Abstract
We have shown that female(F) rat pituicytes were more sensitive to GRF but that male(M) cells responded more vigorously, and how these changes were dependent on sex steroids (ESPE 1987). To further study the effects of sex steroids 22-day-old rats were gonadectomized, and 12 days later their pituitaries dispersed and treated in vitro for 6 days with 5nM estradiol(E-2) or testosterone(T). After adherence to cytodex beads, cells were superfused in 1ml-4 million cell columns. One min. pulses of 6nM GRF produced 130% increment of GH secretion. In the F cells the basal secretion of E-2 treated cells was higher by 105% and the response to GRF greater by 230%, while T had no effect. In M cells T augmented GH response to GRF to 560%, while E-2 had no effect. In plated M pituicytes 1nM SST inhibited GH secretion by 75%. This was additive with the effect of GRF, which by 3nM overcame SST. In E-2 treated cells 64% inhibition with SST was also overcome by 3nM GRF. In pituitary cells which were treated by T, inhibition was only 34%, and overcome by 0.03 nM GRF. IGF-I induced a dose dependent inhibition of GH basal secretion with maximal decrease of 31-35% at 0.5 U/ml. The acute response to GRF was only mildly blunted by IGF-I (8-24%). In E-2 treated cells inhibition of GH basal secretion required 5-fold higher IGF-I conc., maximal inhibition was 15-49%, and acute GH response to GRF was blunted by 18-47%. In T treated cells IGF-I inhibited basal secretion by 48-57% but GH response to GRF was augmented by 24-55%. It is concluded that the rat pituitary acquires its sexual dimorphism of GH secretion perinatally. The unique pattern of GH secretion of each sex is later induced by sex steroid effects on the pituicytes' response to GRF, SST and IGF-I.
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