Decreased NR2B Subunit Synaptic Levels Cause Impaired Long-Term Potentiation But Not Long-Term Depression
العنوان: | Decreased NR2B Subunit Synaptic Levels Cause Impaired Long-Term Potentiation But Not Long-Term Depression |
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المؤلفون: | F. Cattabeni, Sabrina Siliquini, Alessandro Tozzi, Fabrizio Gardoni, Federica Polli, M. Di Luca, Cinzia Costa, Matteo Malinverno, Barbara Picconi, Daniela Mauceri, Paolo Calabresi |
المصدر: | The Journal of Neuroscience. 29:669-677 |
بيانات النشر: | Society for Neuroscience, 2009. |
سنة النشر: | 2009 |
مصطلحات موضوعية: | Patch-Clamp Techniques, Time Factors, Long-Term Potentiation, Nonsynaptic plasticity, Enzyme-Linked Immunosorbent Assay, Biology, Hippocampus, Receptors, N-Methyl-D-Aspartate, Organ Culture Techniques, Synaptic augmentation, Metaplasticity, Animals, Immunoprecipitation, Enzyme Inhibitors, Long-term depression, Cells, Cultured, Neurons, Analysis of Variance, Long-Term Synaptic Depression, musculoskeletal, neural, and ocular physiology, General Neuroscience, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Long-term potentiation, Articles, Embryo, Mammalian, CREB-Binding Protein, Electric Stimulation, Rats, Protein Transport, Synaptic fatigue, nervous system, Synapses, Synaptic plasticity, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Peptides, Disks Large Homolog 4 Protein, Neuroscience, Synaptic tagging, Subcellular Fractions |
الوصف: | 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. |
تدمد: | 1529-2401 0270-6474 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71572381ca57f4e5a799611e79b05f74Test https://doi.org/10.1523/jneurosci.3921-08.2009Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....71572381ca57f4e5a799611e79b05f74 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15292401 02706474 |
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