Electrolytic lesions in the posterior part of the median eminence of rats caused diabetes insipidus, and aldehyde-fuchsin-positive material disappeared from the infundibular process but not from the hypothalamus. The lesions were consistently followed by infarction of the central pars distalis and depression of the thyroid uptake of radioactive iodine, but the effects on the gonads and adrenal cortex were very variable. Chronic adrenal atrophy occurred in some females in association with recurrent pseudopregnancy, atrophic but hyperluteinized ovaries, and cytological changes in the pituitary similar to those in ectopic grafts. After a short post-operative period of pseudopregnancy other rats recovered normal cycles and had, in general, adrenals of normal weight; their pituitaries resembled ectopic grafts returned to the median eminence. It is suggested that the difference between the two groups of rats with chronic lesions depended on the permanence or otherwise of the damage to the long portal veins. No evidence could be found of a separate corticotrophin-releasing mechanism in the median eminence, nor of any dependence of the secretion of corticotrophin on the release of vasopressin.
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