This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Welsch, C. W. Articles by Meites, J. Search for Related Content PubMed PubMed Citation Articles by Welsch, C. W. Articles by Meites, J.

Effects of Hypothalamic and Amygdaloid Lesions on Development and Growth of Carcinogen-induced Mammary Tumors in the Female Rat^1,2,

Department of Physiology, Michigan State University, East Lansing, Michigan 48823

The effects of median eminence and preoptic and amygdaloid lesions on normal and 7,12-dimethylbenzanthracene-induced neoplastic mammary tissue growth were investigated in female Sprague-Dawley rats. Marked stimulation of normal and neoplastic mammary tissue growth was observed in intact rats 10 and 25 days after placement of median eminence lesions. When median eminence lesions and ovariectomy were combined, a striking stimulation of normal and neoplastic tissue was noted 10 days but not 25 days later. If ovariectomy preceded the median eminence lesions by 10 days, no effect was observed on neoplastic mammary growth, and only a slight stimulation of normal mammary growth was observed 10 days after lesion placement. Since lesions in the median eminence result in enhanced prolactin secretion and reduced secretion of all other anterior pituitary hormones, these observations indicate that prolactin is the principal hormone responsible for growth of the 7,12-dimethylbenzanthracene-induced mammary tumors. Lesions in the preoptic or amygdaloid complex of intact rats induced marked tumor regression 10 or 25 days after lesion placement, but they apparently had no effect on normal mammary development 10 days after lesion placement. The reduction in mammary tumor growth was accompanied by decreased ovarian and uterine weights, suggesting that estrogen secretion was lowered. Since the latter can result in diminished prolactin secretion, it is possible that reduced secretion of estrogen and prolactin was responsible for the mammary regression observed in the le-sioned rats.

¹ Supported in part by NIH research Grants AM-04784 and CA-10771 and Grant 68-177TA from the Michigan Cancer Foundation.

² Reported in part at the Annual Meeting of the American Association for Cancer Research, April 1968.

³ Special Research Fellow, National Cancer Institute, NIH, USPHS. Present address: Department of Anatomy, Michigan State University, East Lansing, Michigan 48823.

⁴ NIH predoctoral trainee (GM-1121) during tenure of his work. Present address: Department of Anatomy, University of California at Los Angeles, Los Angeles, California 90024.

Received 9/30/68. Accepted 4/ 1/69.