Enhanced expression of Ca2+ channel α1A and β4 subunits and phosphorylated tyrosine hydroxylase in the adrenal gland of N-type Ca2+ channel α1B subunit-deficient mice with a CBA/JN genetic background

Eiki Takahashi, Takeshi Nagasu

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Electrophysiologic studies have demonstrated that adrenal medulla chromaffin cells express voltage-dependent P/Q-, N-, L-, and R-type Ca 2+ channels and that these channels regulate release of norepinephrine and epinephrine. However, N-type Ca2+ channel α1B-deficient mice with a CBA/JN background show normal plasma norepinephrine and epinephrine levels, presumably owing to compensation by other gene(s). To examine the expression patterns of the P/Q-type α1A, L-type α1C1D, and R-type α1E, β1, β2, β3 and β4 subunits, as well as of tyrosine hydroxylase (Th), dopamine β hydroxylase (Dbh), and phenylethanolamine-N- methyltransferase (Pnmt) in the adrenal gland of α1B-deficient mice, we used real-time quantitative reverse transcription-polymerase chain reaction and Western blot analyses. The expression levels of α1A, β4, Th, and Th phosphorylated at serine 40 were higher in homozygous mice than in wild-type and heterozygous mice, but the expression levels of α1C, α1D, α1E, β1, β2, β3, Dbh, and Pnmt did not differ among wild-type, heterozygous, and homozygous mice. These results suggest that the compensatory mechanisms to maintain normal levels of epinephrine and norepinephrine in the adrenal gland of N-type Ca2+ channel α1B-deficient mice include increased expression of α1A and β4 subunits and increased catecholamine biosynthetic activity.

Original languageEnglish
Pages (from-to)168-175
Number of pages8
JournalComparative Medicine
Volume56
Issue number3
Publication statusPublished - Jun 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • veterinary(all)

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