Long-term potentiation (LTP) at excitatory hippocampal synapses involves the postsynaptic insertion of AMPA receptors triggered by calcium/calmodulin-dependent protein kinase type II (CaMKII)-mediated protein phosphorylation, but the CaMKII substrate remains unclear. Here, mice expressing a mutant form of auxiliary transmembrane AMPA receptor regulatory protein γ8 (TARP γ8), which lacks CaMKII phosphorylation sites, showed reductions in LTP, postsynaptic AMPA receptor insertion and performance in memory tasks compared with controls. This suggests that TARP γ8 is an important substrate for CaMKII during LTP induction.
References
Park, J. et al. CaMKII phosphorylation of TARPγ-8 is a mediator of LTP and learning and memory. Neuron http://dx.doi.org/10.1016/j.neuron.2016.09.002 (2016)
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Lewis, S. TARP target. Nat Rev Neurosci 17, 671 (2016). https://doi.org/10.1038/nrn.2016.146
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DOI: https://doi.org/10.1038/nrn.2016.146
