Involvement of the Snk-SPAR pathway in glutamate-induced excitotoxicity in cultured hippocampal neurons
Autor: | Hui Ma, Chang-kai Sun, Jian Zhang, Ming Fan, Jing Xu, Lan-Xiang Wu, Yumei Zhang |
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Rok vydání: | 2007 |
Předmět: |
Time Factors
Dendritic spine Dendritic Spines Excitotoxicity Glutamic Acid Protein Serine-Threonine Kinases Biology medicine.disease_cause Hippocampus Models Biological Synapse medicine Animals Molecular Biology Cells Cultured Neurons L-Lactate Dehydrogenase General Neuroscience GTPase-Activating Proteins Intracellular Signaling Peptides and Proteins Glutamate receptor Membrane Proteins Glutamic acid Rats Dizocilpine Animals Newborn Gene Expression Regulation NMDA receptor Neurology (clinical) Dizocilpine Maleate Signal transduction Disks Large Homolog 4 Protein Excitatory Amino Acid Antagonists Protein Kinases Neuroscience Signal Transduction Developmental Biology medicine.drug |
Zdroj: | Brain Research. 1168:38-45 |
ISSN: | 0006-8993 |
DOI: | 10.1016/j.brainres.2007.06.082 |
Popis: | The serum-induced kinase (Snk)-spine-associated Rap GTPase-activating protein (SPAR) signaling pathway is reported as a new molecular mechanism in activity-dependent remodeling of synapses. However, the relationship between Snk-SPAR pathway and glutamate-induced excitotoxicity is not well understood. We report here that in cultured hippocampal neurons, glutamate stimulation induces the activation of Snk-SPAR pathway, and leads to a loss of mature dendritic spines. The time-dependent changes in Snk and SPAR expression after glutamate exposure are also elucidated. Furthermore, the activation of Snk-SPAR pathway induced by glutamate treatment can be blocked by an NMDA receptor antagonist, MK801. These results demonstrate that Snk-SPAR pathway may play a pivotal role in glutamate-induced excitotoxic damage in CNS through regulating the stability of synapse. |
Databáze: | OpenAIRE |
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