Growth hormone secretion in the fetal sheep following stereotaxic electrolytic lesioning of the fetal hypothalamus.
Stereotaxic surgery was performed on sheep fetuses at 108 to 110 days of gestation to investigate hypothalamic influences on fetal growth hormone (GH) release. In 5 fetuses the median eminence was destroyed, in 6 damage was confined to the medial basal hypothalamus without total destruction of the median eminence, 6 had misplaced lesions and 4 were sham operated controls. Destruction of the median eminence led to a marked fall in GH secretion and an abolition of pulsatile GH release. Following lesioning of the median eminence, GH values are comparable to resting levels in the infant lamb. Pituitary infarction was excluded in these fetuses both histologically and by a maintained GH response to exogenous growth hormone releasing factor. Lesions of the medial basal hypothalamus without destruction of the median eminence led to a significant but lesser fall in GH secretion and a reduction in the pulsatility of GH release. Sham operated fetuses and those with lesions misplaced outside the endocrine hypothalamus showed maintained high circulating GH concentrations with marked pulsatility of GH release. These studies demonstrate that fetal GH release is solely dependent upon hypothalamic stimulation presumably mediated by growth hormone releasing factor. There is no evidence for pituitary autonomy or for direct extrahypothalamic stimulation of the fetal somatotrope.
D000818:Animals; D002940:Circadian Rhythm; D005333:Fetus / Q000378:metabolism*; D013006:Growth Hormone / Q000378:metabolism*; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology*; D012756:Sheep / Q000196:embryology; D013238:Stereotaxic Techniques
D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone