The infusion of 50 µg norepinephrine (NE) into the third ventricle of the brain was found to be highly effective in stimulating the release of an ovulatory surge of LH from the pituitary gland in estrogen-primed rabbits. Intraventricular dopamine (D), in dosages of 5 and 50 µg, was not only completely ineffective in inducing ovulation, but the higher dosage actually blocked the ovulatory effect of NE, often for a month or more after infusion. In experimentts in which LH was measured by radioimmunoassay, intraventricular NE stimulated a marked rise in LH starting within minutes, peaking at 2 h and returning to pre-infusion levels by 6 h. No rise in serum LH was observed following the intraventricular infusion of D. Both dosages of D were quite effective in blocking LH output in response to NE infused 2 h later, and the 50-µg dosage of D generally prevented any rise in serum LH concentration for some weeks after the infusion of intraventricular NE. The results are consistent with the hypothesis that a noradrenergic synapse is functional in hypothalamic mechanisms activating the release of pituitary LH.

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The effect of cholecystokinin (CCK)-8 was studied on the release of luteinizing hormone (LH) from perifused medial basal hypothalami (MBH) and/or adenohypophyses of castrated bulls in a sequential double chamber perifusion system. LH concentrations in the perifusion efflux from the pituitary in series with the hypothalamus decreased significantly (P<0.05) after perifusion of 10-8M CCK as compared with control levels. In the similar perifusion LH concentrations in the efflux from the pituitary alone decreased significantly (P<0.01) after perifusion of 10-8M CCK. 10-7M CCK induced neither inhibitory nor stimulatory effects in perifusions of the pituitary in series with the hypothalamus except one fraction. Similarly, 10-7M CCK failed to induce a significant change in LH release in perifusion of the pituitary alone. LH concentrations in the perifusion efflux from pituitary in series with the hypothalamus increased significantly at 50 and 60 min after the initiation of 10-6M CCK perifusion as compared with the control level (P<0.05). LH concentrations in the efflux from the pituitary alone increased significantly 40, 50, 60 and 80 min after the initiation of perifusion with 10-6M CCK. The results indicate that CCK acts directly on the adenohypophysis to modulate release of LH in cattle.

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