Participation of transient-type Ca2+ channels in the sustained increase of Ca2+ level in GH3 cells

J Cell Physiol. 1990 Jul;144(1):62-8. doi: 10.1002/jcp.1041440109.

Abstract

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.

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / physiology*
  • Electric Conductivity
  • In Vitro Techniques
  • Membrane Potentials
  • Nickel / pharmacology
  • Nifedipine / pharmacology
  • Peptides, Cyclic / pharmacology
  • Phenytoin / pharmacology
  • Pituitary Gland / physiology*
  • Rats
  • Thyrotropin-Releasing Hormone / pharmacology*
  • Tumor Cells, Cultured
  • Verapamil / pharmacology
  • omega-Conotoxin GVIA

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Peptides, Cyclic
  • Thyrotropin-Releasing Hormone
  • Phenytoin
  • Nickel
  • omega-Conotoxin GVIA
  • Verapamil
  • Nifedipine
  • Calcium