ライフサイエンスコーパス: kainic acid

1 age induced by intraventricular injection of kainic acid.

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

3 cumulation and lipid peroxidation induced by kainic acid.

4 hione peroxidase activity in the presence of kainic acid.

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

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

7 ional distribution using focal injections of kainic acid.

8 o the excitotoxic glutamate receptor agonist kainic acid.

9 tivity to seizures induced by the convulsant kainic acid.

10 al time upon extracellular administration of kainic acid.

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

12 was induced by intrahippocampal injection of kainic acid.

13 at were systemically injected with saline or kainic acid.

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

15 nificantly protected against the excitotoxin kainic acid.

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

17 local injection of a glutamatergic agonist, kainic acid.

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

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

20 lateral intracerebroventricular injection of kainic acid.

21 owing generalized clonic seizures induced by kainic acid.

22 mannitol, but not during seizures induced by kainic acid.

23 G infusion of an excitatory nontoxic dose of kainic acid.

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

25 ensitivity of hippocampal pyramidal cells to kainic acid.

26 administration of the excitatory amino acid kainic acid.

27 ols to focal hippocampal seizures induced by kainic acid.

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

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

30 ampus affects behavioral seizures induced by kainic acid.

31 1(+/+) mice after administration of 15 mg/kg kainic acid.

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

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

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

35 Kainic acid (100 nm) induced coherent network oscillatio

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

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

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

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

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

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

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

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

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

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

46 Beginning 1-2 weeks after kainic acid administration, a progressive increase in th

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

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

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

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

51 against focal cerebral ischemia and systemic kainic acid administration.

52 Kainic acid also produced a loss of mitochondrial membra

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

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

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

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

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

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

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

60 were more susceptible to seizures induced by kainic acid and subsequently exhibited greater neuron in

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

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

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

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

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

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

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

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

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 the excitatory amino acids glutamic acid and kainic acid, has specific effects on brain histology in

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 hich are known to exacerbate the toxicity in kainic acid in CA3 neurons, exacerbate the metabolic eff

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

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

88 aking localized injections of the neurotoxin kainic acid in the NRA in decerebrate cats, most of whic

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

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

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

92 Kainic acid induced DNA laddering and death of neurons e

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

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

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

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

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

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

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

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

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

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

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

104 Kainic acid-induced neuron loss in the hippocampal denta

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

106 Neuroserpin also attenuated kainic acid-induced neuronal death.

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

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

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

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

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

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

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

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

115 Kainic acid-induced seizures elicited production of pro-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 The kainic acid-induced sprouting of mossy fibers containing

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

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

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

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

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

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

138 3 border several weeks after pilocarpine- or kainic acid-induced status epilepticus.

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

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

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

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

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

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

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

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

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

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

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

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

151 e gyrus at progressive time points following kainic acid injection.

152 show less hippocampal cell damage following kainic acid injection.

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

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

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

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

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

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

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

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

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

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

163 Kainic acid is known to induce seizures, neuronal damage

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ) receptors were labeled with [3H]glutamate, kainic acid (KA) receptors were labeled with [3H]KA, and

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

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

194 Kainic acid (KA) selectively damages afferent synapses t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 8a(med) and Scn8a(med-jo), to flurothyl- and kainic acid (KA)-induced seizures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 In intact and kainic acid-lesioned control adult neocortex, transplant

235 Kainic acid lesions elicit reductions in ligand binding

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

237 Kainic acid lesions produced degeneration of CA3 pyramid

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

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

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

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

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

243 mistry to determine the prolonged effects of kainic acid on the distribution of dynorphin- and enkeph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 Kainic acid produced excitotoxic cell death in the CA3 a

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

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

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

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

264 2-carboxylic acid (1b), for cloned homomeric kainic acid receptors subtype 1 (GluK1) was attained (Ki

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

266 Kainic acid resulted in caspase-3 activation in several

267 chronic expression of Delta-FosB elicited by kainic acid seizures may be indicative of a compensatory

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

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

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

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

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

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

277 , 2-deoxyglucose, 3-nitropropionic acid, and kainic acid) to induce acute energy inhibition in C57/B6

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

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

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

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

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

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

284 Kainic acid-treated transgenic mice showed no significan

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

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

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

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

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

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

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

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

293 avage and provides neuroprotection following kainic acid treatment.

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

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

296 4787) in the GRIK4 gene, which codes for the kainic acid-type glutamate receptor KA1, was observed.

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

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

299 ng wild-type and fosB-null mice treated with kainic acid, we establish that the complexes comprise Ju

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