrahypothalamic sites after kainic-acid (KA)-induced seizures in male rats.

232 transcription and cell activation following kainic-acid (KA)-induced seizures.

233 (glutamate, N-methyl-D-aspartate [NMDA], or kainic acid [KA]) were added for 30 minutes or 24 hours,

234 s of Cu(2+) application and chelation (using kainic acid, KA) on the neural retina from wildtype and

235 icities of drugs including acetaminophen and kainic acid, known as RNS inducers.

236 Chronic kainic acid lesion of the STN or chronic levodopa treatm

237 Kainic acid lesions of CA3 dramatically reduced Kv1.1 im

238 Kainic acid lesions produced degeneration of CA3 pyramid

239 Excitation of local neurons with kainic acid mimicked effects of electrical stimulation b

240 We have used genes identified in a kainic acid model of synaptic plasticity as in situ hybr

241 s and that phosphorylation is reduced in the kainic acid model of TLE.

242 epileptogenesis and chronic epilepsy in the kainic acid model of TLE.

243 In both pilocarpine and kainic acid models, there was greater mossy fiber sprout

244 icantly protects against quinolinic acid and kainic acid neurotoxicity in the mouse striatum whereas

245 rmation methodology to efficiently construct kainic acid on the gram scale.

246 Bicuculline, Ro15-4513, finasteride, kainic acid or AMPA, alone or in combination, did not si

247 eizures in postnatal day 10 rats with either kainic acid or flurothyl.

248 as well as those exposed to the neurotoxins kainic acid or methamphetamine were examined.

249 ) mice, BrdUrd labeling was attenuated after kainic acid or middle cerebral artery occlusion, as was

250 most profoundly increased by excitation with kainic acid or mobilization of calcium from intracellula

251 ion after exposure to either sodium cyanide, kainic acid or oxygen glucose deprivation (OGD).

252 , an induction of acidosis by treatment with kainic acid or pH 6.0 medium activated asparaginyl endop

253 ilepsy was induced with injections of either kainic acid or pilocarpine.

254 Injury was induced by exposure to kainic acid or potassium cyanide/2-deoxyglucose (KCN/2-D

255 us or minus an excitotoxic insult (50 microM kainic acid) or 6-h oxygen glucose deprivation.

256 ls of acute seizures induced by pilocarpine, kainic acid, or pentylenetetrazole.

257 ng exposure to either the glutamate agonist, kainic acid, or the inhibitor of mitochondrial respirati

258 to the neurodegenerative effects of MPTP and kainic acid, oxidative stressors affecting the substanti

259 tive than DBH KO mice to seizures induced by kainic acid, pentylenetetrazole, or flurothyl, although

260 A combination of lesioning and systemic kainic acid produced a strong, c-fos expression througho

261 rsal regions of the PAG by microinjection of kainic acid produced wild running, while injections into

262 ith previous studies in the intrahippocampal kainic acid rat model of chronic epilepsy that provide e

263 eover, c-Fos regulates the expression of the kainic acid receptor GluR6 and brain-derived neurotrophi

264 We demonstrated that glutamate acts through kainic acid receptors in the VMH to augment counterregul

265 2-carboxylic acid (1b), for cloned homomeric kainic acid receptors subtype 1 (GluK1) was attained (Ki

266 rolonged seizures induced in adult rats with kainic acid resulted in an increase in activity of the e

267 Kainic acid resulted in caspase-3 activation in several

268 Excitotoxic challenge with kainic acid significantly increased apoE fragmentation i

269 r, exposure of spinal cord slice cultures to kainic acid significantly reduced PMCA2 mRNA levels.

270 in for bicuculline and 6.37 +/- 7.66 min for kainic acid, suggesting the existence of powerful seizur

271 Kainic acid, the flagship member of the kainoid family o

272 o the excitotoxic glutamate-receptor agonist kainic acid: they showed a reduction in seizure activity

273 An efficient synthesis of (-)-kainic acid, through a high-pressure-promoted Diels-Alde

274 ple injections (i.p.) of saline (control) or kainic acid to induce seizures and were euthanized 16 da

275 iet, followed by treatment with low doses of kainic acid to induce seizures.

276 onsider the temporal and multiple effects of kainic acid to optimize conditions for their endpoint of

277 and induction of Fos after administration of kainic acid to wild type mice (NR1(+/+)) and mice with g

278 , 2-deoxyglucose, 3-nitropropionic acid, and kainic acid) to induce acute energy inhibition in C57/B6

279 matic brain injury, Alzheimer's disease, and kainic acid toxicity.

280 euploid, but not trisomic cortical cultures, kainic acid, trans-(+/-)-ACPD, or H2O2 exposure elicited

281 l types in single-channel EEG collected from kainic acid-treated mice.

282 and Bax-dependent excitotoxic cell death in kainic acid-treated primary cortical neurons derived fro

283 Hz [fast ripples (FRs)] in intrahippocampal kainic acid-treated rats with spontaneous seizures, by a

284 sprouted mossy fiber synapses in kindled and kainic acid-treated rats.

285 Kainic acid-treated transgenic mice showed no significan

286 actors regulating the long-term events after kainic acid treatment are not clear.

287 indicate widespread neurotoxicity following kainic acid treatment in C57BL/6J mice, and reveal incre

288 id not express EGFP under normal conditions, kainic acid treatment induced intense expression of EGFP

289 In both wild-type and Prkdc(-/-) neurons, kainic acid treatment resulted in rapid induction of DNA

290 iption factors in the long-term events after kainic acid treatment, gel mobility-shift and Western bl

291 GFP was expressed in <10% of microglia after kainic acid treatment, suggesting that microglia are not

292 ours, but not 4 hours or 96 hours, following kainic acid treatment.

293 nduced in the rat hippocampus after systemic kainic acid treatment.

294 avage and provides neuroprotection following kainic acid treatment.

295 is molecule in mice substantially diminishes kainic acid-triggered neuronal cell death and decreases

296 ings demonstrate that genetic variation in a kainic acid-type glutamate receptor is reproducibly asso

297 4787) in the GRIK4 gene, which codes for the kainic acid-type glutamate receptor KA1, was observed.

298 e if these receptor subunits are functional, kainic acid was injected and c-fos expression monitored.

299 The excitotoxin, kainic acid, was injected into the rostral IO of three c

300 and F(4)-NeuroPs after systemic exposure to kainic acid were not associated with a significant chang