Electrical Stimulation of Several Limbic Areas Suppressed the Growth Hormone (GH) Release Induced by Human Pancreatic GH-Releasing Factor in Pentobarbital-Anesthetized Rats*

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Abstract
The present study was designed to clarify the topography in the limbic system related to the suppression of GH release induced by iv injected human pancreatic GH-releasing factor (hpGRF) in pentobarbital-anesthetized rats. Bipolar concentric stimulating electrodes were implanted in certain limbic areas 1 week before the stimulation. Under pentobarbital anesthesia, 10 .mu.g hpGRF dissolved in 0.3 ml saline were injected iv, which increased the plasma GH level from 19.8 .+-. 3.6 (mean .+-. SE) to 846.0 .+-. 40.5 ng/ml in 10 min. After the plasma GH level showed its highest value (at 10 min), it gradually decreased to 30.5 .+-. 3.0 ng/ml by 60 min. This hpGRF-induced response was suppressed by the electrical stimulation (for the first 10 min) of the medial amygdaloid nucleus (Me), the lateral septum, or the bed nucleus of the stria terminalis. The inhibition rate ranged between 31.9-42.4% of control at 10 min. This inhibition was abolished by prior lesion of the perventricular nucleus of the hypothalamus, where the somatostatinergic nerve terminals in the median eminence originate. Sectioning the stria terminalis also abolished the inhibitory effect of GH release due to Me stimulation. The electrical stimulation of other amygdaloid nuclei or of the medial septum exerted no inhibitory effect on hpGRF-induced GH release. These results indicate that stimulation of the Me, the lateral septum, or the bed nucleus of the stria terminalis exerts an inhibitory effect on GH release, and the periventricular nucleus of the hypothalamus and the stria terminalis (in the case of Me stimulation) are important for this inhibitory effect.