Noradrenergic peripheral denervation of the female rat accelerates the positive feedback mechanisms resulting in pubertal ovulation, and blocks the modifications induced by administration of testosterone propionate at birth.
The noradrenergic innervation of the ovary of prepubertal rats causes an inhibitory response of the follicles to gonadotrophins, leading to ovulation. We investigated the possibility that noradrenergic peripheral denervation at birth, produced by treatment with guanethidine, modifies the positive feedback effects of gonadotrophins and oestradiol in prepubertal rats, and also the possibility that peripheral denervation can modify the anovulatory syndrome induced by androgenization at birth. Noradrenergic peripheral denervated rats of 18 days of age treated with pregnant mare serum gonadotrophin (PMSG) ovulated 96 h later, while normal animals did not ovulate (4/9 vs 0/12, P < 0.05) and the number of ova shed was lower than in rats which ovulated spontaneously at first vaginal oestrus (3.5 +/- 0.6 vs 8.3 +/- 0.4 (S.E.M.), P < 0.01). Oestradiol benzoate (10 micrograms) did not induce ovulation in either normal or denervated animals (0/11 and 0/11). The anovulatory syndrome induced by the administration of testosterone propionate (75 micrograms) at birth was partially blocked by noradrenergic peripheral denervation (4/7 ovulated vs 0/10). The results suggest that some neural information arising from the ovary modulates, in an inhibitory way, the stimulatory feedback mechanisms required to induce ovulation. Partial inhibition of the anovulatory syndrome resulting from androgenization caused by peripheral noradrenergic denervation suggests that noradrenergic neural information sent by the ovary to the hypothalamus results in a decreased concentration of noradrenaline in the hypothalamus and in the aromatization of androgens to oestrogens.[1]References
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