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Slow ventricular conduction in mice heterozygous for a connexin43 null mutation.
To characterize the role of the gap junction protein connexin43 ( Cx43) in ventricular conduction, we studied hearts of mice with targeted deletion of the Cx43 gene. Mice homozygous for the Cx43 null mutation ( Cx43 -/-) die shortly after birth. Attempts to record electrical activity in neonatal Cx43 -/- hearts (n = 5) were unsuccessful. Ventricular epicardial conduction of paced beats, however, was 30% slower in heterozygous ( Cx43 -/+) neonatal hearts (0.14+/-0.04 m/s, n = 27) than in wild-type ( Cx43 +/+) hearts (0.20+/-0.07 m/s, n = 32; P < 0.001). This phenotype was even more severe in adult mice; ventricular epicardial conduction was 44% slower in 6-9 mo-old Cx43 -/+ hearts (0.18+/-0.03 m/s, n = 5) than in wild-type hearts (0.32+/-0.07 m/s, n = 7, P < 0.001). Electrocardiograms revealed significant prolongation of the QRS complex in adult Cx43 -/+ mice (13.4+/-1.8 ms, n = 13) compared with Cx43 +/+ mice (11.5+/-1.4 ms, n = 12, P < 0.01). Whole-cell recordings of action potential parameters in cultured disaggregated neonatal ventricular myocytes from Cx43 -/+ and +/+ hearts showed no differences. Thus, reduction in the abundance of a major cardiac gap junction protein through targeted deletion of a Cx43 allele directly leads to slowed ventricular conduction.[1]References
- Slow ventricular conduction in mice heterozygous for a connexin43 null mutation. Guerrero, P.A., Schuessler, R.B., Davis, L.M., Beyer, E.C., Johnson, C.M., Yamada, K.A., Saffitz, J.E. J. Clin. Invest. (1997) [Pubmed]
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