Functional Development of the Ovarian Noradrenergic Innervation

Abstract

A substantial fraction of the noradrenergic innervation targeting the mammalian ovary is provided by neurons of the celiac ganglion. Although studies in the rat have shown that noradrenergic nerves reach the ovary near the time of birth, it is unknown how the functional capacity of this innervation unfolds during postnatal ovarian development. To address this issue, we assessed the ability of the developing ovary to incorporate and release (3)H-norepinephrine. Incorporation of (3)H-norepinephrine was low during the first 3 wk of postnatal life, but pharmacological inhibition of norepinephrine (NE) neuronal uptake with cocaine showed that an intact transport mechanism for NE into nerve terminals is already in place by the first week after birth. Consistent with this functional assessment, the mRNA encoding the NE transporter was also expressed in the celiac ganglion at this time. During neonatal-infantile development [postnatal (PN) d 5-20], the spontaneous, vesicle-independent outflow of recently taken up NE was high, but the NE output in response to K(+)-induced depolarization was low. After PN d 20, spontaneous outflow decreased and the response to K(+) increased markedly, reaching maximal values by the time of puberty. Tyramine-mediated displacement of NE stored in vesicles, which displace vesicular NE, showed that vesicle-dependent NE storage becomes functional by PN d 12 and that vesicular release increases during the juvenile-peripubertal phases of sexual development. These results indicate that vesicular release of NE from ovarian noradrenergic nerves begins to operate by the third week of postnatal life, becoming fully functional near the time of puberty.

Androstenedione acts on the coeliac ganglion and modulates luteal function via the superior ovarian nerve in the postpartum rat

“…We have shown that under our experimental ex vivo conditions the SON releases catecholamines and nitric oxide to the ovarian compartment [6,14,16]. It has been shown that the CG expresses the enzyme tyrosine hydroxylase that controls the synthesis of norepinephrine [30]. Indeed we have shown that the main neuronal bodies forming the CG express androgen receptor immunoreactive proteins [6] and when we mapped 1510 bp upstream of the transcription starting site of the tyrosine hydroxylase gene using the MatInspector software [31], we identified one putative androgen response element and three putative oestrogen response elements (results not shown).…”

Neonatal Exposure to Estradiol Valerate Programs Ovarian Sympathetic Innervation and Follicular Development in the Adult Rat1

“…It was also expected that the animal recovered estrous cycling activity and ovulation, as we have previously found when estradiol valerate was administrated to adult or prepubertal rats [15,17]. We have recently described that sympathetic nerves develop their functional capacity to release NA after 21 days of age [42]; it could be possible that the administration of EV at the first day of life advanced the age at the ovary developed its nerve activity. It is interesting to note that the morphological aspect of the ovary of denervated rats was almost identical to the one we described after destroying the sympathetic nerves by neonatal treatment with antibodies against NGFB [43].…”

Kisspeptin is involved in ovarian follicular development during aging in rats

“…The procedure was performed as previously described (Wakade 1980, Ricu et al 2008, Acuna et al 2009). The rats were sacrificed at 10 months of age.…”

“…One-minute fractions were collected for an additional 5 min. The total amount of neurotransmitters released was calculated as the area under the curve after stimulation minus that of basal efflux (Ferruz et al 1991, Ricu et al 2008. The release percentages of 3H NE previously incorporated in 6-, 8-and 12-month-old rats were obtained from a previous publication by our laboratory (Acuna et al 2009).…”