T-type Ca2+ channels contribute to IBMX/forskolin- and K+-induced Ca2+ transients in porcine olfactory receptor neurons

被引:6
作者
Gautam, Shree Hari
Otsuguro, Ken-ichi
Ito, Shigeo
Saito, Toshiyuki
Habara, Yoshiaki [1 ]
机构
[1] Hokkaido Univ, Physiol Lab, Dept Biomed Sci, Grad Sch Vet Med, Sapporo, Hokkaido 0600818, Japan
[2] Hokkaido Univ, Pharmacol Lab, Dept Biomed Sci, Grad Sch Vet Med, Sapporo, Hokkaido 0600818, Japan
[3] Natl Inst Agrobiol Sci, Neurobiol Lab, Tsukuba, Ibaraki 3050901, Japan
关键词
olfaction; signal transduction; Ca2+ dynamics; cAMP; mibefradil; Ni2+; pig;
D O I
10.1016/j.neures.2006.09.016
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
T-type Ca2+ channels are low-voltage-activated Ca2+ channels that control Ca2+ entry in excitable cells during small depolarization above resting potentials. Using Ca2+ imaging with a laser scanning confocal microscope we investigated the involvement of T-type Ca2+ channels in IBMX/forskolin- and sparingly elevated extracellular K+-induced Ca2+ transients in freshly isolated porcine olfactory receptor neurons (ORNs). In the presence of mibefradil (10 mu M) or Ni2+ (100 mu M), the selective T-type Ca2+ channel inhibitors, IBMX/forskolin-induced Ca2+ transients in the soma were either strongly (> 60%) inhibited or abolished completely. However, the Ca2+ transients in the knob were only partially (< 60%) inhibited. Ca2+ transients induced by 30 mM K+ were also partially (similar to 60%) inhibited at both the knob and soma. Furthermore, ORNs responded to as little as a 2.5 mM increase in the extracellular K+ concentration (7.5 mM K+), and such responses were completely inhibited by mibefradil or Ni2+. These results reveal functional expression of T-type Ca2+ channels in porcine ORNs, and suggest a role for these channels in the spread Ca2+ transients from the knob to the soma during activation of the cAMP cascade following odorant binding to G-protein-coupled receptors on the cilia/knob of ORNs. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
引用
收藏
页码:129 / 139
页数:11
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