Abstract
Perinatal hypoxic injury is the major cause of normal neural developmental alterations. Recent studies concerning animal models show that an hypoxic/ischaemic event triggers a process taking to a synaptic architecture reorganization which induces a transient change in the synaptic (synapsin 1, SNAP 25, APP) and neuronal (MAP2, N-CAM, GAP-43 and presenilins) protein expression. Here we review the post-translational modifications of some proteins after hypoxic-ischaemic events. A deeper study on synaptic proteins plasticity could give an important key for the understanding of the recovery mechanisms of the nervous system.
MeSH terms
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Amyloid beta-Peptides / physiology
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Disease Models, Animal
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GAP-43 Protein / physiology
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Humans
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Hypoxia-Ischemia, Brain / etiology*
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Membrane Proteins / physiology
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Microtubule-Associated Proteins / physiology
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Nerve Tissue Proteins / physiology*
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Neural Cell Adhesion Molecules / physiology
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Presenilin-1
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Presenilin-2
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Synapsins / physiology
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Synaptosomal-Associated Protein 25
Substances
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Amyloid beta-Peptides
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GAP-43 Protein
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Membrane Proteins
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Microtubule-Associated Proteins
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Nerve Tissue Proteins
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Neural Cell Adhesion Molecules
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PSEN1 protein, human
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PSEN2 protein, human
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Presenilin-1
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Presenilin-2
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SNAP25 protein, human
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Synapsins
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Synaptosomal-Associated Protein 25