Autor: |
Gardoni, Fabrizio, Mauceri, Daniela, Malinverno, Matteo, Polli, Federica, Costa, Cinzia, Tozzi, Alessandro, Siliquini, Sabrina, Picconi, Barbara, Cattabeni, Flaminio, Calabresi, Paolo, Di Luca, Monica |
Předmět: |
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Zdroj: |
Journal of Neuroscience; 1/21/2009, Vol. 29 Issue 3, p669-677, 9p, 8 Diagrams |
Abstrakt: |
The discovery of the molecular mechanisms regulating the abundance of synaptic NMDA receptors is essential for understanding how synaptic plasticity, as well as excitotoxic events, are regulated. However, a complete understanding of the precise molecular mechanisms regulating the composition of the NMDA receptor complex at hippocampal synapse is still missing. Here, we show that 2 h of CaMKII inhibition leads to a specific reduction of synaptic NR2B-containingNMDAreceptors without affecting localization of the NR2A subunit; this molecular event is accompanied by a dramatic reduction in the induction of long-term potentiation (LTP), while long-term depression induction is unaffected. The same molecular and functional results were obtained by disrupting NR2B/PSD-95 complex with NR2B C-tail cell permeable peptide (TAT-2B). These data indicate that NR2B redistribution between synaptic and extrasynaptic membranes represents an important molecular disturbance of the glutamatergic synapse and affects the correct induction of LTP. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
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