Abdominal vagotomy delays the onset of puberty and inhibits ovarian function in the female rat

To examine the influence that the vagus nerve may have on ovarian development and on the timing of puberty, both anterior and posterior vagi were sectioned at the abdominal level in 24-day-old female rats. Abdominal vagotomy (AV) resulted in a marked delay in the onset of puberty, as measured by the age at vaginal opening and at first diestrus. No differences in circulating levels of LH, FSH, PRL, TSH or GH between control and vagotomized rats were observed between the time of AV and vaginal opening. Nevertheless, estradiol (E₂) and progesterone (P) response to human chorionic gonadotropin (hCG) in vitro was profoundly depressed in ovaries of vagotomized rats. This decreased ovarian secretory activity was further reflected in vivo by a reduced ovarian weight and, more prominently, by a reduced uterine weight. Ovarian release of androgens, however, was increased in vagotomized rats suggesting an enhanced activity of the thecal-interstitial gland compartment of the ovary. The reduced E₂ and P response to hCG could not be attributed to changes in hCG-LH or FSH receptor number. Likewise, the inhibitory effect of AV on the ovary was not due to changes in ovarian β-adrenergic receptor content. Cencentration of LHRH binding sites in granulosa cells was increased after AV. However, since LHRH receptor content decreases with ovarian maturation, this change may simply reflect delayed ovarian development rather than being the actual factor mediating the effect of AV. The delay in puberty induced by AV was not due to interference with nutrition of the animal, because at no age examined was the body weight of vagotomized rats different from that of controls. In addition, the effect of AV was not due to a decreased availability of cholesterol to the ovary, because levels of high- and low-density lipoproteins were normal in vagotomized rats. It is concluded hat AV delays the onset of puberty and depresses ovarian function by mechanisms which do not involve alterations in ovarian gonadotropin or β-adrenergic receptors, changes in serum levels of pituitary hormones or availability of precursors for steroid synthesis. The possibility arises that the vagal control of the ovary is, instead, exerted by peptidergic fibers known to be contained in the abdominal vagus.