| First Author | Glukhov AV | Year | 2010 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 299 |
| Issue | 2 | Pages | H482-91 |
| PubMed ID | 20525877 | Mgi Jnum | J:163867 |
| Mgi Id | MGI:4830056 | Doi | 10.1152/ajpheart.00756.2009 |
| Citation | Glukhov AV, et al. (2010) Functional anatomy of the murine sinus node: high-resolution optical mapping of ankyrin-B heterozygous mice. Am J Physiol Heart Circ Physiol 299(2):H482-91 |
| abstractText | The mouse is widely used as a genetic platform to investigate the molecular mechanisms of sinoatrial node (SAN) pacemaking. Recently, it has been shown that isolated SAN cells from the ankyrin-B (AnkB)-deficient mice display severe pacemaking dysfunction similar to individuals harboring ankyrin 2 allele variants. However, these results have been limited to isolated SAN cells only and thus did not evaluate the functional anatomy of the widely distributed atrial pacemaker complex (e.g., the dynamic interaction of primary and subsidiary pacemakers). We studied pacemaker function in an intact mouse atrial preparation, which included the SAN, atrioventricular junction (AVJ), and both atria, excluding most of the septum. Optical mapping with a voltage-sensitive dye and CMOS camera ULTIMA-L was used to map spontaneous pacemaker activity with or without autonomic modulation in wild-type (WT) mice (n = 7) and in the AnkB heterozygous (AnkB(+/-); n = 9) mouse model of human SAN disease. In WT mice, isoproterenol accelerated the SAN rate (for 10 microM: from 325 + or - 19 to 510 + or - 33 beat/min, P < 0.01) and shifted the leading pacemaker site superiorly by 0.77 + or - 0.11 mm within the SAN. ACh decreased the SAN rate (from 333 + or |
