title: Thyrotropin-releasing hormone-induced rise in cytosolic calcium and activation of outward K+ current monitored simultaneously in individual GH3B6 pituitary cells.
abstract: Thyrotropin-releasing hormone (TRH) acts on pituitary cells to raise the cytosolic free Ca2+ concentration ([Ca2+]i) and causes simultaneously a transient hyperpolarization of the plasma membrane. The combination of the microfluorimetric monitoring of [Ca2+]i with electrophysiological recordings obtained using the patch clamp technique in its whole cell configuration, allows the analysis of the correlation between changes in [Ca2+]i and the alterations in ionic currents at the plasma membrane. It was shown that in the absence of hormone stimulation, a depolarization-induced change in steady state [Ca2+]i, as well as the internal perfusion with Ca2+ at microM levels at constant membrane potential led to the activation of outward K+ current. TRH stimulation resulted in a marked but transient rise in [Ca2+]i; concomitantly, there was an increase in membrane conductance and an enhancement of outward current. During the time course of an individual response, an excellent correlation between the changes in [Ca2+]i and those in conductance or current was observed. The relative changes of current and conductance during the TRH response were consistent with the activation of a single type of ionic current, the apparent reversal potential of which coincided with the equilibrium potential for K+. A strong correlation between the TRH-induced changes in [Ca2+]i and K+, conductance was demonstrated in a large number of cells with varied kinetic features: significant correlation coefficients were found both for the transition time from basal to maximal values (r = 0.85, p less than 0.001) as well as for the total duration of the responses (r = 0.68, p less than 0.002). It is concluded that during the early phase of TRH action, the hormone-induced rise in [Ca2+]i is the principal cause of enhanced K+ channel activation.
authors.affiliation: Laboratoire de Neurophysiologie, UA Centre National de la Recherche Scientifique 1200, Bordeaux, France.
authors.forename: P
authors.initials: P
authors.lastname: Mollard
authors.forename: P
authors.initials: P
authors.lastname: Vacher
authors.forename: B
authors.initials: B
authors.lastname: Dufy
authors.forename: B P
authors.initials: BP
authors.lastname: Winiger
authors.forename: W
authors.initials: W
authors.lastname: Schlegel
mesh_terms: D000217:Acyltransferases / Q000235:genetics; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004553:Electric Conductivity; D008564:Membrane Potentials / Q000187:drug effects; D010911:Pituitary Neoplasms; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D013466:Sulfurtransferases / Q000235:genetics; D013972:Thyrotropin / Q000494:pharmacology*; D000637:Transaminases / Q000235:genetics
chemical_list: D015221:Potassium Channels; D013972:Thyrotropin; D000217:Acyltransferases; C021929:8-amino-7-oxononanoate synthase; C020029:7,8-diaminopelargonic acid aminotransferase; D000637:Transaminases; D013466:Sulfurtransferases; C057985:biotin synthetase; D002118:Calcium