Contribution of PSD-95 Protein to Reward Location Memory
bioRxiv (Cold Spring Harbor Laboratory)(2019)
摘要
The molecular mechanisms involved in formation of memory are still poorly understood. We focus here on the function of post-synaptic density protein 95 (PSD-95) and its phosphorylation by CaMKII in spontaneous learning about reward location in female mice. We show that formation of reward location memory leads to downregulation of PSD-95 protein in dendritic spines of the stratum radiatum , area CA1, and selective shrinkage of dendritic spines that contain PSD-95. ShRNA-driven, long-term downregulation of PSD-95 in the area CA1 decreases precision of memory. Autophosphorylation deficient CaMKII mutant mice (CaMKII:T286A) need more time than wild-type animals to learn the location of reward. The same impairment is observed after CA1-targeted overexpression of CaMKII phosphorylation-deficient form of PSD-95 (PSD-95:S73A). In contrast to young adult mice, in aged animals reward location learning affects only spines that lack PSD-95. The frequency and size of the spines without PSD-95 are increased, while shRNA targeted to PSD-95 affects neither speed of learning nor precision of memory indicating alternative mechanisms to support successful memory formation in old mice. Altogether, our data suggest that dynamic regulation of PSD-95 expression is a mechanism that accelerates learning and improves precision of reward location memory in young mice. The function of PSD-95 in memory processes changes in aged animals.
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关键词
Memory
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