The Ca2+ channel α1B subunit is a pore-forming component capable of generating N-type Ca2+ channel activity. Although N-type Ca2+ channel plays a role in a variety of neuronal functions, α1B-deficient mice exhibit normal life span without apparent abnormalities of behavior, histology or plasma norepinephrine level, presumably owing to compensation by some other Ca2+ channel α1 or β subunit. In this study, we studied the levels of α1A, α1C, α1D, α1E, β1, β2, β3 and β4 mRNAs in adrenal gland of α1B-deficient mice. The α1A mRNA in homozygous mice was expressed at higher level than in wild or heterozygous mice, but no difference in the expression levels of α1C, α1D, α1E, β1, β2, β3 and β4 was found among wild, heterozygous and homozygous mice. The protein level of α1A in homozygous mice was also expressed at higher level than in wild or heterozygous mice. To examine whether increased expression is induced by cis-regulatory element within 5′-upstream region of α1A gene, we examined lacZ expression in α1B-deficient × α1A6.3-lacZ mice (carrying a 6.3-kb 5′-upstream fragment of α1A gene fused to E. coli lacZ reporter gene), which express lacZ in medullar chromaffin cells, but not in cortex. The levels of lacZ expression in homozygous α1B-deficient × α1A6.3-lacZ mice were higher than in wild or heterozygous mice. Therefore, a possible explanation of the normal behavior and plasma norepinephrine level of α1B-deficient mice is that compensation by α1A subunit occurs and that 6.3-kb 5′-upstream region of α1A gene contains enhancer cis-element(s) for compensation in adrenal medulla chromaffin cells. (Mol Cell Biochem 271: 91–99, 2005)