help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Koibuchi, N.
Right arrow Articles by Suzuki, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koibuchi, N.
Right arrow Articles by Suzuki, M.

Endocrinology, Vol 122, 659-664, Copyright © 1988 by Endocrine Society

ARTICLES

Suppression of human growth hormone (GH)-releasing hormone-induced GH secretion in pentobarbital-anesthetized rats after electrical stimulation of the midbrain central gray and several raphe nuclei

N Koibuchi, M Kato, T Kakegawa and M Suzuki
Department of Physiology, Gunma University, Maebashi, Japan.

To investigate the neural mechanism involved in suppression of GH secretion, we examined the effect of electrical stimulation of the midbrain central gray (CG) and several raphe nuclei on human (h) GRF- induced GH secretion in pentobarbital-anesthetized rats. A concentric bipolar stimulating electrode was implanted stereotaxically into each nucleus under pentobarbital anesthesia 1 week before stimulation. Blood samples were taken through a cannula placed in the right atrium via the right external jugular vein. Under pentobarbital anesthesia, 5 micrograms hGRF dissolved in 0.3 ml saline were systemically applied through this cannula. Ten minutes after the infusion, plasma GH was increased from the resting value of 28.5 +/- 7.1 ng/ml (mean +/- SE) to 686.1 +/- 62.0 ng/ml. Biphasic electrical stimulation was delivered for the first 10 min. When the CG was stimulated with a current of 500 microA, hGRF-induced GH secretion was markedly suppressed. However, even when the stimulation site was outside the CG, hGRF-induced GH secretion was suppressed. But with a smaller current (100 microA) the suppressive effect was observed only when the medial portion of the CG was stimulated. This suppression was abolished by prior lesioning of the hypothalamic periventricular nucleus (Pe), in which most of the somatostatin-immunoreactive fibers in the median eminence originate. The stimulation of the dorsal raphe with a current of 500 microA suppressed the GH increment at 10 min, but no suppression occurred with a current of 100 microA. This suppression was abolished by prior lesioning of the Pe. Electrical stimulation of the rest of the raphe nuclei had no effect on hGRF-induced GH secretion. These results suggest that electrical stimulation of the CG suppresses hGRF-induced GH secretion, and the most effective area is the ventromedial portion of the CG. These suppressive actions may be achieved by activation of the somatostatin neurons in the Pe.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1988 by The Endocrine Society