Enhanced Expression of Ca2+ Channel α1A and 4 Subunits and Phosphorylated Tyrosine Hydroxylase in the Adrenal Gland of N-type Ca2+ Channel α1B Subunit-deficient Mice with a CBA/JN Genetic Background
Abstract:Electrophysiologic studies have demonstrated that adrenal medulla chromaffin cells express voltage-dependent P/Q-, N-, L-, and R-type Ca2+ 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 α1C/α1D, and R-type α1E, 1, 2, 3, and 4 subunits, as well as of tyrosine hydroxylase (Th), dopamine 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, 4, 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, 1, 2, 3, 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 4 subunits and increased catecholamine biosynthetic activity.
Document Type: Research Article
Publication date: June 1, 2006
Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.
Attention Members: To access the full text of the articles, be sure you are logged in to the AALAS website.
Attention: please note, due to a temporary technical problem, reference linking within the content is not available at this time
- Editorial Board
- Information for Authors
- Submit a Paper
- Subscribe to this Title
- Membership Information
- Information for Advertisers
- For issues prior to 1998
- Institutional Subscription Activation
- ingentaconnect is not responsible for the content or availability of external websites