title: ATP suppresses the K(+) current responses to FSH and adenosine in the follicular cells of Xenopus oocyte.
abstract: The application of either follicle-stimulating hormone (FSH) or adenosine (Ade) induces a K(+)-current response in the follicular cells surrounding a Xenopus oocyte under a voltage clamp. These K(+)-current responses are reported to be produced by an increase in intracellular cAMP. A previous application of ATP to the same cells markedly depressed the K(+)-current responses to FSH and Ade. Furthermore, a 2 min application of phorbol 12,13-dibutyrate (PDBu), an activator of protein kinase C (PKC), significantly depressed the K(+)-current responses to FSH and Ade, but it had no significant effect on the Cl(-)-current response to ATP. An application of either ATP or PDBu also depressed the K(+)-current response induced by intracellularly applied cAMP. In contrast to the effect of PDBu, the application of 1-octanol, an inhibitor of gap junction channel, significantly depressed both the Ade- and ATP-induced responses, indicating that the acting site of 1-octanol is different from that of PKC. The results suggest that the depressing effect of ATP on the FSH- and Ade-induced K(+)-current responses might be mediated by PKC activation and that the site of PKC action might be downstream of the cAMP production involved in the K(+) channel opening.
authors.affiliation: Department of Chemistry, School of Liberal Arts and Sciences, Iwate Medical University, Morioka, 020-0015, Japan. rfujita@iwate-med.ac.jp
authors.forename: R
authors.initials: R
authors.lastname: Fujita
authors.forename: S
authors.initials: S
authors.lastname: Kimura
authors.forename: S
authors.initials: S
authors.lastname: Kawasaki
authors.forename: K
authors.initials: K
authors.lastname: Takashima
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Hirano
authors.forename: K
authors.initials: K
authors.lastname: Sasaki
mesh_terms: D000200:Action Potentials; D000241:Adenosine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002273:Carcinogens / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D003593:Cytoplasm / Q000737:chemistry; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology*; D017629:Gap Junctions / Q000502:physiology; D009865:Oocytes / Q000502:physiology; D006080:Ovarian Follicle / Q000201:enzymology / Q000502:physiology*; D015240:Phorbol 12,13-Dibutyrate / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D011493:Protein Kinase C / Q000378:metabolism*; D014982:Xenopus laevis
chemical_list: D002273:Carcinogens; D015221:Potassium Channels; D015240:Phorbol 12,13-Dibutyrate; D000255:Adenosine Triphosphate; D005640:Follicle Stimulating Hormone; D000242:Cyclic AMP; D011493:Protein Kinase C; D000241:Adenosine