Takahashi Eiki, Nagasu Takeshi
Tsukuba Research Laboratory, Eisai Co. Ltd., Tsukuba, Ibaraki, Japan.
Exp Anim. 2005 Jan;54(1):29-36. doi: 10.1538/expanim.54.29.
The Ca(2+) channel alpha(1B) subunit is a pore-forming component capable of generating N-type Ca(2+) channel activity. Although the N-type Ca(2+) channel plays a role in a variety of neuronal functions, alpha(1B)-deficient mice with a CBA/JN genetic background show no apparent behavioral or anatomical-histological abnormality, presumably owing to compensation by other Ca(2+) channels. In this study, we examined the mRNA expression of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits in the olfactory bulb, cerebral cortex, hippocampus and cerebellum of alpha(1B)-deficient mice. We found that the mRNA expression levels of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits were the same in the olfactory bulbs of wild, heterozygous and homozygous alpha(1B)-deficient mice. In the cerebral cortex, alpha(1A) mRNA in homozygous alpha(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits was found among wild, heterozygous and homozygous mice. In hippocampus and cerebellum, beta(4) mRNA in homozygous alpha(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2) and beta(3) subunits was found among wild, heterozygous and homozygous mice. These results suggest that the compensatory mechanisms differ in different brain regions of alpha(1B)-deficient mice with a CBA/JN genetic background.
钙离子通道α1B亚基是一种能够产生N型钙离子通道活性的孔形成成分。尽管N型钙离子通道在多种神经元功能中发挥作用，但具有CBA/JN遗传背景的α1B基因缺陷小鼠并未表现出明显的行为或解剖组织学异常，这可能是由于其他钙离子通道的代偿作用。在本研究中，我们检测了α1B基因缺陷小鼠嗅球、大脑皮层、海马体和小脑中α1A、α1C、α1D、α1E、β1、β2、β3和β4亚基的mRNA表达。我们发现，野生型、杂合型和纯合型α1B基因缺陷小鼠嗅球中α1A、α1C、α1D、α1E、β1、β2、β3和β4亚基的mRNA表达水平相同。在大脑皮层中，纯合型α1B基因缺陷小鼠的α1A mRNA表达水平高于野生型或杂合型小鼠，但野生型、杂合型和纯合型小鼠之间α1C、α1D、α1E、β1、β2、β3和β4亚基的表达水平没有差异。在海马体和小脑中，纯合型α1B基因缺陷小鼠的β4 mRNA表达水平高于野生型或杂合型小鼠，但野生型、杂合型和纯合型小鼠之间α1A、α1C、α1D、α1E、β1、β2和β3亚基的表达水平没有差异。这些结果表明，具有CBA/JN遗传背景的α1B基因缺陷小鼠不同脑区的代偿机制存在差异。
