Inhibitory Effect of Hypothalamic Stimulation on Growth Hormone (GH) Release Induced by GH-Releasing Factor in the Rat*

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Abstract
The topography of hypothalamic areas related to the suppression of GH [growth hormone] release induced by human pancreatic GH-releasing factor (hpGRF) was clarified. One week before the experiments, bipolar concentric stimulating electrodes were implanted in the organum vasculosum of the lamina terminalis (OVLT), the periventricular nucleus of the hypothalamus (Pe), the ventromedial nucleus of the hypothalamus (VMH), the lateral hypothalamic area (LHA), or the ventral premammillary nucleus (PMV). At the same time, the jugular vein was cannulated for blood sampling, and lesion of the anterior Pe was performed with a cathodal current. One and one half hours before the 1st blood sampling the rats were anesthetized with pentobarbital to prevent spontaneous GH bursts. One minute after the 1st blood sampling, 10 .mu.g hpGRF dissolved in 0.3 ml saline was injected i.v. through the cannula. The blood samples were collected at 10, 20, 30, and 60 min after the zero-time sample. The above mentioned hypothalamic nuclei were electrically stimulated for the first 10 min. Injection of hpGRF increased the plasma GH level from 44.2 .+-. 7.3 ng/ml (mean .+-. SE) to 981.4 .+-. 59.8 ng/ml in 10 min, and the plasma GH level gradually decreased to 50.8 .+-. 8.8 ng/ml by 60 min. The hpGRF-induced GH release was most effectively suppressed by the stimulation of the Pe. After the stimulation of the OVLT, the VMH, the LHA, or the PMV, the suppression of hpGRF-induced GH release was weaker than that of the Pe. This stimulation-induced suppression was fully or partly prevented in Pe-lesioned animals. Apparently the stimulation of the Pe, the OVLT, the VMH, the LHA, or the PMV exerts an inhibitory effect on GH release. For this inhibitory effect, the Pe was essential. The topography of immunoreactive SRIF [somatostatin] neuronal cell bodies and processes in the hypothalamus is discussed.