Functional coupling of voltage-dependent L-type Ca 2+ current to Ca 2+ -activated K + current in pituitary GH 3 cells

Sheng-Nan Wu, Y. K. Lo, H. F. Li, A. Y. Shen

Research output: Contribution to journalArticle

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Abstract

Ca 2+ -activated K + currents (I K(Ca) ) can contribute to action potential repolarization and after-hyperpolarization in GH 3 cells. In this study, we examined how the activation of I K(Ca) at the cellular level could be functionally coupled to Ca 2+ influx through L-type Ca 2+ channels. A 30-msec Ca 2+ influx step to 0 mV was found to exhibit substantial contribution of Ca 2+ influx through the activation of I Ca,L to the activation of I K(Ca) A bell-shaped relationship between the conditioning potentials and the integrated I K(Ca) was observed, suggesting that the magnitude of integrated I Ca,L correlates well with that of integrated I K(Ca) in the same cell. A linear relationship of integrated I Ca,L and integrated I K(Ca) was found with a coupling ratio of 69 ± 7. The value of the coupling ratio was unaffected by the presence of Bay K 8644 or nimodipine, although these compounds could effectively affect the amplitudes of both I K(Ca) and I Ca,L. However, tetrandrine could decrease the coupling ratio. Paxilline or intracellular Ca 2+ buffer with EGTA decreased the coupling ratio, while apamin had no effect on it. Interestingly, phorbol 12-myristate 13-acetate also reduced the coupling ratio significantly, whereas thapsigargin increased this value. Thus, the present study indicates that the activation of I K(Ca) during brief Ca 2+ influx, which is inhibited by paxilline, is coupled to Ca 2+ influx primarily through the L-type channels. The selective modulation of I K(Ca) by second messengers or Ca 2+ release from internal stores may affect the coupling efficiency and hence cellular excitability.

Original languageEnglish
Pages (from-to)161-167
Number of pages7
JournalChinese Journal of Physiology
Volume44
Issue number4
Publication statusPublished - 2001 Jan 1

Fingerprint

Somatotrophs
tetrandrine
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Apamin
Nimodipine
Thapsigargin
Egtazic Acid
Second Messenger Systems
Action Potentials
Buffers
Acetates
paxilline
phorbol-12-myristate

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Functional coupling of voltage-dependent L-type Ca 2+ current to Ca 2+ -activated K + current in pituitary GH 3 cells",
abstract = "Ca 2+ -activated K + currents (I K(Ca) ) can contribute to action potential repolarization and after-hyperpolarization in GH 3 cells. In this study, we examined how the activation of I K(Ca) at the cellular level could be functionally coupled to Ca 2+ influx through L-type Ca 2+ channels. A 30-msec Ca 2+ influx step to 0 mV was found to exhibit substantial contribution of Ca 2+ influx through the activation of I Ca,L to the activation of I K(Ca) A bell-shaped relationship between the conditioning potentials and the integrated I K(Ca) was observed, suggesting that the magnitude of integrated I Ca,L correlates well with that of integrated I K(Ca) in the same cell. A linear relationship of integrated I Ca,L and integrated I K(Ca) was found with a coupling ratio of 69 ± 7. The value of the coupling ratio was unaffected by the presence of Bay K 8644 or nimodipine, although these compounds could effectively affect the amplitudes of both I K(Ca) and I Ca,L. However, tetrandrine could decrease the coupling ratio. Paxilline or intracellular Ca 2+ buffer with EGTA decreased the coupling ratio, while apamin had no effect on it. Interestingly, phorbol 12-myristate 13-acetate also reduced the coupling ratio significantly, whereas thapsigargin increased this value. Thus, the present study indicates that the activation of I K(Ca) during brief Ca 2+ influx, which is inhibited by paxilline, is coupled to Ca 2+ influx primarily through the L-type channels. The selective modulation of I K(Ca) by second messengers or Ca 2+ release from internal stores may affect the coupling efficiency and hence cellular excitability.",
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Functional coupling of voltage-dependent L-type Ca 2+ current to Ca 2+ -activated K + current in pituitary GH 3 cells . / Wu, Sheng-Nan; Lo, Y. K.; Li, H. F.; Shen, A. Y.

In: Chinese Journal of Physiology, Vol. 44, No. 4, 01.01.2001, p. 161-167.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Functional coupling of voltage-dependent L-type Ca 2+ current to Ca 2+ -activated K + current in pituitary GH 3 cells

AU - Wu, Sheng-Nan

AU - Lo, Y. K.

AU - Li, H. F.

AU - Shen, A. Y.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Ca 2+ -activated K + currents (I K(Ca) ) can contribute to action potential repolarization and after-hyperpolarization in GH 3 cells. In this study, we examined how the activation of I K(Ca) at the cellular level could be functionally coupled to Ca 2+ influx through L-type Ca 2+ channels. A 30-msec Ca 2+ influx step to 0 mV was found to exhibit substantial contribution of Ca 2+ influx through the activation of I Ca,L to the activation of I K(Ca) A bell-shaped relationship between the conditioning potentials and the integrated I K(Ca) was observed, suggesting that the magnitude of integrated I Ca,L correlates well with that of integrated I K(Ca) in the same cell. A linear relationship of integrated I Ca,L and integrated I K(Ca) was found with a coupling ratio of 69 ± 7. The value of the coupling ratio was unaffected by the presence of Bay K 8644 or nimodipine, although these compounds could effectively affect the amplitudes of both I K(Ca) and I Ca,L. However, tetrandrine could decrease the coupling ratio. Paxilline or intracellular Ca 2+ buffer with EGTA decreased the coupling ratio, while apamin had no effect on it. Interestingly, phorbol 12-myristate 13-acetate also reduced the coupling ratio significantly, whereas thapsigargin increased this value. Thus, the present study indicates that the activation of I K(Ca) during brief Ca 2+ influx, which is inhibited by paxilline, is coupled to Ca 2+ influx primarily through the L-type channels. The selective modulation of I K(Ca) by second messengers or Ca 2+ release from internal stores may affect the coupling efficiency and hence cellular excitability.

AB - Ca 2+ -activated K + currents (I K(Ca) ) can contribute to action potential repolarization and after-hyperpolarization in GH 3 cells. In this study, we examined how the activation of I K(Ca) at the cellular level could be functionally coupled to Ca 2+ influx through L-type Ca 2+ channels. A 30-msec Ca 2+ influx step to 0 mV was found to exhibit substantial contribution of Ca 2+ influx through the activation of I Ca,L to the activation of I K(Ca) A bell-shaped relationship between the conditioning potentials and the integrated I K(Ca) was observed, suggesting that the magnitude of integrated I Ca,L correlates well with that of integrated I K(Ca) in the same cell. A linear relationship of integrated I Ca,L and integrated I K(Ca) was found with a coupling ratio of 69 ± 7. The value of the coupling ratio was unaffected by the presence of Bay K 8644 or nimodipine, although these compounds could effectively affect the amplitudes of both I K(Ca) and I Ca,L. However, tetrandrine could decrease the coupling ratio. Paxilline or intracellular Ca 2+ buffer with EGTA decreased the coupling ratio, while apamin had no effect on it. Interestingly, phorbol 12-myristate 13-acetate also reduced the coupling ratio significantly, whereas thapsigargin increased this value. Thus, the present study indicates that the activation of I K(Ca) during brief Ca 2+ influx, which is inhibited by paxilline, is coupled to Ca 2+ influx primarily through the L-type channels. The selective modulation of I K(Ca) by second messengers or Ca 2+ release from internal stores may affect the coupling efficiency and hence cellular excitability.

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