The ontogenesis of GABA mediated inhibition of growth hormone release in the sheep.
To investigate the ontogenesis of gamma-aminobutyric acid (GABA) mediated regulation of growth hormone release, the GABA agonist muscimol (250-300 micrograms/kg, i.v.) or antagonist, picrotoxin (300-500 micrograms/kg, i.v.) was administered to the chronically catheterized ovine fetus, infant lamb or adult ewe. Neither agent affected growth hormone release in fetuses younger than 105 days of gestation or in infant lambs or adult sheep. In fetuses between 115 and 140 days of gestation muscimol inhibited (n = 5, P less than 0.02) and picrotoxin stimulated (n = 5, P less than 0.001) fetal growth hormone secretion. These observations indicate the presence of tonic GABA mediated inhibition of growth hormone release in the late gestation fetus and are evidence that fetal GH secretion is not entirely unrestrained. Compared to other neurotransmitter systems potentially regulating growth hormone secretion, the GABA-ergic system is intermediate in its appearance. The presence of a growth hormone response to GABA agonists and antagonists in the fetal but not in the postnatal period is further evidence of the particularly prominent role of GABA as a neurotransmitter in the immature brain.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D005260:Female; D005333:Fetus / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism*; D009118:Muscimol / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D011247:Pregnancy; D012756:Sheep / Q000196:embryology / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D013006:Growth Hormone; D009118:Muscimol; D010852:Picrotoxin; D005680:gamma-Aminobutyric Acid