Characterization of the calcium response to thyrotropin-releasing hormone (TRH) in cells transfected with TRH receptor complementary DNA: importance of voltage-sensitive calcium channels

Mol Endocrinol. 1992 Sep;6(9):1393-402. doi: 10.1210/mend.6.9.1279382.

Abstract

TRH stimulates a biphasic increase in intracellular free calcium ion, [Ca2+]i. Cells stably transfected with TRH receptor cDNA were used to compare the response in lines with and without L type voltage-gated calcium channels. Rat pituitary GH-Y cells that do not normally express TRH receptors, rat glial C6 cells, and human epithelial Hela cells were transfected with mouse TRH receptor cDNA. All lines bound similar amounts of [3H][N3-Me-His2]TRH with identical affinities (dissociation constant = 1.5 nM). Both pituitary lines expressed L type voltage-gated calcium channels; depolarization with high K+ increased 45Ca2+ uptake 20- to 25-fold and [Ca2+]i 12- to 14-fold. C6 and Hela cells, in contrast, appeared to have no L channel activity. GH4C1 cells responded to TRH with a calcium spike (6-fold) followed by a sustained second phase. When TRH was added after 100 nM nimodipine, an L channel blocker, the initial calcium burst was unaffected but the second phase was abolished. GH-Y cells transfected with TRH receptor cDNA responded to TRH with a 6-fold [Ca2+]i spike followed by a plateau phase (>8 min) in which [Ca2+]i remained elevated or increased. Nimodipine did not alter the peak TRH response or resting [Ca2+]i but reduced the sustained phase, which was eliminated by chelation of extracellular Ca2+. In the transfected glial C6 and Hela cells without calcium channels, TRH evoked transient, monophasic 7- to 9-fold increases in [Ca2+]i, and [Ca2+]i returned to resting levels within 3 min. Thapsigargin stimulated a gradual, large increase in [Ca2+]i in transfected C6 cells, and subsequent addition of TRH caused no further rise. Removal of extracellular Ca2+ from transfected C6 cells shortened the [Ca2+]i responses to TRH, to endothelin 1, and to thapsigargin. The TRH responses were pertussis toxin-insensitive. In summary, TRH can generate a calcium spike in pituitary, C6, and Hela cells transfected with TRH receptor cDNA, but the plateau phase of the [Ca2+]i response is not observed when the receptor is expressed in a cell line without L channel activity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
  • Animals
  • Calcium / metabolism*
  • Calcium Channels / drug effects
  • Calcium Channels / physiology*
  • Cell Line
  • DNA / genetics
  • Endothelins / pharmacology
  • HeLa Cells
  • Humans
  • Ion Channel Gating / drug effects
  • Mice
  • Neuroglia / cytology
  • Neuroglia / drug effects
  • Nimodipine / pharmacology
  • Pituitary Neoplasms / pathology
  • Rats
  • Receptors, Neurotransmitter / drug effects
  • Receptors, Neurotransmitter / genetics
  • Receptors, Neurotransmitter / physiology*
  • Receptors, Thyrotropin-Releasing Hormone
  • Recombinant Proteins
  • Stimulation, Chemical
  • Terpenes / pharmacology
  • Thapsigargin
  • Thyrotropin-Releasing Hormone / pharmacology*
  • Transfection
  • Tumor Cells, Cultured

Substances

  • Calcium Channels
  • Endothelins
  • Receptors, Neurotransmitter
  • Receptors, Thyrotropin-Releasing Hormone
  • Recombinant Proteins
  • Terpenes
  • Nimodipine
  • Thyrotropin-Releasing Hormone
  • Thapsigargin
  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
  • DNA
  • Calcium