Effect of Partial Deafferentation of the Hypothalamus on Stress-Induced LH Suppression and Prolactin Release

Abstract

Stress of immobilization suppressed pulsatile LH release and decreased mean serum LH levels within 10 min, lasting at least for 2 h in ovariectomized rats. Anterior cuts (radius, 2 mm) at the level of the caudal border of the suprachi-asmatic nucleus, resulted in elimination of the stress-induced LH suppression. A smaller cut (radius, 1 mm) at the same level induced increased LH secretion without a period of inhibition in some rats by the stress. Extended anterior cut at the level of the border between the medial preoptic and the anterior hypothalamic area, partially inhibited the suppressive effect of the stress on LH secretion; that is, LH pulses resumed within 2 h. A more extended anterior cut at the level of the anterior border of the medial preoptic area, or a posterior or small posterior cut at the level of the midmammillary body, had no effect on the LH suppression by the stress. Basal LH levels prior to the stress were lower in the groups which had neural deafferentation in the anterior area to the mediobasal hypothalamic, but not in the groups with posterior deafferentation, compared with the sham control. Serum prolactin response to the immobilization was inhibited almost completely by an anterior, small anterior, posterior or small posterior cut. Extended anterior cuts inhibited the stress-induced prolactin release in about half of the animals, whereas a more extended anterior cut had no effect. Any kind of deafferentation except the posterior or small posterior cut failed to change basal nonstressed prolactin levels as compared to those in sham-operated rats. The rats bearing a posterior or small posterior cut had significantly lower serum prolactin levels prior to the immobilization. These results indicate that the stimulus necessary for stress-induced LH suppression and for the maintenance of the basal LH levels may reach the mediobasal hypothalamus from the anterior direction. The stress-evoked inhibitory stimulus for LH-RH release may interact, at the anterior hypothalamus-suprachiasmatic region, with the LH-RH neuron or inputs regulating the LH-RH neuron. Both neural connections from anterior and posterior directions to the medial basal hypothalamus seem to be indispensable for the stress-induced prolactin release and the input from the posterior direction for maintaining the nonstressed basal prolactin levels.

Regional Specificity in the Effect of Estrogen Implantation within the Forebrain on the Frequency of Pulsatile Luteinizing Hormone Secretion in the Ovariectomized Rat

“…Lesions of the retrochiasmatic area prevented the inhibition of pulsatile LH release in duced by electrical stimulation of the dorsal raphe nucleus [4]. Stimulation of the perisuprachiasmatic area lengthened the interval between LH pulses [8], Stress-induced suppres sion of pulsatile LH release was inhibited by the anterior neural deafferentation in ovariectomized rats [13]. Taken together with the present result, it is suggested that the mod ulatory, particularly inhibitory, influence comes from the rostral direction to the MBH.…”

Acute Stress Suppresses the N-Methyl-<i>D</i>-Aspartate-Induced Luteinizing Hormone Release in the Ovariectomized Estrogen-Primed Rat

“…It is uncertain, however, whether the acute elevation of circulating pro lactin levels in acutely stressed animals [ 13,20,21 ] may as well play a role in the refractoriness of the hypothalamic LH-RH neuron system to NMDA.…”

“…For example, it has been reported that acute immobilization stress inhibits the existing pulsatile LH release in ovariectomized rats [12][13][14], In intact female rats, acute restraint or foot shock stress can eliminate the expected ovulation [15,16]. Pre vious studies have shown that corticotropin-releasing fac tor (CRF) and endogenous opioid peptides (EOP) are involved in the induction of the hypogonadotropic state by acute stress in the rat, since administration of a CRF antagonist [17] or EOP antagonists or antiserum [14-16, 18, 19], prior to the stress exposure, could inhibit the decline in LH secretion which was otherwise observed in acutely stressed rats.…”

Inhibitory influence of the nuclei of the posterior hypothalamus on the pro-oestrous surge of LH

“…However, an earlier time of onset of the pro-oestrous surge of LH occurred in rats bearing PM cuts interrupting caudal afférents to the hypothalamus. Previous works have indicated that interruption of caudal afférents to the mediobasal hypothalamus did not interfere with ovulation and normal cyclicity in the rat (Halász & Gorski 1967) and the guinea pig (Terasawa & Wiegand 1978) nor with the release of LH in ovariectomized rats (Kawakami & Higuchi 1981). The advanced release of LH by these cuts can not be assigned to the duration of the oestrous cycle and may rather be due to transection of fibres that inhibit LH secretion perhaps by way of sup¬ pressing the secretion from gonadotrophin releas¬ ing hormone-containing neurons.…”