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      Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene.

      Nature

      Animals, Apoptosis, Drug Resistance, Excitatory Amino Acid Agonists, toxicity, Gene Expression, drug effects, Gene Targeting, Glutamic Acid, metabolism, Hippocampus, enzymology, pathology, Kainic Acid, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitogen-Activated Protein Kinase 10, Mitogen-Activated Protein Kinases, Neurons, Phosphorylation, Protein Kinases, deficiency, genetics, physiology, Protein-Serine-Threonine Kinases, Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-fos, Proto-Oncogene Proteins c-jun, Seizures, chemically induced, Signal Transduction, Transcription Factor AP-1

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          Abstract

          Excitatory amino acids induce both acute membrane depolarization and latent cellular toxicity, which often leads to apoptosis in many neurological disorders. Recent studies indicate that glutamate toxicity may involve the c-Jun amino-terminal kinase (JNK) group of mitogen-activated protein (MAP) kinases. One member of the JNK family, Jnk3, may be required for stress-induced neuronal apoptosis, as it is selectively expressed in the nervous system. Here we report that disruption of the gene encoding Jnk3 in mice caused the mice to be resistant to the excitotoxic glutamate-receptor agonist kainic acid: they showed a reduction in seizure activity and hippocampal neuron apoptosis was prevented. Although application of kainic acid imposed the same level of noxious stress, the phosphorylation of c-Jun and the transcriptional activity of the AP-1 transcription factor complex were markedly reduced in the mutant mice. These data indicate that the observed neuroprotection is due to the extinction of a Jnk3-mediated signalling pathway, which is an important component in the pathogenesis of glutamate neurotoxicity.

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          Journal
          9349820
          10.1038/39899

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