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 language | English |
|---|---|
| Pages (from-to) | 2844-2850 |
| Number of pages | 7 |
| Journal | Journal of Neurophysiology |
| Volume | 87 |
| Issue number | 6 |
| Publication status | Published - 2002 Jul 3 |
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All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Physiology
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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 journal › Article
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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M3 - Article
C2 - 12037187
AN - SCOPUS:0036089708
VL - 87
SP - 2844
EP - 2850
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 6
ER -