The peak phase of the proestrous prolactin surge is blocked by either posterior pituitary lobectomy or antisera to vasoactive intestinal peptide.
The proestrous surge of PRL could result from a decrease in dopamine, an increase in PRL-releasing factor (PRF) or both. The objectives were to determine whether PRF from the posterior pituitary regulates the proestrous PRL surge, and to examine if there are interactions between PRF and vasoactive intestinal peptide (VIP). Posterior pituitary lobectomy (LOBEX) and passive immunization against VIP were employed. Adult cycling rats were subjected at 0900 h on proestrus to LOBEX or sham surgery (SHAM) under short term anesthesia, and were injected iv at 1330 h with 0.75 ml anti-VIP serum or normal rabbit serum. Jugular blood was collected hourly from 1400-2300 h and analyzed for PRL and LH by RIA. Oviductal ova were examined on estrus. The rise in plasma PRL in normal rabbit serum-treated SHAM rats was biphasic, with an early peak between 1500-1700 h and a lower plateau between 1900-2100 h. This rise was similar in profile and magnitude to that seen in intact rats. In contrast, LOBEX significantly attenuated the early peak, but did not alter the plateau. Passive immunization against VIP of either SHAM or LOBEX rats mimicked the effect of LOBEX alone on PRL release. Neither surgery nor anti-VIP serum affected the profile of the LH surge which was sharp and symmetrical, and all rats ovulated with 15-16 ova per rat. To determine whether VIP is the posterior pituitary PRF, selected tissues removed on proestrus or diestrus-1 were analyzed for VIP by RIA. VIP was undetectable (less than 20 pg/organ) in the posterior pituitary on either day examined. The contents of VIP in the anterior pituitary, medial basal hypothalamus, and paraventricular nuclei were unchanged between diestrus-1 and proestrus.


CONCLUSIONS
The proestrous surge of PRL consists of two components: an early peak and a late plateau. The peak phase appears to be dependent on PRF input from the posterior pituitary. This input might be regulated by VIP, and interactions between the two could occur at the level of the hypothalamus, anterior pituitary, or both. The plateau phase of the PRL surge is independent of the posterior pituitary and VIP, and might involve hypothalamic dopamine.
Murai
I
I
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46223.
Reichlin
S
S
Ben-Jonathan
N
N
D000818:Animals; D004971:Estrus; D005260:Female; D007106:Immune Sera; D010904:Pituitary Gland, Posterior / Q000502:physiology*; D011359:Proestrus; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D013973:Thyrotropin-Releasing Hormone / Q000276:immunology / Q000502:physiology; D014660:Vasoactive Intestinal Peptide / Q000276:immunology / Q000502:physiology*
D007106:Immune Sera; D014660:Vasoactive Intestinal Peptide; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin