HORMONAL BASIS FOR IMPAIRMENTS IN MILK SYNTHESIS AND MILK EJECTION FOLLOWING HYPOTHALAMIC LESIONS

Abstract

SUMMARY: The placing of electrolytic lesions in the median eminence of the hypothalamic tuber cinereum induces severe impairment of lactation in rats by causing deficiencies in pituitary secretion of adrenocorticotrophic hormone (ACTH; essential for milk synthesis) and of oxytocin (necessary for milk ejection). Thus, in rats with lesions given oxytocin × 2/day to permit milk ejection, it was observed that: (1) the severity of impairment in lactation correlated significantly with the degree of atrophy of the dams' adrenal glands; (2) administration of luteotrophin (LTH) failed to repair this defect in lactation; (3) when cortisol was administered milk production was markedly improved—to about 70–80% of normal for days 5–10—(a further slight increase in milk yield resulted when oxytocin injections were given every 4 hr. 'around the clock' to rats receiving cortisol therapy); and (4) administration of regimens consisting of either LTH and cortisol, or LTH, growth hormone (GH), and cortisol failed to improve lactation beyond levels attained with cortisol therapy alone. In hypophysectomized rats replacement with cortisol and LTH, plus oxytocin × 2/day, permitted substantial synthesis which was not significantly improved further when GH was added to the regimen, and which promptly declined when LTH therapy was withdrawn. Since no deficiency in secretion of LTH could be demonstrated in lactating rats with lesions given hormonal replacement, these data provide evidence that elimination of hypothalamic regulatory mechanisms by hypothalamic lesions is compatible with secretion of large amounts of LTH. This demonstration that lesions in the median eminence block release of ACTH while permitting continued secretion of LTH indicates that the hypothalamic mechanisms regulating their release are not identical.