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• W2163883777 abstract "We used homologous recombination in the mouse to knock-out RC3, a postsynaptic, calmodulin-binding PKC substrate. Mutant brains exhibited lower immunoreactivity to phospho-Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) but had the same synaptic density as wild type and did not exhibit a gross neuroanatomical phenotype. Basal excitatory synaptic transmission in CA1 was depressed, long-term potentiation (LTP) was enhanced, and the depressant effects of the metabotropic glutamate receptor (mGluR) agonist (<i>RS</i>)-3,5-dihydroxyphenylglycine was occluded compared with littermate controls. The frequency–response curve was displaced to the left, and long-term depression (LTD) could not be induced unless low-frequency stimuli were preceded by high-frequency tetani. Depotentiation was much more robust in the mutant, and only one stimulus was required to saturate LTD in primed mutant hippocampi, whereas multiple low-frequency stimuli were required in wild-type slices. Thus, ablation of RC3 appears to render the postsynaptic neuron hypersensitive to Ca²⁺, decreasing its LTD and LTP thresholds and accentuating the effects of priming stimuli. We propose an mGluR-dependent CaM-based sliding threshold mechanism for metaplasticity that is governed by the phosphorylation states of RC3 and CaMKII." @default.
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• W2163883777 date "2002-07-01" @default.
• W2163883777 modified "2023-09-27" @default.
• W2163883777 title "Targeted Disruption of RC3 Reveals a Calmodulin-Based Mechanism for Regulating Metaplasticity in the Hippocampus" @default.
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• W2163883777 doi "https://doi.org/10.1523/jneurosci.22-13-05525.2002" @default.
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