Inoue Yuriko, Honkura Naoki, Kato Akihiko, Ogawa Sachie, Udo Hiroshi, Inokuchi Kaoru, Sugiyama Hiroyuki
Department of Biology, Faculty of Science, Graduate School of Science, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
Neurosci Lett. 2004 Jan 9;354(2):143-7. doi: 10.1016/j.neulet.2003.09.082.
In cultured rat hippocampal neurons, overexpression of Homer1a/Vesl-1S, an inducible protein upregulated by seizure or long-term potentiation, caused a reduction of punctate distribution of a postsynaptic protein Homer1c/Vesl-1L, without significant decrease in its total amount. Clusters of F-actin were also decreased. Treatments of cells with BDNF or a proteasome inhibitor, which cause increase in the expression level of endogenous Homer1a, also resulted in the reduction of Homer1c puncta. These results indicate that the accumulation of Homer1a, either exogenously expressed or endogenously induced, caused redistribution and dispersion of postsynaptic clusters of Homer1c and F-actin, suggesting an important role of Homer1a in synaptic remodeling.
在培养的大鼠海马神经元中，癫痫发作或长期增强作用上调的诱导型蛋白Homer1a/Vesl-1S的过表达，导致突触后蛋白Homer1c/Vesl-1L的点状分布减少，但其总量没有显著下降。F-肌动蛋白簇也减少。用BDNF或蛋白酶体抑制剂处理细胞，这会导致内源性Homer1a表达水平增加，也会导致Homer1c斑点减少。这些结果表明，外源性表达或内源性诱导的Homer1a的积累导致Homer1c和F-肌动蛋白的突触后簇重新分布和分散，提示Homer1a在突触重塑中起重要作用。
