A protein phosphatase 2A deficit in the hippocampal CA1 area impairs memory extinction

Molecular Brain

Rui Liu¹  Weiyan You¹  Jing Wang¹  Cui Qi¹  Ran Xie¹  Jun Gao¹  Xiaolin Kou¹  Yu Liu¹  Xiang Gao² 

[1] 0000 0000 9255 8984, grid.89957.3a, Department of Neurobiology, Nanjing Medical University, 211166, Nanjing, Jiangsu, China;0000 0001 2314 964X, grid.41156.37, Model Animal Research Center and MOE Key Laboratory of Model Animals for Disease Study, Nanjing University, 210093, Nanjing, Jiangsu, China;

关键词: PP2A;    Extinction;    Learning and memory;    Synaptic plasticity;    Hippocampus;   

DOI  :  10.1186/s13041-019-0469-9

来源: publisher

【 摘 要 】

Protein phosphorylation plays an important role in learning and memory. Protein phosphatase 2A (PP2A) is a serine/threonine phosphatase involved in the regulation of neural synaptic plasticity. Here, to determine if PP2A is necessary for successful learning and memory, we have utilized a Tg (Camk2a-cre) T29–2Stl mice to specific knock down the expression of hippocampal PP2A in mice. By analysing behavioural, we observed that loss of PP2A in the hippocampal CA1 area did not affect the formation of memory but impaired contextual fear memory extinction. We use the electrophysiological recording to find the synaptic mechanisms. The results showed that the basic synapse transmission and synaptic plasticity of PP2A conditional knockout (CKO) mice were impaired. Moreover, PP2A CKO mice exhibited a saturating long-term potentiation inducted by strong theta burst stimulation but no depotentiation after low-frequency stimulation. Taken together, our results provide the evidence that PP2A is involved in synaptic transmission and hippocampus-dependent memory extinction.

【 授权许可】

CC BY