| First Author | Martinez-Espinosa PL | Year | 2014 |
| Journal | J Gen Physiol | Volume | 144 |
| Issue | 4 | Pages | 275-95 |
| PubMed ID | 25267913 | Mgi Jnum | J:225860 |
| Mgi Id | MGI:5694639 | Doi | 10.1085/jgp.201411253 |
| Citation | Martinez-Espinosa PL, et al. (2014) Knockout of the BK beta2 subunit abolishes inactivation of BK currents in mouse adrenal chromaffin cells and results in slow-wave burst activity. J Gen Physiol 144(4):275-95 |
| abstractText | Rat and mouse adrenal medullary chromaffin cells (CCs) express an inactivating BK current. This inactivation is thought to arise from the assembly of up to four beta2 auxiliary subunits (encoded by the kcnmb2 gene) with a tetramer of pore-forming Slo1 alpha subunits. Although the physiological consequences of inactivation remain unclear, differences in depolarization-evoked firing among CCs have been proposed to arise from the ability of beta2 subunits to shift the range of BK channel activation. To investigate the role of BK channels containing beta2 subunits, we generated mice in which the gene encoding beta2 was deleted (beta2 knockout [KO]). Comparison of proteins from wild-type (WT) and beta2 KO mice allowed unambiguous demonstration of the presence of beta2 subunit in various tissues and its coassembly with the Slo1 alpha subunit. We compared current properties and cell firing properties of WT and beta2 KO CCs in slices and found that beta2 KO abolished inactivation, slowed action potential (AP) repolarization, and, during constant current injection, decreased AP firing. These results support the idea that the beta2-mediated shift of the BK channel activation range affects repetitive firing and AP properties. Unexpectedly, CCs from beta2 KO mice show an increased tendency toward spontaneous burst firing, suggesting that the particular properties of BK channels in the absence of beta2 subunits may predispose to burst firing. |
