首页> 外文期刊>Experimental Animals >Pattern of Compensatory Expression of Voltage-Dependent Ca~(2+) Channel α_1 and β Subunits in Brain of N-type Ca~(2+) Channel α_(1B) Subunit Gene-Deficient Mice with a CBA/JN Genetic Background
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Pattern of Compensatory Expression of Voltage-Dependent Ca~(2+) Channel α_1 and β Subunits in Brain of N-type Ca~(2+) Channel α_(1B) Subunit Gene-Deficient Mice with a CBA/JN Genetic Background

机译:具有CBA / JN遗传背景的N型Ca〜(2+)通道α_(1B)亚基基因缺陷小鼠脑中电压依赖性Ca〜(2+)通道α_1和β亚基的补偿表达模式

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The Ca~(2+) channel α_(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, α_(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 α_(1A), α_(1C), α_(1D), α_(1E), β_1, β_2, β_3 and 耞4 subunits in the olfactory bulb, cerebral cortex, hippocampus and cerebellum of α_(1B)-deficient mice. We found that the mRNA expression levels of the α_(1A), α_(1C), α_(1D), α_(1E), β_1, β_2, β_3 and β_4 subunits were the same in the olfactory bulbs of wild, heterozygous and homozygous α_(1B)-deficient mice. In the cerebral cortex, α_(1A) mRNA in homozygous α_(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the α_(1C), α_(1D), α_(1E), β_1, β_2, β_3 and ft subunits was found among wild, heterozygous and homozygous mice. In hippocampus and cerebellum, β_4 mRNA in homozygous α_(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the α_(1A), α_(1C), α_(1D), α_(1E), β_1, β_2 and β_3 subunits was found among wild, heterozygous and homozygous mice. These results suggest that the compensatory mechanisms differ in differentbrain regions of α_(1B)-deficient mice with a CBA/JN genetic background.
机译:Ca〜(2+)通道α_(1B)亚基是能够产生N型Ca〜(2+)通道活性的成孔组分。尽管N型Ca〜(2+)通道在多种神经元功能中起作用,但具有CBA / JN遗传背景的α_(1B)缺陷型小鼠没有表现出明显的行为或解剖组织异常,这可能是由于补偿引起的通过其他Ca〜(2+)通道。在这项研究中,我们检查了嗅球,大脑皮层,海马中α_(1A),α_(1C),α_(1D),α_(1E),β_1,β_2,β_3和耞4亚基的mRNA表达α_(1B)缺陷小鼠的小脑和小脑。我们发现在野生,杂合和纯合的嗅球中,α_(1A),α_(1C),α_(1D),α_(1E),β_1,β_2,β_3和β_4亚基的mRNA表达水平相同。 α_(1B)缺陷小鼠。在大脑皮层中,纯合α_(1B)缺陷小鼠中的α_(1A)mRNA的表达水平高于野生或杂合小鼠,但α_(1C),α_(1D)的表达水平没有差异在野生,杂合和纯合小鼠中发现了α,(1E),β_1,β_2,β_3和ft亚基。在海马和小脑中,纯合α_(1B)缺陷型小鼠的β_4mRNA的表达水平高于野生或杂合小鼠,但α_(1A),α_(1C),α_(在野生,杂合和纯合小鼠中发现了1D),α_(1E),β_1,β_2和β_3亚基。这些结果表明,在具有CBA / JN遗传背景的α_(1B)缺陷型小鼠的不同大脑区域,其补偿机制不同。

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