At present the origin of the signal(s) to initiate parturition remains unknown. Experimental studies in sheep have shown that interruption of the fetal hypothalamohypophyseal-adrenal axis will prolong gestation but no studies have shown prolongation of gestation after destruction of fetal neural structures. In this study we placed bilateral lesions of the paraventricular nucleus in five fetal sheep at 118 to 122 days' gestation. Cortiocotropin-releasing factor staining in the median eminence of the hypothalamus was markedly decreased after fetal paraventricular nucleus lesions. Paraventricular nucleus lesions prevented the fetal adrenocorticotropic hormone rise in response to hypotension and the normal predelivery increase in fetal plasma adrenocorticotropic hormone and cortisol and resulted in impaired fetal adrenal growth relative to the rest of the fetus. Lesioned fetuses had not been delivered at 157 days' gestation when they were removed by cesarian section to obtain tissue for histology. Four control fetuses were delivered at 146.5 ± 0.9 days' gestation (mean ± SEM). These findings indicate that a structure in the fetal brain, the fetal hypothalamic paraventricular nucleus, is necessary for parturition to occur.
- Paraventricular nuclei
- corticotropin-releasing hormone
- fetal adrenal
ASJC Scopus subject areas
- Obstetrics and Gynecology