Involvement of extracellular sodium in agonist-induced gonadotropin release from goldfish (Carassius auratus) gonadotrophs

F. Van Goor
1996 Endocrinology  
I ONIC FLUX across the plasma membrane through voltage-dependent and -independent ionic channels are important in the regulation of many cellular functions, including hormone release. In mammals, LH release is stimulated by the hypothalamic decapeptide, mammalian GnRH (1). Activation of GnRH-receptors in the plasma membrane results in the oscillatory release of intracellular Ca*+ from InsI',-sensitive stores, which leads to the generation of periodic membrane hyperpolarizations followed by one
more » ... r more regenerative action potentials (2, 3), as well as exocytosis (3). These GnRH-induced membrane potential changes are mediated by multiple ionic channels, including voltagedependent Na+ and Cazt channels, as well as Ca'+-activated, apamin-sensitive K+ channels (2, 3). In addition, GnRH action has also been linked to the activation of transport proteins such as Na+ /H+ exchangers (4, 5). Recently, the signal transduction mechanisms mediating GnRH action on pituitary cells have also been investigated in goldfish. The goldfish pituitary cell system, with its unique features, is an important model for studying the control of gonadotropin (GTH) release (1,6-8). First, two endogenous GnRHs, salmon (s) GnRH and chicken (c)GnRH-II, are released from hypothalamic neurons directly at the level of the pars distalis to stimulate the secretion of maturational GTH
doi:10.1210/en.137.7.2859 pmid:8770907 fatcat:bcnrjdts5faoxpyhvshxdwc65i