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Okadaic acid and calyculin A enhance the effect of thyrotropin‐releasing hormone on GH 3 rat anterior pituitary cells excitability
Author(s) -
Delgado Luis M.,
de la Peña Pilar,
del Camino Donato,
Barros Francisco
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)81362-p
Subject(s) - okadaic acid , medicine , thyrotropin releasing hormone , endocrinology , phosphatase , anterior pituitary , hormone , chemistry , hyperpolarization (physics) , biology , phosphorylation , biochemistry , stereochemistry , nuclear magnetic resonance spectroscopy
Thyrotropin‐releasing hormone (TRH) causes a transient hyperpolarization followed by several minutes of increased action potential frequency in patch‐perforated current‐clamped GH 3 cells. Treatment of cells for 5 min with either 2 or 100 nM of the protein phosphatase inhibitor okadaic acid does not affect electrical activity of the cells, but potentiates the enhancement of action potential frequency elicited by a subsequent addition of TRH. Alternatively, 100 nM (but not 2 nM) of okadaic acid added during the second phase of TRH action, further increases the frequency of firing above that produced by the hormone. Similar effects to those of 2 nM okadaic acid are observed with 20 nM calyculin A. These data suggest that a protein phosphatase plays a major role in regulating the delayed effects of TRH on cell excitability in GH 3 cells.

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