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Loss of MsrB1 perturbs spatial learning and long-term potentiation/long-term depression in mice
Tengrui Shi1, Yujie Yang2, Zhonghao Zhang2
1College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China; College of Optoelectronic Engineering, Shenzhen University, Shenzhen, China.
Abstract:
MsrB1 belongs to the methionine sulfoxide reductase family, it is also known as selenoprotein R for the sake of possessing a selenocysteine residue. It has been reported that MsrB1 could interact with actin, TRPM6, clusterin, and amyloid-beta in vitro. Thus, we presumed that MsrB1 may play an important role in central nervous system. To examine whether MsrB1 knockout has any effects on brain development or learning behavior, we carried out histological study on brains of MsrB1 deficient mice, and further tested spatial learning ability and long-term synaptic plasticity of these mice by using Morris water maze and electrophysiological methods. It was observed that loss of MsrB1 did not perturb the overall development of central nervous system except for the astrogliosis in hippocampus, however, it led mice to be incapable in spatial learning and severe impairments in LTP/LTD expression in CA1 of brain slices, along with the down-regulation of the synaptic proteins including PSD95, SYP, GluN2A and GluN2B, as well as the dramatic decrease of CaMKIIs phosphorylation at 286(287) compared with wild type mice. Taken together, these results suggest that MsrB1 is essential for mice spatial learning and LTP/LTD induction, and the MsrB1 related redox homeostasis may be involved in regulating the phosphorylation of CaMKIIs.
Insights
Methionine sulfoxide reductase B1 (MsrB1) is vital for spatial learning and synaptic plasticity in mice. Its absence impairs long-term potentiation/depression and affects key synaptic proteins.
Area of Science:
- Neuroscience
- Biochemistry
- Genetics
Background:
- MsrB1, also known as selenoprotein R, is a methionine sulfoxide reductase.
- MsrB1 interacts with proteins like actin, TRPM6, clusterin, and amyloid-beta in vitro.
- Potential role of MsrB1 in the central nervous system is suggested by its interactions.
Purpose of the Study:
- To investigate the role of MsrB1 in brain development and learning behavior.
- To determine the effects of MsrB1 deficiency on spatial learning and memory.
- To analyze the impact of MsrB1 knockout on synaptic plasticity and related molecular mechanisms.
Main Methods:
- Histological examination of brains from MsrB1 deficient mice.
- Behavioral testing using the Morris water maze for spatial learning assessment.
- Electrophysiological recordings in brain slices to evaluate long-term potentiation (LTP) and long-term depression (LTD).
Main Results:
- MsrB1 deficiency did not affect overall central nervous system development but caused hippocampal astrogliosis.
- MsrB1 knockout mice exhibited deficits in spatial learning and severe impairments in CA1 LTP/LTD.
- Down-regulation of synaptic proteins (PSD95, SYP, GluN2A, GluN2B) and decreased CaMKII phosphorylation were observed.
Conclusions:
- MsrB1 is essential for spatial learning and LTP/LTD induction in mice.
- MsrB1-mediated redox homeostasis may regulate CaMKII phosphorylation.
- These findings highlight MsrB1's critical role in synaptic function and cognitive processes.
