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1 Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
2 Neurosurgery, Wake Forest University School of Medicine, Winston-Salem, NC, USA
3 Obstetrics/Gynecology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
4 EICS Summer Program, Wake Forest University School of Medicine, Winston-Salem, NC, USA
5 Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Obstetrics/Gynecology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
* To whom correspondence should be addressed. E-mail: youngsha{at}mail.nih.gov.
Corticotropin-releasing hormone receptor type 1 (CRH-R1) expression1 and vasopressin type 1b (V1b) receptor protein decrease in late gestation fetal sheep. Since hypothalamo-pituitary disconnection (HPD) has been demonstrated to prevent the morphological maturation of corticotrophs, we hypothesized that hypothalamic input is necessary for the maturational changes in CRH-R1 and V1b receptor levels. We measured CRH-R1 and V1b receptor expression in the anterior pituitaries of fetuses at 140 days gestational age (dGA) that underwent HPD or sham surgery at 120dGA. CRH-R1 mRNA decreased similarly in HPD and sham fetuses compared to 120dGA naive fetuses. However, CRH-R1 protein levels were elevated in HPD fetuses compared to sham and were not different from 120dGA values. V1b protein levels decreased similarly in HPD and sham fetuses compared to 120dGA naive fetuses. We conclude that hypothalamic input to the pituitary is necessary for the decrease in CRH-R1 receptor protein levels in late gestation fetal sheep. However, hypothalamic input is not necessary for the decrease in V1b receptor expression seen in late gestation.
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