AI Article Synopsis
- PSD-95 is a key protein in glutamatergic synapses, helping anchor AMPA receptors and influencing their activity.
- During NMDA-induced long-term depression (NMDA-LTD), levels of PSD-95 decrease, but this downregulation is not necessary for the expression of NMDA-LTD.
- The study found that while CaMKII activation leads to the phosphorylation of PSD-95, this process is not required for the actual changes in synaptic functionality associated with NMDA-LTD.
Article Abstract
PSD-95 is a major scaffolding protein of the post-synaptic density (PSD) of a glutamatergic synapse. PSD-95, via interactions with stargazin, anchors AMPA receptors at the synapse and regulates AMPAR currents. The expression of PSD-95 is regulated during synaptic plasticity. It is, however, unknown whether this regulation is required for induction of functional plasticity of glutamatergic synapses. Here, we show that NMDA-induced long-term depression of synaptic transmission (NMDA-LTD) is accompanied by downregulation of PSD-95 protein levels. Using pharmacologic and molecular manipulations, we further demonstrate that the NMDA-induced downregulation of PSD-95 depends on the activation of CaMKII and CaMKII-driven phosphorylation of PSD-95 serine 73. Surprisingly, neither CaMKII activity nor CaMKII-dependent phosphorylation of PSD-95 serine 73 are required for the expression of NMDA-LTD. These results support the hypothesis that synaptic plasticity of AMPARs may occur without dynamic regulation of PSD-95 protein levels.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005143 | PMC |
| http://dx.doi.org/10.1038/s41598-020-58989-2 | DOI Listing |
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