Although the N-type Ca2+ channel plays a role in a variety of neuronal functions, N-type Ca2+ channel α1B- deficient mice exhibit normal life span without apparent behavioral or histologic abnormalities. To examine whether the reason for their normal behavior is compensation by other Cav2 channel α1 or β subunit genes and to analyze whether genetic background influences the subunit expression pattern, we studied the α1A, α1E, β1b, β2, β3 and β4 subunit mRNA levels in cerebellum of α1B-deficient mice with CBA x C57BL/6 or CBA/JN background. In cerebellum of the mice with a CBA x C57BL/6 background, α1A mRNA was expressed at a higher level than that in wild-type or heterozygous mice, but difference in the expression levels of α1E, β1b, β2, β3 and β4 subunits was not found among wild-type, heterozygous, and homozygous mice. In cerebellum of α1B-deficient mice with CBA/JN background, β4 mRNA was expressed at a higher level than that in wild-type or heterozygous mice, but α1A, α1E, β1b, α2 and β3 transcripts were expressed at similar levels in all genotypes. Therefore, a possible explanation of the normal behavior of α1B-deficient mice is that Cav2 channel family members compensate for the deficiency, and that the change of functional subunit expression pattern for compensation differs in animals with different genetic backgrounds.
|Number of pages
|Published - Dec 2004
All Science Journal Classification (ASJC) codes
- General Biochemistry,Genetics and Molecular Biology
- General Veterinary