Comparison of seizure phenotype and neurodegeneration induced by systemic kainic acid in inbred, outbred, and hybrid mouse strains.
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Insights into the Pathology of the α3 Na(+)/K(+)-ATPase Ion Pump in Neurological Disorders; Lessons from Animal ModelsThe Effects of Exercise on Cognitive Recovery after Acquired Brain Injury in Animal Models: A Systematic ReviewPathobiology of aging mice and GEM: background strains and experimental designImmediate Epileptogenesis after Kainate-Induced Status Epilepticus in C57BL/6J Mice: Evidence from Long Term Continuous Video-EEG TelemetryCognitive deficits caused by a disease-mutation in the α3 Na(+)/K(+)-ATPase isoform.Advantages of repeated low dose against single high dose of kainate in C57BL/6J mouse model of status epilepticus: behavioral and electroencephalographic studiesRegulation of GABA(A) and glutamate receptor expression, synaptic facilitation and long-term potentiation in the hippocampus of prion mutant miceCaspase 3 involves in neuroplasticity, microglial activation and neurogenesis in the mice hippocampus after intracerebral injection of kainic acidLack of kainic acid-induced gamma oscillations predicts subsequent CA1 excitotoxic cell death.Variation in Galr1 expression determines susceptibility to exocitotoxin-induced cell death in mice.Galanin receptor 1 deletion exacerbates hippocampal neuronal loss after systemic kainate administration in mice.The CREB/CRE transcriptional pathway: protection against oxidative stress-mediated neuronal cell deathSusceptibility to seizure-induced excitotoxic cell death is regulated by an epistatic interaction between Chr 18 (Sicd1) and Chr 15 (Sicd2) loci in mice.Kainic acid-induced neurodegenerative model: potentials and limitationsCongenic strains provide evidence that a mapped locus on chromosome 15 influences excitotoxic cell deathPost-exposure administration of diazepam combined with soluble epoxide hydrolase inhibition stops seizures and modulates neuroinflammation in a murine model of acute TETS intoxicationLong term changes in phospho-APP and tau aggregation in the 3xTg-AD mice following cerebral ischemia.Genome-wide profiling of the activity-dependent hippocampal transcriptome.Kainic Acid-induced neurotoxicity: targeting glial responses and glia-derived cytokines.Early life seizures: evidence for chronic deficits linked to autism and intellectual disability across species and models.Neuroprotection requires the functions of the RNA-binding protein HuR.The relevance of individual genetic background and its role in animal models of epilepsyStrain differences in seizure-induced cell death following pilocarpine-induced status epilepticus.Effect of pioglitazone on excitotoxic neuronal damage in the mouse hippocampusHomeostatic regulation of KCC2 activity by the zinc receptor mZnR/GPR39 during seizures.Allosteric modulation of sigma-1 receptors elicits anti-seizure activitiesNeurodegeneration and functional impairments associated with glycogen synthase accumulation in a mouse model of Lafora diseaseLoss of CDKL5 disrupts kinome profile and event-related potentials leading to autistic-like phenotypes in mice.Altered GABAergic neurotransmission is associated with increased kainate-induced seizure in prostaglandin-endoperoxide synthase-2 deficient miceLack of Chronic Histologic Lesions Supportive of Sublethal Spontaneous Seizures in FVB/N Mice.Lack of influence of prion protein gene expression on kainate-induced seizures in mice: studies using congenic, coisogenic and transgenic strains.Age-Dependent Resistance to Excitotoxicity in Htt CAG140 Mice and the Effect of Strain Background.Cyclin D1 in excitatory neurons of the adult brain enhances kainate-induced neurotoxicity.Acute and chronic responses to the convulsant pilocarpine in DBA/2J and A/J miceMicroarray-assisted fine mapping of quantitative trait loci on chromosome 15 for susceptibility to seizure-induced cell death in mice.The relevance of inter- and intrastrain differences in mice and rats and their implications for models of seizures and epilepsy.One hour of pilocarpine-induced status epilepticus is sufficient to develop chronic epilepsy in mice, and is associated with mossy fiber sprouting but not neuronal death.A Standardized Protocol for Stereotaxic Intrahippocampal Administration of Kainic Acid Combined with Electroencephalographic Seizure Monitoring in Mice.Dual leucine zipper kinase is required for excitotoxicity-induced neuronal degeneration.The Rho-kinase (ROCK) inhibitor Y-27632 protects against excitotoxicity-induced neuronal death in vivo and in vitro.
P2860
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P2860
Comparison of seizure phenotype and neurodegeneration induced by systemic kainic acid in inbred, outbred, and hybrid mouse strains.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
@wuu
2006年学术文章
@zh
2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
2006年學術文章
@zh-hant
name
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@en
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@nl
type
label
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@en
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@nl
prefLabel
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@en
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@nl
P1476
Comparison of seizure phenotyp ...... red, and hybrid mouse strains.
@en
P2093
Jessica Pilar McLin
P304
P356
10.1111/J.1460-9568.2006.05111.X
P407
P577
2006-10-01T00:00:00Z