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pubmed:abstractText |
Learning-related modifications of synaptic transmission at CA1 hippocampal excitatory synapses are activity- and NMDA receptor (NMDAR)-dependent. While a postsynaptic increase in Ca(2+) is absolutely required for synaptic plasticity induction, the molecular mechanisms underlying the transduction of synaptic signals to postsynaptic changes are not clearly understood. In our recent study, we found that the postsynaptic calmodulin (CaM)-binding protein neurogranin (Ng) enhances synaptic strength in an activity- and NMDAR-dependent manner. Furthermore we have shown that Ng is not only required for the induction of long-term potentiation (LTP), but its mediated synaptic potentiation also mimics and occludes LTP. Our results demonstrate that Ng plays an important role in the regulation of hippocampal synaptic plasticity and synaptic function. Here, we summarize our findings and further discuss their possible implications in aging-related synaptic plasticity deficits.
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