Premium
Effects of overexpression of Sim2 on spatial memory and expression of synapsin I in rat hippocampus
Author(s) -
Meng Xianfang,
Peng Bin,
Shi Jing,
Zheng Yao,
Chen Hao,
Zhang Jing,
Li Lingli,
Zhang Chun
Publication year - 2006
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2006.07.003
Subject(s) - synapsin i , synapsin , hippocampus , immunohistochemistry , morris water navigation task , transfection , synaptic plasticity , microbiology and biotechnology , biology , chemistry , neuroscience , gene , immunology , biochemistry , receptor , vesicle , membrane , synaptic vesicle
The single‐minded 2 gene (Sim2) plays a crucial role in the mental retardation of Down Syndrome (DS). To explore how Sim2 influences spatial memory, a DNA plasmid‐encoding mouse Sim2 (mSim2) wrapped with liposome was bilaterally injected into the hippocampus of rats. The effect of overexpressing mSim2 on spatial learning was determined by a Morris water maze task. The expression of synapsin I was detected by reverse transcriptional‐polymerase chain reaction (RT‐PCR) analysis and immunohistochemistry, respectively. The phosphosynapsin was also examined by immunohistochemistry. As demonstrated by RT‐PCR, mSim2 was overexpressed in the hippocampus of rats, and pcDNA3/mSim2‐transfected rats showed longer latency to find the hidden platform compared with pcDNA3‐transfected rats ( P < 0.05). Synapsin I mRNA and protein expression were decreased significantly by mSim2 transfection, as demonstrated by RT‐PCR and immunohistochemistry. Moreover, the expression profile of phosphosynapsin was similar to that of synapsin I. So it is concluded that Sim2 could impair the ability of learning and memory by inhibiting synaptic plasticity, and may play a crucial role in the pathogenesis of DS.