The iv injection of crude methanol or acid extracts of porcine hypothalamic fragments (SME) induces at ten min a significant rise in radioimmunoassayable prolactin levels in male rats treated with 50 μg estradiol benzoate, and 25 mg progesterone daily for three days prior to assay. The response is log-dose dependent over the range of 2–25 SME equivalents. Although vasopressin in large doses also induces prolactin release, the effects of SME extract cannot be accounted for solely by the relatively small amounts of this hormone present in the extract; moreover, vasopressin can be separated from prolactin releasing activity (PRA) by thin-layer chromatography. Thyrotrophin-releasing hormone (TRH) in amounts far in excess of those found in SME extracts with PRA does not release prolactin, and by Sephadex G-10 chromatography a distinct fraction that exhibits PRA can be separated from TRH. As judged by the distribution on Sephadex G-10, PRA is distinct from luteinizing hormone-releasing factor (LRF). The sensitizing effect of the estrogenprogesterone treatment on PRA is due to the estradiol component of the steroid mixture since SME extracts are effective in stimulating prolactin release in animals pretreated with estrogen alone, but not with progesterone alone. Rat hypothalamic extracts also induce prolactin release in estrogen-progesterone (EP) sensitized animals. These results indicate that extracts of porcine and rat hypothalamic tissue contain a prolactin releasing substance distinct from other recognized hormones of the hypothalamus, and give support to the view that in addition to the long recognized prolactin inhibitory effects of the hypothalamus there may be an additional stimulatory control of mammalian prolactin secretion. (Endocrinology91: 982, 1972)
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Valverde et al. (1972) studied this question.