L-type Ca 2+ channel function in the avian embryonic heart after cardiac neural crest ablation

Carol A Nichols, Tony L. Creazzo

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

In avian and mammalian embryos, surgical ablation or severely reduced migration of the cardiac neural crest leads to a failure of outflow tract septation known as persistent truncus arteriosus (PTA) and leads to embryo lethality due partly to impaired excitation-contraction coupling stemming primarily from a reduction in the L-type Ca 2+ current (I Ca,L ). Decreased I Ca,L occurs without a corresponding reduction in the α 1 -subunit of the Ca 2+ channel. We hypothesize that decreased I Ca,L is due to reduced function at the single channel level. The cell-attached patch clamp with Na + as the charge carrier was used to examine single Ca 2+ channel activity in myocytes from normal hearts from sham-operated embryos and from hearts diagnosed with PTA at embryonic days (ED) 11 and 15 after laser ablation of the cardiac neural crest. In normal hearts, the number of single channel events per 200-ms depolarization and the mean open channel probability (P O ) was 1.89 ± 0.17 and 0.067 ± 0.008 for ED11 and 1.14 ± 0.17 and 0.044 ± 0.005 for ED15, respectively. These values represent a normal reduction in channel function and I Ca,L observed with development. However, the number of single channel events was significantly reduced in hearts with PTA at both ED11 and ED15 (71% and 47%, respectively) with a corresponding reduction in P O (75% and 43%). The open time frequency histograms were best fitted by single exponentials with similar decay constants (τ ≅ 4.5 ms) except for the sham operated at ED15 (τ = 3.4 ms). These results indicate that the cardiac neural crest influences the development of myocardial Ca 2+ channels.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume288
Issue number3 57-3
DOIs
StatePublished - Mar 1 2005

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Persistent Truncus Arteriosus
Neural Crest
Embryonic Structures
Mammalian Embryo
Excitation Contraction Coupling
Laser Therapy
Muscle Cells

Keywords

  • Excitation-contraction coupling
  • Heart defect
  • Heart development

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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title = "L-type Ca 2+ channel function in the avian embryonic heart after cardiac neural crest ablation",
abstract = "In avian and mammalian embryos, surgical ablation or severely reduced migration of the cardiac neural crest leads to a failure of outflow tract septation known as persistent truncus arteriosus (PTA) and leads to embryo lethality due partly to impaired excitation-contraction coupling stemming primarily from a reduction in the L-type Ca 2+ current (I Ca,L ). Decreased I Ca,L occurs without a corresponding reduction in the α 1 -subunit of the Ca 2+ channel. We hypothesize that decreased I Ca,L is due to reduced function at the single channel level. The cell-attached patch clamp with Na + as the charge carrier was used to examine single Ca 2+ channel activity in myocytes from normal hearts from sham-operated embryos and from hearts diagnosed with PTA at embryonic days (ED) 11 and 15 after laser ablation of the cardiac neural crest. In normal hearts, the number of single channel events per 200-ms depolarization and the mean open channel probability (P O ) was 1.89 ± 0.17 and 0.067 ± 0.008 for ED11 and 1.14 ± 0.17 and 0.044 ± 0.005 for ED15, respectively. These values represent a normal reduction in channel function and I Ca,L observed with development. However, the number of single channel events was significantly reduced in hearts with PTA at both ED11 and ED15 (71{\%} and 47{\%}, respectively) with a corresponding reduction in P O (75{\%} and 43{\%}). The open time frequency histograms were best fitted by single exponentials with similar decay constants (τ ≅ 4.5 ms) except for the sham operated at ED15 (τ = 3.4 ms). These results indicate that the cardiac neural crest influences the development of myocardial Ca 2+ channels.",
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AU - Nichols, Carol A

AU - Creazzo, Tony L.

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N2 - In avian and mammalian embryos, surgical ablation or severely reduced migration of the cardiac neural crest leads to a failure of outflow tract septation known as persistent truncus arteriosus (PTA) and leads to embryo lethality due partly to impaired excitation-contraction coupling stemming primarily from a reduction in the L-type Ca 2+ current (I Ca,L ). Decreased I Ca,L occurs without a corresponding reduction in the α 1 -subunit of the Ca 2+ channel. We hypothesize that decreased I Ca,L is due to reduced function at the single channel level. The cell-attached patch clamp with Na + as the charge carrier was used to examine single Ca 2+ channel activity in myocytes from normal hearts from sham-operated embryos and from hearts diagnosed with PTA at embryonic days (ED) 11 and 15 after laser ablation of the cardiac neural crest. In normal hearts, the number of single channel events per 200-ms depolarization and the mean open channel probability (P O ) was 1.89 ± 0.17 and 0.067 ± 0.008 for ED11 and 1.14 ± 0.17 and 0.044 ± 0.005 for ED15, respectively. These values represent a normal reduction in channel function and I Ca,L observed with development. However, the number of single channel events was significantly reduced in hearts with PTA at both ED11 and ED15 (71% and 47%, respectively) with a corresponding reduction in P O (75% and 43%). The open time frequency histograms were best fitted by single exponentials with similar decay constants (τ ≅ 4.5 ms) except for the sham operated at ED15 (τ = 3.4 ms). These results indicate that the cardiac neural crest influences the development of myocardial Ca 2+ channels.

AB - In avian and mammalian embryos, surgical ablation or severely reduced migration of the cardiac neural crest leads to a failure of outflow tract septation known as persistent truncus arteriosus (PTA) and leads to embryo lethality due partly to impaired excitation-contraction coupling stemming primarily from a reduction in the L-type Ca 2+ current (I Ca,L ). Decreased I Ca,L occurs without a corresponding reduction in the α 1 -subunit of the Ca 2+ channel. We hypothesize that decreased I Ca,L is due to reduced function at the single channel level. The cell-attached patch clamp with Na + as the charge carrier was used to examine single Ca 2+ channel activity in myocytes from normal hearts from sham-operated embryos and from hearts diagnosed with PTA at embryonic days (ED) 11 and 15 after laser ablation of the cardiac neural crest. In normal hearts, the number of single channel events per 200-ms depolarization and the mean open channel probability (P O ) was 1.89 ± 0.17 and 0.067 ± 0.008 for ED11 and 1.14 ± 0.17 and 0.044 ± 0.005 for ED15, respectively. These values represent a normal reduction in channel function and I Ca,L observed with development. However, the number of single channel events was significantly reduced in hearts with PTA at both ED11 and ED15 (71% and 47%, respectively) with a corresponding reduction in P O (75% and 43%). The open time frequency histograms were best fitted by single exponentials with similar decay constants (τ ≅ 4.5 ms) except for the sham operated at ED15 (τ = 3.4 ms). These results indicate that the cardiac neural crest influences the development of myocardial Ca 2+ channels.

KW - Excitation-contraction coupling

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