Pattern of compensatory expression of voltage-dependent Ca2+ channel α1 and β subunits in brain of N-type Ca2+ channel α1B subunit gene-deficient mice with a CBA/JN genetic background

Eiki Takahashi, Takeshi Nagasu

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5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)29-36
Number of pages8
JournalExperimental Animals
Volume54
Issue number1
DOIs
Publication statusPublished - 2005
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Animal Science and Zoology
  • Biochemistry, Genetics and Molecular Biology(all)
  • veterinary(all)

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