Effects of the Interruption of Amygdaloid and Hippocampal Afferents to the Medial Hypothalamus on Gonadotrophin Release

Abstract

The effects of interruption of amygdaloid and hippocampal afferents to the hypothalamus on ovulation and on the release of luteinizing hormone (LH) were studied in rats. Animals acutely deprived on the morning of pro-oestrus of amygdaloid influences either by transection of the stria terminalis (ST) or lesions of the amygdala, failed to show the expected ovulation. Control lesions had no effect. In contrast, rats with long-term transection of either the ST, the cortico-hypothalamic tract (CHT), or both, had regular oestrus cycles and ovulated normally. Studies of ovulation which was induced after the administration of ovarian steroids revealed a differential response to oestrogen and progesterone. In animals with long-term transection of the ST the ovulatory response to oestrogen was similar to that induced in non-lesioned rats but fewer ovulations were induced by progesterone administration. The decreased ovulatory response after progesterone treatment was attributed to activation of inhibitory influences originating in the hippocampus, since administration of picrotoxin or section of the fornix re-established a normal response. Long-term interruption of the limbic efferents did not alter the increased levels of plasma LH found after ovariectomy. However, the release of LH induced by progesterone in ovariectomized rats primed with gonadal steroids was decreased after transection of the ST and increased after interruption of the CHT. These results are consistent with the concept that the amygdala and the hippocampus exert a modulating influence on gonadotrophin release; the influence of the amygdala being facilitatory and that of the hippocampus inhibitory.

Acute Effect of Neural Deafferentation on Timing of Gonadotropin Secretion Before Proestrus in the Female Rat

“…Whether estrogen feeds back to the amygdala itself or rather the septal complex in inducing ovulatory hormone release, was not clear in the present experiment. Although Velasco and Taleisnik (1971) showed that estrogen acts to the preoptic basal hypothalamus to release LH in the rats with amygdaloid lesions, author observed facts that the bed nucleus of stria terminalis or nucleus of accumbens could originate the neural triggering for the ovulatory hormone release under estrogen influences. That is, characteristic increases of multiunit activity was observed in the bed nucleus of stria terminalis during the critical period of the proestrous day , and estrogen induced remarkable increase of multiunit activity in the same nuclei (Kawakami et al, unpublished observation).…”

“…The medial corticohypothalamic tract was suggested as a pathway from hippocampus to the basal hypothalamus (Grudjian, 1927;Krieg, 1932;Nauta, 1956;Raisman et al, 1966). Recently Velasco and Taleisnik (1971) have reported that the transection of this tract, but not the fornix longus, resulted in the loss of the inhibitory function of the hippocampus on LH release. In the present experiment the destruction of the septal complex, including the parolfactory area, the nucleus of accumbens, the bed nucleus of stria terminalis, the bed nucleus of anterior commissure, but not rather simply the fornix or the medial corticohypothalamic tract, revealed blocking effect of an increase of folliculotropin and estrogen responsible for the events of proestrus and estrus.…”

The sexual and reproductive health in men with generalized epilepsy: a multidisciplinary evaluation

“…5,40 This possibility is supported by the previously reported improved seizure control achieved with the adjunctive use of the aromatase inhibitor testolactone or the antiestrogen clomiphene than testosterone alone. 41 (2) Poor seizure control and untreated groups of epileptics exhibited more hormonal abnormalities than the controlled group on AED(s). Many evidences support our findings, including the following: free testosterone levels are usually low in reproductive endocrine disorders that are associated with TLE in men and therefore favor the occurrence of epileptiform activity, 26 testosterone has been found to raise the threshold of some induced seizures in experimental animals, 15,16 and previous studies demonstrated that patients with refractory epilepsy had improved sexual performance after temporal lobectomy.…”

“…1,2 Epileptic patients frequently exhibited sexual and reproduction dysfunctions. Changes in central control, peripheral hormone levels, and/or antiepileptic drug (AED) medications may all contribute to decreased libido, potency, and fertility in patients with epilepsy.…”

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

“…Several other experiments indicated the higher brain areas as the important location. Deafferentation of the MPO area the morning of proestrus or on the days before proestrus blocked expected ovulation (Velasco andTaleisnik, 1971, Kawakami andTerasawa, 1972). Terasawa and Kawami (1974) showed that EB implantation into the medial amygdala (AMYL) or the bed nucleus of stria terminalis (BST) on the night of diestrus day 2 in 4-day cyclic rats pretreated with progestrone overcame the inhibitory effect of progesterone on LH release during the critical period of proestrus.…”