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Immunocytochemical studies have identified immunoreactive prolactin (IR-PRL) in the hypothalamus and other areas of the rat brain. However, neither the release of IR-PRL from the hypothalamus nor its subcellular localization have been demonstrated. In this study, the release of IR-PRL from hypothalami obtained from female rats was examined using hypothalamic units incubated in vitro in Krebs-Ringer bicarbonate-glucose buffer. Hypothalamic tissue spontaneously released IR-PRL, and this release was increased by depolarizing concentrations of potassium by a calcium-dependent mechanism. Hypothalamic IR-PRL was also released from hypothalamic tissue obtained from hypophysectomized rats (14 days). The subcellular localization of IR-PRL was investigated using equilibrium-density centrifugation. Tissue homogenates from intact or hypophysectomized rats were centrifuged at 150 g at 4 °C for 10 min, and the supernatants were layered onto continuous sucrose gradients (1.00–1.27 g/ml) and centrifuged at 100,000 g (max.) for 16 h. IR-PRL in pituitary supernatants showed a high equilibrium-density peak with a modal density of 1.23 g/ml. Fractionation of the supernatant from ventral or dorsal hypothalamic tissue resulted in two high-equilibrium density peaks, a primary peak with a modal density of 1.23 g/ml and a smaller peak with a modal density of 1.10 g/ml. Both high-density peaks were maintained in tissue obtained from hypophysectomized rats and were disrupted by homogenization in hypo-osmotic medium. Together, these data suggest that hypothalamic IR-PRL is stored in membrane-bound particles which have densities similar to those of secretory granules and is released by a calcium-dependent mechanism when the tissue is depolarized.

Anterior hypothalamic implantations of crystalline atropine markedly inhibit the adrenocortical responses evoked by surgical stress, ether anesthesia, or intravenolus injection of arginine vasopressin. Similar implants in nearby regions of the brain or sham implantations in the same region were ineffective. The data suggest that the hypothalamic control of pituitary corticotropin may have a cholinergic component.

Thyroid function was studied in unanesthetized female rats by determining ¹²⁵I levels in sequential blood samples obtained via chronic jugular catheters. On the basis of plasma corticosterone determinations, nothing associated with the sampling procedure was stressful for the animals. Synthetic TRF and TSH injections resulted in rather rapid increases in blood ¹²⁵I levels. Exposure to cold (either continuous or transient) caused a similar but somewhat delayed response. The response to cold was abolished by thyroxine pretreatment. Pentobarbital anesthesia, when maintained by hourly injections, also abolished the cold response. This was, at least in part, due to decreased responsiveness of the thyroid to TSH.