Growth hormone release induced by electrical stimulation of the basolateral amygdala, observed in pentobarbital anesthetized rats.
The aim of this study was to clarify the neural pathway leading to the growth hormone (GH) release when the basolateral amygdala (ABL) was electrically stimulated. Concentric bipolar stimulating electrode was implanted in the unilateral ABL. Blood samples were taken from a cannula implanted into the right atrium via the right external jugular vein. Electrical stimulation of the ABL for 10 min caused a significant increase in plasma GH level from resting value 27.5 +/- 5.7 ng/ml (mean +/- S.E.M.) to 62.2 +/- 7.5 ng/ml at the termination of stimulation. This increase in GH level was markedly augmented to 152.0 +/- 23.0 ng/ml after lesion of the periventricular hypothalamic nucleus (Pe), where somatostatinergic neurons send their axons to the median eminence. Lesion of the stria terminalis (st) fully or partly abolished GH release induced by ABL stimulation. These results suggest that stimulation of the ABL accelerates GH secretion. The st is an essential pathway for this release, whereas the activity of Pe-neurons is rather inhibitory to this release.
D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000502:physiology*; D004558:Electric Stimulation; D013006:Growth Hormone / Q000097:blood / Q000378:metabolism*; D008297:Male; D010424:Pentobarbital; D051381:Rats; D011919:Rats, Inbred Strains
D013006:Growth Hormone; D010424:Pentobarbital