Summary
In nine baboons (Papio papio) guide cannulae and electrodes were stereotaxically implanted
into the medial basal or lateral hypothalamus, the anterior hypothalamus or the dorsal
amygdala. Plasma GH responses were measured after microinfusion (1 μl) of the α2 adrenergic agonist, clonidine, or the β adrenergic antagonist, propranolol, or electrical
stimulation, in each of these sites.
Clonidine, 100 nmol/μl, infused into the medial basal or lateral hypothalamus elevated
plasma GH levels by 5-30 ng/ml, 30-45 min post-infusion. Plasma GH responses to clonidine
infused into the anterior hypothalamus or the dorsal amygdala were all less than 10
ng/ml. The prior, intravenous, administration of piperoxane, 1.0 mg/kg prevented GH
responses to clonidine.
Propranolol, 50 nmol/μl, infused into the dorsal amygdala consistently increased plasma
GH levels by 5-15 ng/ml.
Electrical stimulation of the medial basal or lateral hypothalamus elevated plasma
GH levels by 7-35 ng/ml, 15-45 min post stimulation. Electrical stimulation of anterior
hypothalamus or dorsal amygdala did not alter plasma GH levels.
The stimulation of α2 adrenergic receptors in the medial basal or lateral hypothalamus of the baboons appears
to facilitate GH release.
Key-Words:
Growth Hormone
-
α
2
-Adrenoceptors
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Hypothalamus
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Clonidine
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Baboons