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

スポンサーリンク

概要

• 論文の詳細を見る

• The Ca2+ channel α1B subunit is a pore-forming component capable of generating N-type Ca2+ channel activity. Although the N-type Ca2+ channel plays a role in a variety of neuronal functions, α1B-deficient mice with a CBA/JN genetic background show no apparent behavioral or anatomical-histological abnormality, presumably owing to compensation by other Ca2+ channels. In this study, we examined the mRNA expression of the α1A, α1C, α1D, α1E, β1, β2, β3 and β4 subunits in the olfactory bulb, cerebral cortex, hippocampus and cerebellum of α1B-deficient mice. We found that the mRNA expression levels of the α1A, α1C, α1D, α1E, β1, β2, β3 and β4 subunits were the same in the olfactory bulbs of wild, heterozygous and homozygous α1B-deficient mice. In the cerebral cortex, α1A mRNA in homozygous α1B-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the α1C, α1D, α1E, β1, β2, β3 and β4 subunits was found among wild, heterozygous and homozygous mice. In hippocampus and cerebellum, β4 mRNA in homozygous α1B-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the α1A, α1C, α1D, α1E, β1, β2 and β3 subunits was found among wild, heterozygous and homozygous mice. These results suggest that the compensatory mechanisms differ in different brain regions of α1B-deficient mice with a CBA/JN genetic background.

• 2005-01-01

著者

• Nagasu Takeshi

  Tsukuba Research Laboratories Eisai Co. Ltd.

• Takahashi Eiki

  Tsukuba Research Laboratory Eisai Co. Ltd.

関連論文

• Synthesis and Evaluation of Novel Pyrimido-Acridone, -Phenoxadine, and -Carbazole as Topoisomerase II Inhibitors
• A novel carbazole topoisomerase II poison, ER-37328 : potent tumoricidal activity against human solid tumors in vitro and in vivo
• Decreases in pheromonal responses at the accessory olfactory bulb of mice with a deficiency of the alpha(1B) or beta 3-subunits of voltage-dependent Ca2+-channels
• Pattern of Compensatory Expression of Voltage-Dependent Ca^ Channel α_1 and β Subunits in Brain of N-type Ca^ Channel α_ Subunit Gene-Deficient Mice with a CBA/JN Genetic Background

スポンサーリンク