The mechanisms by which vasoactive intestinal peptide (VIP) and thyrotropin releasing hormone (TRH) stimulate prolactin release from pituitary cells

1990 ◽  
Vol 10 (2) ◽  
pp. 189-199 ◽  
Author(s):  
Trine Bjøro ◽  
Olav Sand ◽  
Bjørn Chr. Østberg ◽  
Jan O. Gordeladze ◽  
Peter Torjesen ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Adenylate Cyclase ◽  
Vasoactive Intestinal Peptide ◽  
Lag Time ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Inositol Polyphosphates ◽  
Releasing Hormone ◽  
Electrophysiological Properties

The effect of vasoactive intestinal peptide (VIP) on prolactin (PRL) secretion from pituitary cells is reviewed and compared to the effect of thyrotropin releasing hormone (TRH). These two peptides induced different secretion profiles from parafused lactotrophs in culture. TRH was found to increase PRL secretion within 4 s and induced a biphasic secretion pattern, while VIP induced a monophasic secretion pattern after a lag time of 45–60 s. The secretion profiles are compared to changes in adenylate cyclase activity, production of inositol polyphosphates, changes in intracellular calcium concentrations and changes in electrophysiological properties of the cell membrane.

Electrophysiological response to thyrotropin-releasing hormone of rat lactotrophs in primary culture

1990 ◽  
Vol 258 (2) ◽  
pp. E311-E319 ◽  
Author(s):  
P. Sartor ◽  
L. Dufy-Barbe ◽  
J. B. Corcuff ◽  
A. Taupignon ◽  
B. Dufy
Keyword(s):  
Primary Culture ◽  
Input Resistance ◽  
Thyrotropin Releasing Hormone ◽  
Female Rats ◽  
Resting Potential ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Electrophysiological Properties ◽  
L Cells ◽  
D Cells

The response of rat pituitary cells to thyrotropin-releasing hormone (TRH) in primary culture was studied in the whole-cell configuration with the patch-clamp technique. Prolactin (PRL)-containing cells were identified in the culture with a peroxidase-antiperoxidase immunocytochemical method. The cells were cultured from the pituitaries of diestrous (D) and lactating (L) female rats. Membrane electrophysiological properties (resting potential and input resistance) of pituitary cells in primary culture varied widely. Under the recording conditions reported here, the mean resting potential of lactotrophs was about -30 mV. There were spontaneous fluctuations in membrane resting potential (10-15 mV) as well as of membrane input resistance, making these parameters difficult to evaluate accurately. Most of the cells exhibited spontaneous firing activity that was shown to be mainly calcium-dependent. There was no difference between L and D cells in resting membrane electrophysiological properties. TRH (10(-7) M) induced a transient hyperpolarization of the membrane similar to that previously described in the GH3 clonal pituitary cell line. Voltage-clamp studies showed that this hyperpolarization resulted from activation of an outward current, the reversal potential of which ranged from -48 to -86.5 mV. Experimental manipulations of the ionic composition of internal and external recording media suggested that both K+ and Cl- were involved. This hyperpolarizing response was observed both in D and L cells, although L cells had larger and faster responses than D cells. This observation may be of physiological significance because lactotrophs have been reported to exist in various subtypes.

scholarly journals Subsecond and second changes in inositol polyphosphates in GH4C1 cells induced by thyrotropin-releasing hormone

1987 ◽  
Vol 243 (1) ◽  
pp. 305-308 ◽  
Author(s):  
A H Tashjian ◽  
J P Heslop ◽  
M J Berridge
Keyword(s):  
Intracellular Calcium ◽  
Inositol Phosphates ◽  
Thyrotropin Releasing Hormone ◽  
Current View ◽  
Free Calcium ◽  
Calcium Stores ◽  
Pituitary Cells ◽  
Inositol Polyphosphates ◽  
Releasing Hormone ◽  
Polyphosphate Metabolism

It has been demonstrated previously that thyrotropin-releasing hormone (TRH) induces changes in inositol polyphosphates in the GH3 and GH4C1 strains of rat pituitary cells within 2.5-5.0 s. TRH also causes a rapid rise in cytosolic free calcium concentration ([Ca2+]i) in these cells which is due largely to redistribution of cellular calcium stores. Therefore, it has been concluded that TRH acts to release sequestered calcium in these cells via enhanced generation of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. If this conclusion were correct, TRH-enhanced accumulation of Ins(1,4,5)P3 should occur at least as rapidly as the increase in [Ca2+]i. We have shown previously that the rise in [Ca2+]i induced by TRH occurs within about 400 ms; thus, it was important to investigate the subsecond time-course of changes in inositol phosphates caused by TRH. Using a rapid mixing device, we have measured changes in inositol polyphosphates on a subsecond time scale in GH4C1 cells prelabelled with myo-[2-3H]inositol. Although TRH did alter inositol polyphosphate metabolism within 500 ms, the changes observed did not reveal a statistically significant increase in Ins(1,4,5)P3 within time intervals of less than 1000 ms. Thus, we have been unable to demonstrate that a TRH-induced rise in Ins(1,4,5)P3 precedes or occurs concomitantly with the rise in [Ca2+]i in GH4C1 cells. Although these results do not disprove the current view that Ins(1,4,5)P3 mediates the action of TRH on intracellular calcium redistribution, we conclude that caution should be exercised in this, and possibly other cell systems, in accepting the dogma that all of the rapid, agonist-induced redistributions of intracellular calcium are mediated by Ins(1,4,5)P3.

Extracellular ATP as an autocrine/paracrine regulator of prolactin release

1997 ◽  
Vol 272 (6) ◽  
pp. E1117-E1123 ◽  
Author(s):  
L. Nunez ◽  
C. Villalobos ◽  
L. S. Frawley
Keyword(s):  
Secretory Granules ◽  
Extracellular Atp ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Cells Cultured ◽  
Local Regulator

Recent evidence demonstrates that ATP, costored with a number of hormones and neurotransmitters in secretory granules, is coreleased during exocytosis of these agents. Here, we explored the possibility that extracellular ATP subserves an autocrine and/or paracrine role in the regulation of prolactin (PRL) release by subjecting rat pituitary cells to various experimental manipulations aimed at evaluating putative interactions between ATP and mammotropes. Our results strongly support the view that ATP functions as a local regulator of PRL secretion. To be more specific, we observed that ATP is released in a predictable manner by physiologically relevant secretagogues that are reasonably targeted to mammotropes. Moreover, we found that ATP can act directly on pituitary cells to stimulate the release of PRL from most (if not all) mammotropes. Finally, we determined that antagonism or removal of ATP leads to a diminution of PRL export from pituitary cells cultured under basal or thyrotropin-releasing hormone-stimulated conditions. On the basis of these results, we propose that ATP acts locally to amplify and prolong the PRL secretory response elicited by a more traditional hypophysiotropic signal.

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