Excitotoxicity-related endocytosis in cortical neurons - PubMed (original) (raw)
. 2007 Aug;102(3):789-800.
doi: 10.1111/j.1471-4159.2007.04564.x. Epub 2007 Apr 16.
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- PMID: 17437546
- DOI: 10.1111/j.1471-4159.2007.04564.x
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Excitotoxicity-related endocytosis in cortical neurons
A Vaslin et al. J Neurochem. 2007 Aug.
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Abstract
Recent studies showed that endocytosis is enhanced in neurons exposed to an excitototoxic stimulus. We here confirm and analyze this new phenomenon using dissociated cortical neuronal cultures. NMDA-induced uptake (FITC-dextran or FITC or horseradish peroxidase) occurs in these cultures and is due to endocytosis, not to cell entry through damaged membranes; it requires an excitotoxic dose of NMDA and is dependent on extracellular calcium, but occurs early, while the neuron is still intact and viable. It involves two components, NMDA-induced and constitutive, with different characteristics. Neither component involves specific binding of the endocytosed molecules to a saturable receptor. Strikingly, molecules internalized by the NMDA-induced component are targeted to neuronal nuclei. This component, but not the constitutive one, is blocked by a c-Jun N-terminal protein kinase inhibitor. In conclusion, an excitotoxic dose of NMDA triggers c-Jun N-terminal protein kinase-dependent endocytosis in cortical neuronal cultures, providing an in vitro model of the excitotoxicity-induced endocytosis reported in intact tissues.
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