N-type and P/Q-type Ca2+ channels play an important role in the processing of olfactory information. However, N-type Ca2+ channel α1B-deficient mice show normal behavior, presumably owing to compensation by other Ca2+ channels. P/Q-type Ca2+ channel α1A mRNA was expressed at a higher level in olfactory bulb of homozygous α1B-deficient mice than wild-type or heterozygous mice. LacZ expression in olfactory mitral cells of homozygous α1B-deficient x α1A1.5-lacZ mice, carrying a 1.5-kb 5′-upstream fragment of the α1A gene fused to the lacZ reporter gene, was increased compared to that in wild-type or heterozygous mice. Therefore, a possible explanation for the normal behavior of α1B-deficient mice is compensation by the α1A gene and that the 1.5-kb 5′-upstream region of this gene contains an enhancer cis-element for compensation in olfactory mitral cells.
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