期刊
EMBO JOURNAL
卷 26, 期 23, 页码 4879-4890出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.emboj.7601884
关键词
AKAP; AMPA receptors; calcium; PKA; synapse
资金
- NIDA NIH HHS [DA015916, P01 DA015916] Funding Source: Medline
- NIGMS NIH HHS [R01 GM032875, GM032875, T32 GM007337, T32 GM067795] Funding Source: Medline
- NINDS NIH HHS [R01 NS046450, R01 NS054614] Funding Source: Medline
Association of PKA with the AMPA receptor GluR1 subunit via the A kinase anchor protein AKAP150 is crucial for GluR1 phosphorylation. Mutating the AKAP150 gene to specifically prevent PKA binding reduced PKA within postsynaptic densities (470%). It abolished hippocampal LTP in 7-12 but not 4- week-old mice. Inhibitors of PKA and of GluR2- lacking AMPA receptors blocked single tetanus LTP in hippocampal slices of 8 but not 4- weekold WT mice. Inhibitors of GluR2-lacking AMPA receptors also prevented LTP in 2 but not 3-week-old mice. Other studies demonstrate that GluR1 homomeric AMPA receptors are the main GluR2-lacking AMPA receptors in adult hippocampus and require PKA for their functional postsynaptic expression during potentiation. AKAP150-anchored PKA might thus critically contribute to LTP in adult hippocampus in part by phosphorylating GluR1 to foster postsynaptic accumulation of homomeric GluR1 AMPA receptors during initial LTP in 8-week-old mice.
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