期刊
NEURON
卷 56, 期 3, 页码 488-502出版社
CELL PRESS
DOI: 10.1016/j.neuron.2007.09.007
关键词
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资金
- Biotechnology and Biological Sciences Research Council [BB/D013232/2] Funding Source: researchfish
- BBSRC [BB/D013232/2] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/D013232/2] Funding Source: Medline
- NIDA NIH HHS [DA017310] Funding Source: Medline
- NIMH NIH HHS [MH076936] Funding Source: Medline
The scaffold protein PSD-95 promotes the maturation and strengthening of excitatory synapses, functions that require proper localization of PSD-95 in the postsynaptic density (PSD). Here we report that phosphorylation of ser-295 enhances the synaptic accumulation of PSD-95 and the ability of PSD-95 to recruit surface AMPA receptors and potentiate excitatory postsynaptic currents. We present evidence that a Rac1-JNK1 signaling pathway mediates ser-295 phosphorylation and regulates synaptic content of PSD-95. Ser-295 phosphorylation is suppressed by chronic elevation, and increased by chronic silencing, of synaptic activity. Rapid dephosphorylation of ser-295 occurs in response to NMDA treatment that causes chemical long-term depression (LTD). Overexpression of a phosphomimicking mutant (S295D) of PSD-95 inhibited NMDA-induced AMPA receptor internalization and blocked the induction of LTD. The data suggest that synaptic strength can be regulated by phosphorylation-dephosphorylation of ser-295 of PSD-95 and that synaptic depression requires the dephosphorylation of ser-295.
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