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,
β1,
β2,
β3 and
β4 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,
β1,
β2,
β3 and
β4 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,
β1,
β2,
β3 and
β4 subunits was found among wild, heterozygous and homozygous mice. In hippocampus and cerebellum,
β4 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,
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 α
1B-deficient mice with a CBA/JN genetic background.
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