J. C. Chapman, J. J. Christian, M. Pawlikowski, N. Yasukawa, S. D. Michael
{"title":"Female house mice develop a unique ovarian lesion in colonies that are at maximum population density.","authors":"J. C. Chapman, J. J. Christian, M. Pawlikowski, N. Yasukawa, S. D. Michael","doi":"10.1111/J.1525-1373.2000.22510.X","DOIUrl":null,"url":null,"abstract":"Colonies of house mice reach maximum population density in 120-180 days, irrespective of cage size and initial number of colonizing animals. Reproduction ceases because the females become aggressive and unreceptive to mating. The aggressive behavior is correlated with elevated levels of testosterone (T) and corticosterone (B) (Chapman et al., Phys Behav 64:529-533, 1998). In two of seven strains of mice, females developed ovarian lesions. The occurrence of the lesion in one strain was correlated with the age of the animal and duration of the study. In the second strain, cage size was the determining factor. Lesioned ovaries weighed significantly more than nonlesioned ovaries. The lesion consisted of accumulations of luteal membrane and organelle fragments, and other cellular debris, suggestive of incomplete and prolonged luteolysis. Electron microscopic (EM) analyses revealed the presence of deposits of permanganate-resistant congophilic amyloid fibrils in the intima and smooth muscle cells of luteal thecal arteries. Population females had thymus glands and uteri that weighed significantly less than the same organs from females housed in the breeding colony, whereas the adrenal glands from the population females weighed significantly more. It is proposed that the female aggression is due to high levels of T. It is also proposed that the high levels of B suppress the immune cells involved in normal luteolysis and contribute to the incomplete and prolonged luteolysis.","PeriodicalId":20618,"journal":{"name":"Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/J.1525-1373.2000.22510.X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
Colonies of house mice reach maximum population density in 120-180 days, irrespective of cage size and initial number of colonizing animals. Reproduction ceases because the females become aggressive and unreceptive to mating. The aggressive behavior is correlated with elevated levels of testosterone (T) and corticosterone (B) (Chapman et al., Phys Behav 64:529-533, 1998). In two of seven strains of mice, females developed ovarian lesions. The occurrence of the lesion in one strain was correlated with the age of the animal and duration of the study. In the second strain, cage size was the determining factor. Lesioned ovaries weighed significantly more than nonlesioned ovaries. The lesion consisted of accumulations of luteal membrane and organelle fragments, and other cellular debris, suggestive of incomplete and prolonged luteolysis. Electron microscopic (EM) analyses revealed the presence of deposits of permanganate-resistant congophilic amyloid fibrils in the intima and smooth muscle cells of luteal thecal arteries. Population females had thymus glands and uteri that weighed significantly less than the same organs from females housed in the breeding colony, whereas the adrenal glands from the population females weighed significantly more. It is proposed that the female aggression is due to high levels of T. It is also proposed that the high levels of B suppress the immune cells involved in normal luteolysis and contribute to the incomplete and prolonged luteolysis.