Involvement of extracellular sodium in agonist-induced gonadotropin release from goldfish (Carassius auratus) gonadotrophs.
In goldfish, gonadotropin (GTH-II) responses to the two endogenous GnRHs, salmon-GnRH and chicken-GnRH-II, are mediated by activation of protein kinase C (PKC) and voltage-sensitive Ca2+ channels. In this study, we investigated the role of extracellular Na+, voltage-dependent Na+ channels, and the plasma membrane Na+/H+ exchanger in mediating GnRH-stimulated GTH-II release from dispersed goldfish pituitary cells. Perifusion with Na+-depleted medium reduced the GTH-II response to both GnRHs and the response to the protein kinase C activator, phorbol 12-myristate 13-acetate. Conversely, increasing Na+ influx with veratridine (100 microM) stimulated GTH-II release in the presence and in the absence of extracellular Ca2+. However, the voltage-sensitive Na+ channel blocker, tetrodotoxin (1 microM), did not affect GnRH- stimulated GTH-II release, and the GnRHs did not affect voltage-sensitive Na+ currents. In contrast, the Na+/H+ antiport inhibitors, amiloride or its analog, DMA, reduced GTH-II responses to the GnRHs and phorbol 12-myristate 13-acetate. The Na+/H+ antiport inhibitors did not affect voltage-sensitive Ca2+ or Na+ currents or the GTH-II release response to the Ca2+ ionophore, ionomycin. These findings indicate that extracellular Na+ and the Na+/H+ exchanger are involved in the mediation of GnRH-stimulated GTH-II release. In addition, Na+ entry may modulate GTH-II release independent of extracellular Ca2+.
Van Goor
F
F
Department of Biological Sciences, University of Alberta, Edmonton, Canada.
Goldberg
J I
JI
Chang
J P
JP
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D002478:Cells, Cultured; D002645:Chickens; D004789:Enzyme Activation; D005260:Female; D006054:Goldfish; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology*; D006065:Gonadotropins, Pituitary / Q000378:metabolism*; D015759:Ionomycin / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010902:Pituitary Gland / Q000187:drug effects / Q000502:physiology*; D011493:Protein Kinase C / Q000378:metabolism; D012474:Salmon; D012741:Sexual Maturation; D012964:Sodium / Q000494:pharmacology*; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014701:Veratridine / Q000494:pharmacology
D015220:Calcium Channels; D006065:Gonadotropins, Pituitary; D015222:Sodium Channels; D017923:Sodium-Hydrogen Exchangers; D007987:Gonadotropin-Releasing Hormone; D013779:Tetrodotoxin; D015759:Ionomycin; D014701:Veratridine; C047717:LHRH, His(5)-Trp(7)-Tyr(8)-; D012964:Sodium; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate