Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons

Jung Ha Lee, Eun Gi Kim, Byong Gon Park, Kyoung Han Kim, Seung Kyu Cha, In Deok Kong, Joong Woo Lee, Seong Woo Jeong

Research output: Contribution to journalArticle

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Abstract

Among autonomic neurons, sympathetic neurons of the major pelvic ganglia (MPG) are unique by expressing low-voltage-activated T-type Ca2+ channels. To date, the T-type Ca2+ channels have been poorly characterized, although they are believed to be potentially important for functions of the MPG neurons. In the present study, thus we investigated characteristics and molecular identity of the T-type Ca2+ channels using patch-clamp and RT-PCR techniques. When the external solution contained 10 mM Ca2+ as a charge carrier, T-type Ca2+ currents were first activated at -50 mV and peaked around -20 mV. Besides the low-voltage activation, T-type Ca2+ currents displayed typical characteristics including transient activation/inactivation and voltage-dependent slow deactivation. Overlap of the activation and inactivation curves generated a prominent window current around resting membrane potentials. Replacement of the external Ca2+ with 10 mM Ba2+ did not affect the amplitudes of T-type Ca2+ currents. Mibefradil, a known T-type Ca2+ channel antagonist, depressed T-type Ca2+ currents in a concentration-dependent manner (IC50 = 3 μM). Application of Ni2+ also produced a concentration-dependent blockade of T-type Ca2+ currents with an IC50 of 10 μM. The high sensitivity to Ni2+ implicates α1H in generating the T-type Ca2+ currents in MPG neurons. RTPCR experiments showed that MPG neurons predominantly express mRNAs encoding splicing variants of α1H (called pelvic Ta and Tb, short and long forms of α1H, respectively). Finally, we tested whether the low-threshold spikes could be generated in sympathetic MPG neurons expressing T-type Ca2+ channels. When hyperpolarizing currents were injected under a current-clamp mode, sympathetic neurons produced postanodal rebound spikes, while parasympathetic neurons were silent. The number of the rebound spikes was reduced by 10 μM Ni2+ that blocked 50% of T-type Ca2+ currents and had a little effect on HVA Ca2+ currents in sympathetic MPG neurons. Furthermore, generation of the rebound spikes was completely prevented by 100 μM Ni2+ that blocked most of the T-type Ca2+ currents. In conclusions, T-type Ca2+ currents in MPG neurons mainly arise from α1H among the three isoforms (α1G, α1H, and α1I) and may contribute to generation of low-threshold spikes in sympathetic MPG neurons.

Original languageEnglish
Pages (from-to)2844-2850
Number of pages7
JournalJournal of Neurophysiology
Volume87
Issue number6
Publication statusPublished - 2002 Jul 3

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Ganglia
Neurons
Inhibitory Concentration 50
Mibefradil
Membrane Potentials
Protein Isoforms
Polymerase Chain Reaction
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Physiology

Cite this

Lee, J. H., Kim, E. G., Park, B. G., Kim, K. H., Cha, S. K., Kong, I. D., ... Jeong, S. W. (2002). Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons. Journal of Neurophysiology, 87(6), 2844-2850.
Lee, Jung Ha ; Kim, Eun Gi ; Park, Byong Gon ; Kim, Kyoung Han ; Cha, Seung Kyu ; Kong, In Deok ; Lee, Joong Woo ; Jeong, Seong Woo. / Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons. In: Journal of Neurophysiology. 2002 ; Vol. 87, No. 6. pp. 2844-2850.
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abstract = "Among autonomic neurons, sympathetic neurons of the major pelvic ganglia (MPG) are unique by expressing low-voltage-activated T-type Ca2+ channels. To date, the T-type Ca2+ channels have been poorly characterized, although they are believed to be potentially important for functions of the MPG neurons. In the present study, thus we investigated characteristics and molecular identity of the T-type Ca2+ channels using patch-clamp and RT-PCR techniques. When the external solution contained 10 mM Ca2+ as a charge carrier, T-type Ca2+ currents were first activated at -50 mV and peaked around -20 mV. Besides the low-voltage activation, T-type Ca2+ currents displayed typical characteristics including transient activation/inactivation and voltage-dependent slow deactivation. Overlap of the activation and inactivation curves generated a prominent window current around resting membrane potentials. Replacement of the external Ca2+ with 10 mM Ba2+ did not affect the amplitudes of T-type Ca2+ currents. Mibefradil, a known T-type Ca2+ channel antagonist, depressed T-type Ca2+ currents in a concentration-dependent manner (IC50 = 3 μM). Application of Ni2+ also produced a concentration-dependent blockade of T-type Ca2+ currents with an IC50 of 10 μM. The high sensitivity to Ni2+ implicates α1H in generating the T-type Ca2+ currents in MPG neurons. RTPCR experiments showed that MPG neurons predominantly express mRNAs encoding splicing variants of α1H (called pelvic Ta and Tb, short and long forms of α1H, respectively). Finally, we tested whether the low-threshold spikes could be generated in sympathetic MPG neurons expressing T-type Ca2+ channels. When hyperpolarizing currents were injected under a current-clamp mode, sympathetic neurons produced postanodal rebound spikes, while parasympathetic neurons were silent. The number of the rebound spikes was reduced by 10 μM Ni2+ that blocked 50{\%} of T-type Ca2+ currents and had a little effect on HVA Ca2+ currents in sympathetic MPG neurons. Furthermore, generation of the rebound spikes was completely prevented by 100 μM Ni2+ that blocked most of the T-type Ca2+ currents. In conclusions, T-type Ca2+ currents in MPG neurons mainly arise from α1H among the three isoforms (α1G, α1H, and α1I) and may contribute to generation of low-threshold spikes in sympathetic MPG neurons.",
author = "Lee, {Jung Ha} and Kim, {Eun Gi} and Park, {Byong Gon} and Kim, {Kyoung Han} and Cha, {Seung Kyu} and Kong, {In Deok} and Lee, {Joong Woo} and Jeong, {Seong Woo}",
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Lee, JH, Kim, EG, Park, BG, Kim, KH, Cha, SK, Kong, ID, Lee, JW & Jeong, SW 2002, 'Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons', Journal of Neurophysiology, vol. 87, no. 6, pp. 2844-2850.

Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons. / Lee, Jung Ha; Kim, Eun Gi; Park, Byong Gon; Kim, Kyoung Han; Cha, Seung Kyu; Kong, In Deok; Lee, Joong Woo; Jeong, Seong Woo.

In: Journal of Neurophysiology, Vol. 87, No. 6, 03.07.2002, p. 2844-2850.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Identification of T-type α1H Ca2+ channels (Cav3.2) in Major pelvic ganglion neurons

AU - Lee, Jung Ha

AU - Kim, Eun Gi

AU - Park, Byong Gon

AU - Kim, Kyoung Han

AU - Cha, Seung Kyu

AU - Kong, In Deok

AU - Lee, Joong Woo

AU - Jeong, Seong Woo

PY - 2002/7/3

Y1 - 2002/7/3

N2 - Among autonomic neurons, sympathetic neurons of the major pelvic ganglia (MPG) are unique by expressing low-voltage-activated T-type Ca2+ channels. To date, the T-type Ca2+ channels have been poorly characterized, although they are believed to be potentially important for functions of the MPG neurons. In the present study, thus we investigated characteristics and molecular identity of the T-type Ca2+ channels using patch-clamp and RT-PCR techniques. When the external solution contained 10 mM Ca2+ as a charge carrier, T-type Ca2+ currents were first activated at -50 mV and peaked around -20 mV. Besides the low-voltage activation, T-type Ca2+ currents displayed typical characteristics including transient activation/inactivation and voltage-dependent slow deactivation. Overlap of the activation and inactivation curves generated a prominent window current around resting membrane potentials. Replacement of the external Ca2+ with 10 mM Ba2+ did not affect the amplitudes of T-type Ca2+ currents. Mibefradil, a known T-type Ca2+ channel antagonist, depressed T-type Ca2+ currents in a concentration-dependent manner (IC50 = 3 μM). Application of Ni2+ also produced a concentration-dependent blockade of T-type Ca2+ currents with an IC50 of 10 μM. The high sensitivity to Ni2+ implicates α1H in generating the T-type Ca2+ currents in MPG neurons. RTPCR experiments showed that MPG neurons predominantly express mRNAs encoding splicing variants of α1H (called pelvic Ta and Tb, short and long forms of α1H, respectively). Finally, we tested whether the low-threshold spikes could be generated in sympathetic MPG neurons expressing T-type Ca2+ channels. When hyperpolarizing currents were injected under a current-clamp mode, sympathetic neurons produced postanodal rebound spikes, while parasympathetic neurons were silent. The number of the rebound spikes was reduced by 10 μM Ni2+ that blocked 50% of T-type Ca2+ currents and had a little effect on HVA Ca2+ currents in sympathetic MPG neurons. Furthermore, generation of the rebound spikes was completely prevented by 100 μM Ni2+ that blocked most of the T-type Ca2+ currents. In conclusions, T-type Ca2+ currents in MPG neurons mainly arise from α1H among the three isoforms (α1G, α1H, and α1I) and may contribute to generation of low-threshold spikes in sympathetic MPG neurons.

AB - Among autonomic neurons, sympathetic neurons of the major pelvic ganglia (MPG) are unique by expressing low-voltage-activated T-type Ca2+ channels. To date, the T-type Ca2+ channels have been poorly characterized, although they are believed to be potentially important for functions of the MPG neurons. In the present study, thus we investigated characteristics and molecular identity of the T-type Ca2+ channels using patch-clamp and RT-PCR techniques. When the external solution contained 10 mM Ca2+ as a charge carrier, T-type Ca2+ currents were first activated at -50 mV and peaked around -20 mV. Besides the low-voltage activation, T-type Ca2+ currents displayed typical characteristics including transient activation/inactivation and voltage-dependent slow deactivation. Overlap of the activation and inactivation curves generated a prominent window current around resting membrane potentials. Replacement of the external Ca2+ with 10 mM Ba2+ did not affect the amplitudes of T-type Ca2+ currents. Mibefradil, a known T-type Ca2+ channel antagonist, depressed T-type Ca2+ currents in a concentration-dependent manner (IC50 = 3 μM). Application of Ni2+ also produced a concentration-dependent blockade of T-type Ca2+ currents with an IC50 of 10 μM. The high sensitivity to Ni2+ implicates α1H in generating the T-type Ca2+ currents in MPG neurons. RTPCR experiments showed that MPG neurons predominantly express mRNAs encoding splicing variants of α1H (called pelvic Ta and Tb, short and long forms of α1H, respectively). Finally, we tested whether the low-threshold spikes could be generated in sympathetic MPG neurons expressing T-type Ca2+ channels. When hyperpolarizing currents were injected under a current-clamp mode, sympathetic neurons produced postanodal rebound spikes, while parasympathetic neurons were silent. The number of the rebound spikes was reduced by 10 μM Ni2+ that blocked 50% of T-type Ca2+ currents and had a little effect on HVA Ca2+ currents in sympathetic MPG neurons. Furthermore, generation of the rebound spikes was completely prevented by 100 μM Ni2+ that blocked most of the T-type Ca2+ currents. In conclusions, T-type Ca2+ currents in MPG neurons mainly arise from α1H among the three isoforms (α1G, α1H, and α1I) and may contribute to generation of low-threshold spikes in sympathetic MPG neurons.

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