Reanalysis of the Preoptic Afferents and Efferents Involved in the Surge of LH, FSH and Prolactin Release in the Proestrous Rat

Female Wistar rats treated with a single subcutaneous injection of 2 mg estradiol valerate (EV) develop gradually progressive, multifocal lesions of the arcuate nucleus. They also exhibit persistent vaginal estrus and endocrine profiles characteristic of animals sustaining anterior hypothalamic deafferentation. In this study, EV-treated females with the arcuate lesions released significantly less LH 1 h following electrochemical stimulation of the medial preoptic area (MPOA) than did normally cycling controls in proestrus. FSH release in response to MPOA stimulation was the same for both groups. As plasma LH concentrations were not significantly different between EV-treated and control animals 1 h after the injection of a potent LHRH analog, the reduced LH response to MPOA stimulation appears to reflect a primarily hypothalamic defect. However, the EV treatment also affected pituitary responsiveness to long-term stimulation as evidenced by reduced LH responses to the LHRH analog after 2 and 3 h. No such differences were seen in the FSH response.

Section: Discussionmentioning

confidence: 61%

Effects of Estradiol-Induced Lesions of the Arcuate Nucleus on Gonadotropin Release in Response to Preoptic Stimulation in the Rat

Brawer¹,

Ruf²,

Naftolin³

1980

“…The likelihood of differential control for the two Received: April 4,1984 Accepted after revision: July 5,1984 surges by the MPOA has received further support in studies involving MPOA stimulation. Both increases and decreases in prolactin secretion have been noted during stimulation of the MPOA [4,6,15]. In conscious, cervically stimulated (CS) females MPOA stimulation can inhibit the nocturnal and diurnal surges of prolactin [12], Appropriately timed stimulation of the MPOA in pentobarbital (PB)-anesthetized females can, however, induce a diurnal surge of pro lactin [12], The MPOA therefore has the capacity to inhibit the nocturnal and diurnal surges.…”

mentioning

confidence: 99%

The Interaction of the Medial Preoptic Area and the Dorsomedial-Ventromedial Nuclei of the Hypothalamus in the Regulation of the Mating-Induced Release of Prolactin

Gunnet

Freeman

1985

The medial preoptic area (MPOA) and the dorsomedial-ventromedial nuclei (DMN-VMN) of the hypothalamus regulate the mating-induced nocturnal and diurnal surges of prolactin in rats. The neural mechanisms governing the release of the two surges differ. For the nocturnal surge the MPOA serves an inhibitory role while the DMN-VMN serves a stimulatory role. The diurnal surge is controlled by both areas functioning as stimulatory centers. The goal of the present study was to explore the possibility of functional interactions between the MPOA and the DMN-VMN in control of mating-induced prolactin secretion. Stimulation of the MPOA in conscious, cervically stimulated (CS) females suppresses the nocturnal surge of prolactin. To determine if the inhibitory effects of the MPOA operate through the DMN-VMN, electrical stimulation was applied to the MPOA of conscious ovariectomized female rats bearing bilateral electrolytic lesions of the DMN-VMN. In the first experiment, control (sham-stimulated, sham-lesioned) CS females exhibited normal nocturnal surges which peaked at 03.00 h. MPOA stimulation (01.00–05.00 h) of both sham-lesioned and DMN-VMN lesioned CS females inhibited the release of their nocturnal surges. This suggests that the inhibitory function of the MPOA is independent of the DMN-VMN. MPOA stimulation can induce the release of a diurnal surge if the females are anesthetized with pentobarbital. In the second experiment, MPOA stimulation (15.00–19.00 h) of sham-lesioned anesthetized females produced elevated prolactin levels with significant peaks at 15.30 and 19.00 h. Anesthetized females with DMN-VMN lesions did not respond to MPOA stimulation with any change in prolactin secretion. Such data show that the stimulatory function of the MPOA requires an intact DMN-VMN. The data suggest that the MPOA does not operate through or affect the activity of the DMN-VMN for regulation of the nocturnal surge. The stimulatory role of the MPOA, however, does require interaction with an intact DMN-VMN for control of the diurnal surge.

“…Stimulation or lesion of this area has been report ed to increase [3,5,12] and decrease [1,9] prolactin release. In female rats destruction of the MPOA initiates pseudo pregnancy as does coital stimulation but.…”

mentioning

confidence: 99%

Hypothalamic Regulation of Mating-Induced Prolactin Release

Gunnet¹,

Freeman²

1984

Lesions of the medial preoptic area (MPOA) induce nocturnal prolactin surges similar to those initiated by cervical stimulation (CS). These same lesions can abolish diurnal prolactin surges previously initiated by CS. Based on these results the MPOA has been suggested to contain two functionally dissimilar sets of neurons, one inhibitory for the nocturnal surge and the other stimulatory for the diurnal surge. The present study sought to demonstrate the existence of these neural elements by electrically stimulating the MPOA of conscious ovariectomized female rats during those times of day when these neurons would be most active. Serial blood samples were collected via cannula before, during and after the stimulation. Stimulation of the MPOA (01.00–05.00 h) on day 2 after CS inhibited the nocturnal surge of prolactin while sham MPOA stimulation of CS females did not disturb the nocturnal surge. MPOA stimulation in non-CS females had no effect upon prolactin secretion. Application of MPOA stimulation (15.00–19.00 h) to CS females also suppressed the diurnal surge of prolactin. Sham-stimulated CS females, however, secreted a diurnal surge peaking at 17.00 h. Basal prolactin levels were unaffected by MPOA stimulation (15.00–19.00 h) in non-CS females. The results from these experiments suggest that the MPOA contains neurons inhibitory for both the nocturnal and diurnal prolactin surges. In a further attempt to show a stimulatory role for the MPOA in prolactin regulation, MPOA stimulation was applied (15.00–19.00 h) to pentobarbital anesthetized non-CS females. Pentobarbital treatment allowed the MPOA stimulation to trigger two prolactin peaks, one at 16.00 h and the other at 19.00 h. The anesthesia did not alter prolactin release in the sham controls. From these stimulation studies and previous lesion experiments we conclude that the MPOA exerts monophasic inhibitory control over the nocturnal prolactin surge and biphasic, stimulatory and inhibitory control over the diurnal prolactin surge. CS must then act upon the MPOA to depress its inhibitory and activate its stimulatory elements for the secretion of the nocturnal and diurnal surges of prolactin to occur.