Participation of transient-type Ca2+ channels in the sustained increase of Ca2+ level in GH3 cells.
Participation of two types of Ca2+ channels (T- and L-types) in the sustained increase of cytosolic-free Ca2+ concentration [( Ca2+]i) was studied in thyrotropin-releasing hormone (TRH)-stimulated clonal GH3 pituitary cells. The effects of Ca2+ channel blockers were analyzed by measuring Ca2+ channel current and [Ca2+]i, using whole-cell voltage-clamp and Fura-2 fluorometry, respectively. Phenytoin (100 microM) and Ni2+ (100 microM) selectively blocked T-type Ca2+ channels and suppressed the TRH-induced sustained [Ca2+]i increase in single cells. Synthetic omega-conotoxin (omega-CgTX, 2 microM) preferentially blocked L-type Ca2+ channels, but it did not suppress the TRH-induced sustained [Ca2+]i increase. The present results suggest that the sustained elevations of [Ca2+]i triggered by TRH may be mediated by T-type Ca2+ channels in GH3 cells.
Suzuki
N
N
Department of Physiology, School of Medicine, Kitasato University, Kanagawa, Japan.
Kudo
Y
Y
Takagi
H
H
Yoshioka
T
T
Tanakadate
A
A
Kano
M
M
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D004553:Electric Conductivity; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010456:Peptides, Cyclic / Q000494:pharmacology; D010672:Phenytoin / Q000494:pharmacology; D010902:Pituitary Gland / Q000502:physiology*; D051381:Rats; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D014700:Verapamil / Q000494:pharmacology; D020866:omega-Conotoxin GVIA
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D010456:Peptides, Cyclic; D013973:Thyrotropin-Releasing Hormone; D010672:Phenytoin; D009532:Nickel; D020866:omega-Conotoxin GVIA; D014700:Verapamil; D009543:Nifedipine; D002118:Calcium