The role of adrenergic nerves in estrous cyclicity and follicular growth was studied in sympathectomized hamster ovaries. Specific ovarian sympathectomy was accomplished by injection of 6-hydroxydopamine (6-OHDA) into the ovarian bursal sac. Ovarian sympathectomy abolished all fluorescent adrenergic nerves 4, 8 or 12 days after treatment. Bilateral ovarian sympathectomy on metestrus altered the first estrous cycle in 53% of the animals and 20% had an altered second cycle. All sham injected animals had normal cycles. Four days after sympathectomy, there was a decrease in healthy follicles 80-240 microns and 250-340 microns in diameter and increased atresia of follicles 80-240 microns and 350-440 microns in diameter compared to solvent treated ovaries. Bilateral 6-OHDA treatment did not affect ovarian weight, number of corpora lutea or the total number of follicles per ovary. These observations suggest that ovarian adrenergic nerves modulate healthy follicular development in the golden hamster.

The postcastration increase in gonadotropins was studied in intact and vagotomized male rats. Rats underwent vagotomy or sham surgery immediately prior to castration. In the first experiment, rats were bled before castration and at 1, 2, 4, and 7 days after castration. Serum LH and FSH were significantly lower in vagotomized rats 1 day after castration. On Days 2, 4, and 7 postcastration, serum gonadotropin levels were generally not different among experimental groups. In a second experiment, rats were decapitated at 12 or 24 hr after surgery and castration. Trunk blood was collected for assay of LH. Vagotomy had no effect on LH levels at 12 hr postcastration, but, at 24 hr postcastration, vagotomized rats had significantly lower serum LH than did sham-operated rats. These experiments indicate that vagotomy has a transient suppressive effect on gonadotropin release following castration. Such observations support the hypothesis that the vagus nerve may play a modulatory role in gonadotropin secretion. 613