Actions of growth-hormone-releasing hormone on rat pituitary cells: intracellular calcium and ionic currents

1994 ◽  
Vol 427 (5-6) ◽  
pp. 414-421 ◽  
Author(s):  
Alexander P. Naumov ◽  
James Herrington ◽  
Bertil Hille
Keyword(s):  
Growth Hormone ◽  
Intracellular Calcium ◽  
Ionic Currents ◽  
Pituitary Cells ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

scholarly journals Mechanism of spontaneous intracellular calcium fluctuations in single GH4C1 rat pituitary cells

1993 ◽  
Vol 292 (1) ◽  
pp. 175-182 ◽  
Author(s):  
K A Wagner ◽  
P W Yacono ◽  
D E Golan ◽  
A H Tashjian
Keyword(s):  
Intracellular Calcium ◽  
Thyrotropin Releasing Hormone ◽  
Bay K 8644 ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Quiescent Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Ca2 Channels

Individual unstimulated GH4C1 cells exhibited spontaneous dynamic fluctuations in cytosolic free Ca2+ concentration ([Ca2+]i). Either chelation of extracellular Ca2+ with EGTA or treatment with nifedipine inhibited spontaneous [Ca2+]i fluctuations, indicating that the [Ca2+]i profile was dependent on the entry of extracellular Ca2+ via voltage-operated Ca2+ channels (VOCC). Spontaneous [Ca2+]i fluctuations did not resume immediately after exposure of EGTA-pretreated cells to extracellular Ca2+, supporting the hypothesis that the complex [Ca2+]i profiles observed in unstimulated cells required filling of an intracellular Ca2+ pool. BAY K 8644 elicited large rapid oscillations in [Ca2+]i. After chelation of extracellular Ca2+, however, re-addition of Ca2+ plus BAY K 8644 did not result in [Ca2+]i oscillations. The intracellular Ca2+ pool necessary for BAY K-induced oscillations was not the same Ins(1,4,5)P3-sensitive pool stimulated by thyrotropin-releasing hormone (TRH), because the TRH-stimulated Ins(1,4,5)P3-induced [Ca2+]i spike and the BAY K 8644-induced oscillations were differentially sensitive to chelation of extracellular Ca2+ and thapsigargin. Caffeine caused an increase in [Ca2+]i fluctuations in quiescent cells, supporting a role for Ca(2+)-induced Ca2+ release (CICR) in the generation of spontaneous [Ca2+]i fluctuations. In conclusion, the complex spontaneous changes in [Ca2+]i observed in single GH4C1 cells depend on both the influx of extracellular Ca2+ through VOCC and the action of an intracellular Ca2+ pool that increases [Ca2+]i through a CICR-like mechanism.

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