First Author | Ohta T | Year | 2010 |
Journal | Biochem Biophys Res Commun | Volume | 394 |
Issue | 3 | Pages | 464-9 |
PubMed ID | 20144588 | Mgi Jnum | J:159255 |
Mgi Id | MGI:4442133 | Doi | 10.1016/j.bbrc.2010.01.036 |
Citation | Ohta T, et al. (2010) Decreased calcium channel currents and facilitated epinephrine release in the Ca2+ channel beta3 subunit-null mice. Biochem Biophys Res Commun 394(3):464-9 |
abstractText | The beta subunits of voltage-dependent calcium channels are known to modify calcium channel currents through pore-forming alpha1 subunits. The beta3 subunit is expressed in the adrenal gland and participates in forming various calcium channel types. We performed a series of experiments in beta3-null mice to determine the role of the beta3 subunit in catecholamine release from the adrenal chromaffin system. Protein levels of N-type channel forming CaV2.2 and L-type forming CaV1.2 decreased. The beta3-null mice showed a decreased baroreflex, suggesting decreased sympathetic tonus, whereas plasma catecholamine levels did not change. Pulse-voltage stimulation revealed significantly increased amperometrical currents in beta3-null mice, while patch-clamp recordings showed a significant reduction in Ca(2+)-currents due to reduced L- and N-type currents, indicating facilitated exocytosis. A biochemical analysis revealed increased InsP3 production. In conclusion, our results indicate the importance of the beta3 subunit in determining calcium channel characteristics and catecholamine release in adrenal chromaffin cells. |