On the mechanism of synaptic depression induced by CaMKIIN, an endogenous inhibitor of CaMKII

Activity-dependent synaptic plasticity underlies, at least in part, learning and memory processes. NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) is a major synaptic plasticity model. During LTP induction, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated, autophospho...

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Veröffentlicht in:	PloS one 2012-11, Vol.7 (11), p.e49293-e49293
Hauptverfasser:	Gouet, Camilo, Aburto, Belen, Vergara, Cecilia, Sanhueza, Magdalena
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biology Brain Brain slice preparation Ca2+/calmodulin-dependent protein kinase II Calcium binding proteins Calcium Signaling - physiology Calcium signalling Calcium-binding protein Calcium-Calmodulin-Dependent Protein Kinase Type 2 - analysis Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Calmodulin Carrier Proteins - metabolism Carrier Proteins - physiology Cerebral blood flow Dendritic spines Glutamatergic transmission Glutamic acid receptors (ionotropic) Hippocampus Hippocampus - metabolism Homeostatic plasticity Inhibitors Ischemia Kinases Learning Long-term depression Long-Term Potentiation Long-Term Synaptic Depression Medical screening Memory Metabolic pathways N-Methyl-D-aspartic acid receptors Occlusion Peptides Phosphorylation Plasticity Postsynaptic density Proteasomes Protein biosynthesis Protein kinases Protein synthesis Protein Transport Proteins Rats Rats, Sprague-Dawley Receptors, N-Methyl-D-Aspartate - metabolism Receptors, N-Methyl-D-Aspartate - physiology Regulators RNA, Messenger - metabolism Saturation Synapses Synaptic depression Synaptic plasticity Synaptic strength
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