Abstract

The aims of the present study were to investigate the sexual dimorphism and the role of sex steroids in GH secretion at the pituitary level, and to evaluate the ontogenesis of these effects. Towards these aims we used an in vitro perifusion system of hemipituitaries under a simulated milieu of hypothalamic factors: two 3-min pulses of GHRH at 3-hour intervals were separated by continuous flow of somatostatin. Rat GH was measured in 2.4-min fractions and analyzed by the pulse analysis program PULSAR. Pulses were similar in prepubertal male and female rats, but sexual dimorphism was evident in adults. In adult males, who had undergone neonatal gonadectomy, GH pulse amplitude and area under the curve (AUC) were lower compared to control. When gonadectomy had been performed at a prepubertal age, the pulse amplitude was still lower, but the AUC was not different from control. The gap between orchiectomy at neonatal and prepubertal age indicates the perinatal imprint, which induces an increase in AUC. Neonatal testosterone treatment of intact female rats had no effect on GH secretion by adult pituitaries. In neonatally gonadectomized female rats, under neonatal testosterone treatment, the pulse amplitude increased. A similar increase was observed after neonatal gonadectomy without testosterone treatment. We conclude that the sexual dimorphism of GH secretion is partially induced at the pituitary level and its response to the hypothalamic hormones. We assume that a neonatal imprint effect of testosterone in the male induces primarily an increase in AUC in response to GHRH. The imprint in females influences the GH pulse amplitude and AUC.

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