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Metaplasticity describes the stabilization of synaptic strength such that strong synapses are likely to remain strong while weak synapses are likely to remain weak. A potential mechanism for metaplasticity is a correlated change in both N-methyl-D-aspartate (NMDA) receptor-mediated postsynaptic conductance and synaptic strength. Synchronous activation of CA3-CA3 synapses during spontaneous bursts of population activity caused long-term potentiation (LTP) of recurrent CA3-CA3 glutamatergic synapses under control conditions and depotentiation when NMDA receptors were partially blocked by competitive antagonists. LTP was associated with a significant increase in membrane-bound NMDA receptors, whereas depotentiation was associated with a significant decrease in membrane-bound NMDA receptors. During burst activity, further depotentiation could be induced by sequential reductions in antagonist concentration, consistent with a depotentiation-associated reduction in membrane-bound NMDA receptors. The decrease in number of membrane-bound NMDA receptors associated with depotentiation reduced the probability of subsequent potentiation of weakened synapses in the face of ongoing synchronous network activity. This molecular mechanism stabilizes synaptic strength, which in turn stabilizes the state of the CA3 neuronal network, reflected in the frequency of spontaneous population bursts.

Original publication

DOI

10.1152/jn.00346.2007

Type

Journal article

Journal

J Neurophysiol

Publication Date

11/2007

Volume

98

Pages

2818 - 2826

Keywords

2-Amino-5-phosphonovalerate, Algorithms, Analysis of Variance, Animals, Biphenyl Compounds, Dose-Response Relationship, Drug, Electric Stimulation, Excitatory Amino Acid Antagonists, Gene Expression Regulation, Hippocampus, In Vitro Techniques, Long-Term Potentiation, Male, Models, Biological, Nerve Net, Propionates, Protein Transport, Pyramidal Cells, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate, Synapses