Abstract
To determine the central neuronal mekchanisms essentially involved in the regulation of ovulatory LH release in cycling female rats, and to confirm the role of ovarian steroid feedback on the central regulatory mechanisms, the following experiments were carried out. A) The effects of electrical stimulation of the preoptic area (MPO) upon unit firing in the periventricular arcuate uncleus (ARC) were investigated in Wister female rats throughout the 4-day estrous cycle. Unit activity was recorded using a stereo-taxic oriented tungsten microelectrode under light urethane anesthesia. Repetitive stimulation of monophasic square waves varying only in current intensity was used. The following results were obtained. (a) An increase in activity of all ARC neurones recorded was induced by MPO stimulation on each day of the estrous cycle. (b) The minimum current (threshold) effective in increasing activity in the ARC neurones varied throughout the estrous cycle; the lowest threshold was observed in the proestrus and the highest on the first day of diestrus. Moreover, thereshold current of MPO stimulation required to increase ARC activity was found to be 'elevated after long-term ovariectomy and markedly lowered to the level of proestrus by estrogen treatment, but less affected by progesterone. (c) The spontaneous activity of the MPO and ARC neurones were increased at proestrus in cycling rats and after estrogen injection in spayed rats.
B) To clarify the conflicting data in the literature on which a dual regulatory mechanism for gonadotrophine release has been proposed, the ovulatory responses to electrochemical stimulation (ECS) of the medical septal-preoptic complex were compared in pentobarbital blocked normal proestrus and neonatally androgenized female rats. Increasing the stimulus strength enhanced the induction of ovulation in normal but not in androgenized rats. However, the ovaries in androgenized rats are relatively insensitive to LH, while pituitary responsiveness to LRH is identical. Therefore, the response to ECS was further evaluated in terms of plasma LH concentration. Radioimmunoassayable plasma LH was significantly elevated 30 min after ECS. Peak LH levels occured 90 min after ECS and were returning toward basseline after 120 min. There was no difference in mean plasma LH values in normal and androgenized rats at any time in each stimulus strength. Stimulation of the diagonal band of Broca, antero-medial septum as well as MPO equally elicited similar LH responses in both animals.
C) Changes of plasma LH were investigated in ovariectomized rats to study the effects of electrolytic lesions of medial or lateral septum by platinum electrode or preoptichypothalamic deafferentation (supracommissural roof cut) upon plasma LH rise after ovari-ectomy, on decrease of LH secretion after a single injection of 20 jig estradiol benzoate (EB) in long-term spayed rats, and on LH release induced by a second injection of EB or 5 mg progesterone given 72 hours after the first EB injection. Septal interruptions did not alter the time sequence and the level of plasma LH rise after ovariectomy, LH decrease created by the first injection of EB and LH release inducted by progesterone in the after-noon of the injection. However, LH release in the afternoon of the day after the second injection of EB was remarkably reduced in rats with supracommissural roof cut in which all the transseptal fiber connections were completely transected. This reduction of LH release was not observed in the cases where in postcommissural component of stria terminalis was left untransected or even partially so. In the rats with either medial or lateral septal lesions, estrogen-induced LH release appeared to differ from intact spayed rats in timing and quantity of peak LH secretion on each afternoon of the second EB injection.
