Polyphosphoinositide hydrolysis by phospholipase C is accelerated by thyrotropin releasing hormone (TRH) in clonal rat pituitary cells (GH<sub>3</sub> cells)

Schlegel, Werner; Roduit, Claude; Zahnd, G

doi:10.1016/0014-5793(84)80205-7

Cited by 44 publications

(22 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under basal conditions, IPi and IP2 repre¬ sented approximately 98% of the inositol polyphosphates, and the non-stimulated level of IP3 was very low. Several studies have demonstrated that lithium blocks inositol 1-phosphomonoesterase (for review see Berridge, Downes & Hanley, 1989) and induces accumulation of inositol polyphosphates in GH3 cells Schlegel, Roduit & Zahnd, 1984). In our model, addition of 10 mmol LiCl/1 enhanced the concentration of all inositol phosphates.…”

Section: Effect Of Trh On A-msh Secretionmentioning

confidence: 99%

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Desrues

Tonon²,

Vaudry³

1990

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Previous studies have demonstrated that TRH is a potent stimulator of alpha-MSH secretion from frog pituitary melanotrophs. In order to determine the intracellular events responsible for TRH-evoked alpha-MSH release, we have investigated the effect of TRH on polyphosphoinositide breakdown in frog pars intermedia. Neurointermediate lobes were labelled to isotopic equilibrium with myo-[3H]inositol. TRH stimulated the rate of incorporation of [3H]inositol into the phospholipid fraction. The effect of TRH was concentration-dependent; half-maximal stimulation of alpha-MSH release and inositol incorporation occurred at 12 and 28 nmol TRH/l respectively. In prelabelled neurointermediate lobes, lithium (10 mmol/l) enhanced the radioactivity in inositol monophosphate, bisphosphate (IP2) and trisphosphate (IP3). LiCl (10 mmol/l) induced a 38% inhibition of alpha-MSH release from perifused neurointermediate lobes but did not impair TRH-induced alpha-MSH secretion. In the presence of LiCl, TRH (1 mumol/l) induced a transient increase of the radioactivity in IP3, which was evident by 30 s and maximal by 1 min (+100%). TRH treatment also increased the radioactivity in IP2, which reached a plateau after 5 min (+100%). The increase in radioactivity in IP3 induced by TRH was closely paralleled by a rapid loss of [3H]phosphatidylinositol bisphosphate (PIP2), which was maximal by 1 min (-70%). These results indicate that, in frog pars intermedia, TRH-evoked alpha-MSH secretion is coupled to breakdown of PIP2. The data suggest that, in amphibian melanotrophs, as previously shown in GH3 tumour cells and in rat pituitary mammotrophs, TRH causes rapid stimulation of polyphosphoinositide-hydrolysing phospholipase C.

show abstract

Section: Effect Of Trh On A-msh Secretionmentioning

confidence: 99%

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Desrues

Tonon²,

Vaudry³

1990

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…Taken together these findings suggest that a GTP binding protein similar or identical to Ni is involved in the coupling of receptors to enhanced PIP2 breakdown. We and others have shown that TRH, similar to fMLP in neutrophils, acts in GH3 cells to enhance PIP2 hydraiysis by phospholipase C, generating IFS ] [18][19][20][21] which in turn mubilizes Ca2+ from intracellular stores [22,23]_ A further aim of this study was therefore to investigate whether FT would affect the Ca" mobilizing action of TRH in GH3 cells.…”

Section: Introductionmentioning

confidence: 99%

Pertussis toxin selectively abolishes hormone induced lowering of cytosolic calcium in GH₃ cells

et al. 1985

Self Cite

View full text Add to dashboard Cite

Pertussis toxin, PT, abolishes inhibitory regulation of adenylate cyclase by cell surface receptors. Inhibitors of adenylate cyclase in GH, cells, namely somatostatin and the muscarinic cholinergic agonist carbachol, lower the cytosolic free Ca2+ concentration.[Ca2+], and cause hyperpolarization. These responses are selectively abolished by PT. It is concluded that the effects of somatostatin and carbachol to lower [Ca'+]i and to hyperpolarize are secondary to their inhibitory action on adenylate cyclase. In contrast, PT does not impair the TRH induced rise in [Ca'+]i in GH, cells demonstrating that the coupling of TRH receptors to Ca2+ mobilization is not mediated by a P'I' substrate.

show abstract

“…23). Patch pipettes had an average resistance of [1][2][3][4][5] Mfl (open diameter, 1-3 ,um). Recording of currents was usually started 5 min after disruption of the membrane patch for intracellular dialysis with the pipette solution.…”

mentioning

confidence: 99%

Thyrotropin-releasing hormone induces opposite effects on Ca2+ channel currents in pituitary cells by two pathways.

Gollasch

Haller

Schultz

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Thyrotropin-releasing hormone (TRH) stimulates pituitary secretion by steps involving a cytosolic Ca2+ rise. We examined various pathways of Ca2' elevation in pituitary GH3 cells. By using the patch clamp technique in the whole-cell configuration and Ba2+ as divalent charge carrier through Ca2+ channels, TIH (1 uM) reversibly reduced the current by about 55%. This hormonal effect was prevented by infusing guanine 5'-[ji-thioldlphosphate (GDP(IJS]) intracellularly but not by pretreating the cell with pertussis toxin (PT). Since PT-insensitive guanine nucleotide-binding regulatory (G) proteins are known to mediate a hormone-stimulated inositol trisphosphate-mediated Ca2+ release from intracellular stores, we assume that the inhibitory effect of TRH on Ba2+ currents through Ca2+ channels is caused by the increased intracellular Ca2+. To prevent a Ca2+-release-dependent inhibition of Ca2+ channels, we preincubated GH3 cells in a medium free of divalent charge carriers and measured the Na+ current through Ca2+ channels. When fura-2 was used as indicator for the cytosolic Ca2+, TRB induced a release from intracellular stores only once and had no effect on the intracellular Ca2+ concentration during further applications. In line with this observation, TRH initially reduced the Na' current through Ca2+ channels but stimulated it during subsequent applications. The stimulation was sensitive to GDP[.3S] and was abolished by pretreatment with PT, suggesting that the stimulatory action of TRH is mediated by a G protein different from the one that functionally couples the receptor to phosphatidylinositol 4,5-bisphosphate hydrolysis. In conclusion, the rent data suggest that TRH increases the intracellular Ca + concentration by two interacting pathways, that release from intracellular stores causes a secondary blockage of Ca2l channels, and that, especially with empty intracellular Ca2+ stores, Ca2+ channels are stimulated by a PT-sensitive G protein.Pituitary-hormone-releasing factors such as thyrotropinreleasing hormone (TRH), luteinizing-hormone-releasing hormone (LHRH), and angiotensin II (ATII) increase the cytosolic Ca2l in anterior pituitary cells in two successive phases. They first induce an inositol trisphosphatedependent Cal' release (1-6) and then stimulate extracellular Ca2l entry, which is sustained in the presence ofthe releasing factor (7,8). The nature of this retarded and prolonged Ca2+ entry remains unclear (9-12). A biphasic TRH action was also seen in membrane potential recordings. The membrane potential hyperpolarized within the first phase (about 2 min); action potentials induced thereafter occurred at a higher rate than the basal activity (13, 14). The hyperpolarization was attributed to an activation of Ca2l-dependent K+ channels, which may be related to the intracellular Ca2+ mobilization (11,15), and the increased firing pattern was thought to be associated with an inhibition of inwardly rectifying K+ channels (16). However, the TRH-induced inhibition of voltagedependent Ca2l channels previo...

show abstract

Polyphosphoinositide hydrolysis by phospholipase C is accelerated by thyrotropin releasing hormone (TRH) in clonal rat pituitary cells (GH₃ cells)

Cited by 44 publications

References 30 publications

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Pertussis toxin selectively abolishes hormone induced lowering of cytosolic calcium in GH₃ cells

Thyrotropin-releasing hormone induces opposite effects on Ca2+ channel currents in pituitary cells by two pathways.

Contact Info

Product

Resources

About

Polyphosphoinositide hydrolysis by phospholipase C is accelerated by thyrotropin releasing hormone (TRH) in clonal rat pituitary cells (GH3 cells)

Cited by 44 publications

References 30 publications

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Thyrotrophin-releasing hormone stimulates polyphosphoinositide metabolism in the frog neurointermediate lobe

Pertussis toxin selectively abolishes hormone induced lowering of cytosolic calcium in GH3 cells

Thyrotropin-releasing hormone induces opposite effects on Ca2+ channel currents in pituitary cells by two pathways.

Contact Info

Product

Resources

About

Polyphosphoinositide hydrolysis by phospholipase C is accelerated by thyrotropin releasing hormone (TRH) in clonal rat pituitary cells (GH₃ cells)

Pertussis toxin selectively abolishes hormone induced lowering of cytosolic calcium in GH₃ cells