Decreased NR2B Subunit Synaptic Levels Cause Impaired Long-Term Potentiation But Not Long-Term Depression
Articolo
Data di Pubblicazione:
2009
Citazione:
Decreased NR2B Subunit Synaptic Levels Cause Impaired
Long-Term Potentiation But Not Long-Term Depression / F. Gardoni, D. Mauceri, M. Malinverno, F. Polli, C. Costa, A. Tozzi, S. Siliquini, B. Picconi, F. Cattabeni, P. Calabresi, M. Di Luca. - In: THE JOURNAL OF NEUROSCIENCE. - ISSN 0270-6474. - 29:3(2009 Jan 21), pp. 669-677.
Abstract:
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-containing NMDA receptors 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
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
NMDA receptor ; synaptic plasticity ; trafficking ; CaMKII ; MAGUK ; postsynaptic density
Elenco autori:
F. Gardoni, D. Mauceri, M. Malinverno, F. Polli, C. Costa, A. Tozzi, S. Siliquini, B. Picconi, F. Cattabeni, P. Calabresi, M. Di Luca
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