Radical ovarian resection advances the onset of persistent vaginal cornification but only transiently disrupts hypothalamic-pituitary regulation of cyclicity in C57BL/6J mice.
In aging laboratory rodents, neuroendocrine failure to support estrous cyclicity is in part the consequence of exposure to ovarian secretions during adulthood. Moreover, some evidence suggests that those secretions associated with the predominant postcyclic state, persistent vaginal cornification (PVC), are more deleterious than those associated with cyclicity. However, it is not clear whether postcyclic hormonal secretions are intrinsically more deleterious or whether vulnerability to ovarian secretions, regardless of their nature, increases during aging. Using relatively young, age-matched mice, this study was designed to control for age and to determine if the hormonal milieu associated with PVC would be more deleterious to neuroendocrine function than that associated with regular cyclicity. Onset of PVC was advanced about 5 mo by resecting 90-95% of the ovarian tissue from 5-mo-old mice. The resultant PVC was similar in duration, vaginal cytology and ovarian histology to that seen in normally aging mice. At age 13 mo, when mean duration of PVC was 3 mo in resected mice but only 1 mo in sham-operated controls, the ability of mice to support cyclicity upon receipt of ovarian grafts from 4-mo-old donors was tested as an index of neuroendocrine function. The response of resected mice was slightly impaired, but only during the first month after grafting. This transient disruption of neuroendocrine function in mice prematurely exposed to PVC stands in contrast to the irreversible loss of cycling potential in older animals.(ABSTRACT TRUNCATED AT 250 WORDS)
D000375:Aging; D000818:Animals; D004971:Estrus; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000254:growth & development* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010052:Ovariectomy; D010053:Ovary / Q000166:cytology / Q000502:physiology*; D014621:Vagina / Q000254:growth & development* / Q000473:pathology