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Cardiovascular Research 2001 51(4):681-690; doi:10.1016/S0008-6363(01)00341-8
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

High resolution optical mapping reveals conduction slowing in connexin43 deficient mice

Benjamin C Eloffa, Deborah L Lernerb, Kathryn A Yamadab, Richard B Schuesslerb, Jeffrey E Saffitzb and David S Rosenbauma,*

aThe Heart and Vascular Research Center and the Department of Biomedical Engineering, MetroHealth Campus, Case Western Reserve University, 2500 MetroHealth Drive, Hamman 322, Cleveland, OH 44109-1998, USA
bThe Departments of Medicine, Pediatrics, Surgery and Pathology, and the Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, MO, USA

* Corresponding author. Tel.: +1-216-778-2005; fax: 1-216-778-4924 drosenbaum{at}metrohealth.org

Analysis of mice with genetically altered expression of cardiac connexins can provide insights into the role of individual gap junction channel proteins in cell-to-cell communication, impulse propagation, and arrhythmias. However, conflicting results have been reported regarding conduction velocity slowing in mice heterozygous for a null mutation in the gene encoding connexin43 (Cx43). Methods: High-resolution optical mapping was used to record action potentials from 256 sites, simultaneously, on the ventricular surface of Langendorff perfused hearts from 15 heterozygous (Cx43+/–) and 8 wildtype (Cx43+/+) mice (controls). A sensitive method for measuring epicardial conduction velocity was developed to minimize confounding influences of subepicardial breakthrough and virtual electrode effects. Results: Epicardial conduction velocity was significantly slower (23 to 35%, P<0.01) in Cx43+/– mice compared to wildtype. There was no change in conduction patterns or anisotropic ratio (Cx43+/– 1.54±0.33; Cx43+/+ 1.57±0.17) suggesting that Cx43 expression was reduced uniformly throughout myocardium. The magnitude of reductions in conduction velocity and Cx43 protein expression (45%) were similar in mice in which the null allele occurred in a pure C57BL/6J genetic background versus a mixed (C57BL/6J X 129) background. Action potential duration did not differ between mice of different genotypes. Conclusions: A ~50% reduction of Cx43 expression causes significant conduction velocity slowing in the Cx43+/– mouse heart. The apparent lack of conduction velocity changes reported in previous studies may be related to technical factors rather than variations in genetic background. High-resolution optical mapping is a powerful tool for investigating molecular determinants of propagation and arrhythmias in genetically engineered mice.

KEYWORDS Cell communication; Gap junctions; Gene expression; Mapping


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[Abstract] [Full Text] [PDF]


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