Localization of .ALPHA.2-adrenergic agonist sensitive area in the hypothalamus for growth hormone release in the rat.

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Abstract
To determine the localization of the clonidine sensitive area responsible for GH release, a minute amount of the α2-agonist (67ng/0.2μl) was injected into the hypothalamus and vicinity of adult male concious rats. The animals were chronically implanted with double metal cannulae fixed on the skull for clonidine microinjection and with silastic tubing into the right atria for collecting blood samples. Ten hr prior to the microinjection, α-methyl-p-tyrosine (250mg/kg body weight) was intraperitoneally injected to prevent spontaneous pulsatile GH release. Localization of the microinjection was assessed by histological examination after the experiment. Clonidine microinjection into the amygdala nucleus had no effect on GH release, while the injection into the preoptic and anterior hypothalamic area (PO/AH) significantly stimulated GH release by causing it to begin 30 min earlier. However, the paraventricular nucleus, the dorsomedial nucleus, the lateral hypothalamus and the ventromedial hypothalamus areas did not respond to the injection, although the latter nucleus has been shown to be a specific locus sensitive to electrical stimulation of release. In the area from the posterior hypothalamus to the mammillary body, several injections stimulated GH release (6/15), but the stimulatory effect was statistically insignificant when comparison was made with the mean (±SE) for all 15 rats. These findings suggest that the α2-agonist acts on the PO/AH to induce an increase in GH release in α-methyl-p-tyrosine-pretreated rats, probably mediating the inhibitory input to somatostatinergic neurons which reside in the periventricular nucleus of the PO/AH area.