Ionic channels in hormone release from adenohypophysial cells—an electrophysiological approach |
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Authors: | J.D. Vincent J.M. Israel J.L. Brigant |
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Affiliation: | INSERM U.176, Domaine de Carreire, Rue Camille Saint-Saëns, 33077, Bordeaux-Cedex, France |
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Abstract: | Electrophysiological experiments were performed on pituitary cells grown in culture. Two types of cells were studied, one of tumoral origin (GH3-B6; GH4-C1; human adenoma) and another type isolated from normal male and female rat pituitaries. Intracellular recordings showed that these cells displayed action potentials which were blocked by calcium antagonists (cobalt, manganese, cadmium, methoxyverapamil). The electrical activity of the cells was affected by substances known to modify hormone release. Dopamine and γ-aminobutyric acid inhibited action potential discharge of GH3 and prolactin-secreting cells, whereas thyreoliberin and estrogen led to an increase of the electrical activity of GH3, acromegalic and “non-functioning” tumor cells. Patch clamp experiments on clonal growth hormone-secreting cells make it possible to record specific ionic currents (e.g. calcium current), through the total membrane of the cell, in adequate voltage clamp conditions. Increase of the calcium current was observed after addition of growth hormone releasing factor, somatocrinin. It was also possible to observe the behaviour of individual ionic channels. We may conclude from intracellular and patch clamp recordings that modulation of the membrane electrical activity may alter the amount of cytosolic calcium and consequently may control hormone release in endocrine cells. |
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