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Arrhythmia in isolated prenatal hearts after ablation of the Ca(v)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels

Arrhythmia in isolated prenatal hearts after ablation of the Ca(v)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels
Arrhythmia in isolated prenatal hearts after ablation of the Ca(v)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels
A voltage-gated calcium channel containing Cav2.3e (1Ee) as the ion conducting pore has recently been detected in rat heart. Functional evidence for this Ca2+ channel to be involved in the regulation of heart beating, besides L- and T-type channels, was derived from murine embryos where the gene for Cav1.2 had been ablated. The remaining ''L-type like“ current component was not related to recombinant splice variants of Cav1.3 containing channels. As recombinant Cav2.3 channels from rat were reported to be weakly dihydropyridine sensitive, the spontaneous activity of the prenatal hearts from Cav2.3(-|-) mice was compared to that of Cav2.3(+|+) control animals to investigate if Cav2.3 could represent such a L-type like Ca2+ channel. The spontaneous activity of murine embryonic hearts was recorded by using a multielectrode array. Between day 9.5 p.c. to 12.5 p.c., the beating frequency of isolated embryonic hearts from Cav2.3-deficient mice did not differ significantly from control mice but the coefficient of variation within individual episodes was more than four-fold increased in Cav2.3-deficient mice indicating arrhythmia. In isolated hearts from wild type mice, arrhythmia was induced by superfusion with a solution containing 200 nM SNX-482, a blocker of some R-type voltage gated Ca2+ channels, suggesting that R-type channels containing the splice variant Cav2.3e as ion conducting pore stabilize a more regular heart beat in prenatal mice.
1015-8987
11-22
Lu, Z.J.
aa7f02fd-28a4-4bca-bd04-1bc8f703bc4c
Pereverzev, A.
4ad3b4f9-81f3-4560-97d8-1c28b1a0f263
Liu, H.L.
0752a74a-0624-4090-80c6-c5f84fc77e16
Weiergraber, M.
e42756d4-2de8-40f1-98de-87f2fbf54ba6
Henry, M.
f20af19b-884c-45b7-a263-276113bbb327
Krieger, A.
67f00586-61ae-4083-b742-e4c4a021c816
Smyth, N.
0eba2a40-3b43-4d40-bb64-621bd7e9d505
Hescheler, J.
b974a26f-9019-43f5-bf03-776f4886224c
Schneider, T.
ddc7c577-d358-4713-bb39-7c3db06b78ab
Lu, Z.J.
aa7f02fd-28a4-4bca-bd04-1bc8f703bc4c
Pereverzev, A.
4ad3b4f9-81f3-4560-97d8-1c28b1a0f263
Liu, H.L.
0752a74a-0624-4090-80c6-c5f84fc77e16
Weiergraber, M.
e42756d4-2de8-40f1-98de-87f2fbf54ba6
Henry, M.
f20af19b-884c-45b7-a263-276113bbb327
Krieger, A.
67f00586-61ae-4083-b742-e4c4a021c816
Smyth, N.
0eba2a40-3b43-4d40-bb64-621bd7e9d505
Hescheler, J.
b974a26f-9019-43f5-bf03-776f4886224c
Schneider, T.
ddc7c577-d358-4713-bb39-7c3db06b78ab

Lu, Z.J., Pereverzev, A., Liu, H.L., Weiergraber, M., Henry, M., Krieger, A., Smyth, N., Hescheler, J. and Schneider, T. (2004) Arrhythmia in isolated prenatal hearts after ablation of the Ca(v)2.3 (alpha 1E) subunit of voltage-gated Ca2+ channels. Cellular Physiology and Biochemistry, 14 (1-2), 11-22. (doi:10.1159/000076922).

Record type: Article

Abstract

A voltage-gated calcium channel containing Cav2.3e (1Ee) as the ion conducting pore has recently been detected in rat heart. Functional evidence for this Ca2+ channel to be involved in the regulation of heart beating, besides L- and T-type channels, was derived from murine embryos where the gene for Cav1.2 had been ablated. The remaining ''L-type like“ current component was not related to recombinant splice variants of Cav1.3 containing channels. As recombinant Cav2.3 channels from rat were reported to be weakly dihydropyridine sensitive, the spontaneous activity of the prenatal hearts from Cav2.3(-|-) mice was compared to that of Cav2.3(+|+) control animals to investigate if Cav2.3 could represent such a L-type like Ca2+ channel. The spontaneous activity of murine embryonic hearts was recorded by using a multielectrode array. Between day 9.5 p.c. to 12.5 p.c., the beating frequency of isolated embryonic hearts from Cav2.3-deficient mice did not differ significantly from control mice but the coefficient of variation within individual episodes was more than four-fold increased in Cav2.3-deficient mice indicating arrhythmia. In isolated hearts from wild type mice, arrhythmia was induced by superfusion with a solution containing 200 nM SNX-482, a blocker of some R-type voltage gated Ca2+ channels, suggesting that R-type channels containing the splice variant Cav2.3e as ion conducting pore stabilize a more regular heart beat in prenatal mice.

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Published date: 1 January 2004

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Local EPrints ID: 56411
URI: http://eprints.soton.ac.uk/id/eprint/56411
ISSN: 1015-8987
PURE UUID: 006a5a8b-5dac-475e-8c0f-91a1cc0a30a2

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Date deposited: 08 Aug 2008
Last modified: 08 Jan 2022 16:02

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Contributors

Author: Z.J. Lu
Author: A. Pereverzev
Author: H.L. Liu
Author: M. Weiergraber
Author: M. Henry
Author: A. Krieger
Author: N. Smyth
Author: J. Hescheler
Author: T. Schneider

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