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The Journal of Neuroscience, January 21, 2009, 29(3):669-677; doi:10.1523/JNEUROSCI.3921-08.2009

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Cellular/Molecular
Decreased NR2B Subunit Synaptic Levels Cause Impaired Long-Term Potentiation But Not Long-Term Depression

Fabrizio Gardoni,^1 * Daniela Mauceri,^1 * Matteo Malinverno,¹ Federica Polli,¹ Cinzia Costa,^2,3 Alessandro Tozzi,^2,3 Sabrina Siliquini,^2,3 Barbara Picconi,³ Flaminio Cattabeni,¹ Paolo Calabresi,^2,3 and Monica Di Luca¹

¹Department of Pharmacological Sciences and Centre of Excellence on Neurodegenerative Diseases, University of Milan, 20133 Milan, Italy, ²Clinica Neurologica, Università di Perugia, 06156 Perugia, Italy, and ³Laboratorio di Neurofisiologia, Fondazione Santa Lucia, Istituto di Ricovero e Cura a Carattere Scientifico c/o Centro Europeo di Ricerca sul Cervello, 00143 Rome, Italy

Correspondence should be addressed to Dr. Fabrizio Gardoni, Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133 Milan, Italy. Email: fabrizio.gardoni{at}unimi.it

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.

Key words: NMDA receptor; synaptic plasticity; trafficking; CaMKII; MAGUK; postsynaptic density

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Received Aug. 18, 2008; accepted Dec. 10, 2008.

Correspondence should be addressed to Dr. Fabrizio Gardoni, Department of Pharmacological Sciences, University of Milan, Via Balzaretti 9, 20133 Milan, Italy. Email: fabrizio.gardoni{at}unimi.it

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