Sexually Differentiated Role of Calcium Ions in Chicken GnRH-I-Stimulated Release of LH from Anterior Pituitary Glands from Adult Domestic Chickens

Abstract

Continuous perifusion of quartered anterior pituitary glands from juvenile and adult chickens of both sexes with chicken gonadotrophin-releasing hormone-I (eGnRH-I) stimulated a spike-plateau profile of luteinizing hormone (LH) secretion. When perifused in CA 2+-free medium, pituitary glands from juveniles of both sexes and from adult cockerels but not those from laying hens, released LH in response to cGnRH-I. This release occurred at the same time as the spike phase of the response seen in the presence of extracellular Ca 2+ and was not accompanied by a plateau phase of secretion. The magnitude of the plateau but not the spkie phase of LH secretion from pituitary glands from adult males and females was reduced by the L-type Ca 2+ channel blocker, nifedipine. This suggests that the mechanism of cGnRH-I-induced LH release from pituitary glands from laying hens is independent of mobilization of intracellular Ca 2+ during the spike phase of LH secretion occurs through non-L-type Ca 2+ channels. Both non-L-type Ca 2+ channels operate during the plateau phase of secretion in adults of both sexes. The duration of the spike phase of LH release from pituitary glands from adult cockerels was curtailed in the presence of nifedipine. The spike phase of LH release from the adult cockerel pituitary therefore involves three modes of Ca 2+ flux, comprising an intracellular Ca 2+-dependent component and extracellular components involving Ca 2+ entry through L-type and non-L-type Ca 2+ channels. The finding that the extracellular Ca 2+-independent component of cGnRH-I-stimulated LH release from pituitary glands from juvenile hens is not present in adult hens suggests that this difference is related to sexual maturation. The maturational and sexual differences in the LH response to cGnRH-I could be mediated through the high concentrations of plasma 17β-oestradiol in adult hens which suppress the mobilization of intracellular stores of Ca 2+ in the gonadotrophes.