Abstract

Acute and chronic changes in calbindin (Mr28,000) mRNA and calbindin concentrations were determined to assess the roles of steroid hormones in calbindin mRNA and calbindin synthesis in the eggshell gland (ESG). The results support an earlier suggestion that calbindin gene expression in the ESG is associated with Ca2+flux through the ESG. The evidence includes wide oscillation of the mRNA during the diurnal egg cycle, in close temporal association with egg shell calcification. Progesterone (single im injection of 1 mg/kg body weight, BW) prolonged the period of egg formation and reduced the rate of Ca2+transport and the concentration of calbindin mRNA in the ESG. Dexamethasone (single im injection of 5 mg/kg BW) prolonged the period of egg formation, increased shell Ca2+, and reduced calbindin mRNA in the ESG and intestine. Testosterone (single im injection of 2 mg/kg BW) did not affect calbindin mRNA synthesis in the ESG. The effects of estradiol on the synthesis of calbindin mRNA in the ESG of sexually immature or laying birds were minor, while it affected plasma Ca in the same birds. The antiestrogen Tamoxifen (60 mg/kg BW, given orally) reduced plasma Ca, but did not affect the synthesis of calbindin mRNA in the ESG. The antiprogesterone RU-38486 (20 mg/kg BW, orally) increased shell Ca2+but had no effect on plasma Ca or the synthesis of calbindin mRNA. It appears that estrogens alone cannot account for the markedly elevated synthesis of calbindin mRNA in the ESG of the laying bird. The hypothesis that the regulatory mechanism for the synthesis of calbindin mRNA in the ESG may involve a stimulator(s), associated with the onset of production, and an oscillating depressor(s) is supported and both appear to be closely linked to the reproductive cycle. The specificin vivoeffect of progesterone on calbindin mRNA in the ESG, together with its already known changes during the ovulatory cycle in birds, supports the idea that it is a depressor.

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