Abstract
In this study, we investigated the interactions between synapse adhesion molecules neurexin, neuroligin1, neuroligin2 and postsynaptic density protein 95 (PSD-95) in transient cerebral ischemia and possible regulatory mechanism of these interactions. Our data show that preconditioning ischemia can down-regulate the increased neurexin-neuroligin1-PSD-95 interaction induced by ischemia injury and exerts a neuroprotective effect. Pre-treatment of N-methyl-D-aspartate (NMDA) receptor antagonist ketamine can demolish this neuroprotective effect of preconditioning by increasing neurexin-neuroligin1-PSD-95 interaction. These results indicate that the neurexin-neuroligin1-PSD-95 is an important signalling module in ischemic injury and a novel possible target in therapeutics of brain ischemia.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Cell Adhesion Molecules, Neuronal / drug effects
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Cell Adhesion Molecules, Neuronal / metabolism*
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Disks Large Homolog 4 Protein
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Excitatory Amino Acid Antagonists / pharmacology
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Hippocampus / blood supply*
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Hippocampus / metabolism
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Hippocampus / pathology
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Immunoprecipitation
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Intracellular Signaling Peptides and Proteins / drug effects
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Intracellular Signaling Peptides and Proteins / metabolism*
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Ischemic Attack, Transient / metabolism*
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Ischemic Attack, Transient / physiopathology
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Ischemic Preconditioning*
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Ketamine / pharmacology
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Male
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Membrane Proteins / drug effects
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Membrane Proteins / metabolism*
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Nerve Tissue Proteins / drug effects
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Nerve Tissue Proteins / metabolism*
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / metabolism
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Synapses / metabolism
Substances
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Cell Adhesion Molecules, Neuronal
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Disks Large Homolog 4 Protein
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Dlg4 protein, rat
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Excitatory Amino Acid Antagonists
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Intracellular Signaling Peptides and Proteins
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Membrane Proteins
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Nerve Tissue Proteins
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Receptors, N-Methyl-D-Aspartate
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neuroligin 1
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Ketamine