Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression

Fabrizio Gardoni, Daniela Mauceri, Matteo Malinverno, Federica Polli, Cinzia Costa, Alessandro Tozzi, Sabrina Siliquini, Barbara Picconi, Flaminio Cattabeni, Paolo Calabresi, Monica Di Luca

Research output: Contribution to journalArticle

91 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)669-677
Number of pages9
JournalJournal of Neuroscience
Volume29
Issue number3
DOIs
Publication statusPublished - Jan 21 2009

Fingerprint

Long-Term Potentiation
N-Methyl-D-Aspartate Receptors
Synapses
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Synaptic Membranes
Neurotransmitter Receptor
Neuronal Plasticity
Peptides
NR2B NMDA receptor

Keywords

  • CaMKII
  • MAGUK
  • NMDA receptor
  • Postsynaptic density
  • Synaptic plasticity
  • Trafficking

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Gardoni, F., Mauceri, D., Malinverno, M., Polli, F., Costa, C., Tozzi, A., ... Di Luca, M. (2009). Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression. Journal of Neuroscience, 29(3), 669-677. https://doi.org/10.1523/JNEUROSCI.3921-08.2009

Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression. / Gardoni, Fabrizio; Mauceri, Daniela; Malinverno, Matteo; Polli, Federica; Costa, Cinzia; Tozzi, Alessandro; Siliquini, Sabrina; Picconi, Barbara; Cattabeni, Flaminio; Calabresi, Paolo; Di Luca, Monica.

In: Journal of Neuroscience, Vol. 29, No. 3, 21.01.2009, p. 669-677.

Research output: Contribution to journalArticle

Gardoni, F, Mauceri, D, Malinverno, M, Polli, F, Costa, C, Tozzi, A, Siliquini, S, Picconi, B, Cattabeni, F, Calabresi, P & Di Luca, M 2009, 'Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression', Journal of Neuroscience, vol. 29, no. 3, pp. 669-677. https://doi.org/10.1523/JNEUROSCI.3921-08.2009
Gardoni, Fabrizio ; Mauceri, Daniela ; Malinverno, Matteo ; Polli, Federica ; Costa, Cinzia ; Tozzi, Alessandro ; Siliquini, Sabrina ; Picconi, Barbara ; Cattabeni, Flaminio ; Calabresi, Paolo ; Di Luca, Monica. / Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression. In: Journal of Neuroscience. 2009 ; Vol. 29, No. 3. pp. 669-677.
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