Prepubertal ovarian function is finely regulated by direct adrenergic influences. Role of noradrenergic innervation

L. I. Aguado, Sergio Ojeda

Research output: Contribution to journalArticle

106 Citations (Scopus)

Abstract

In the rat, the main source of adrenergic fibers innervating nonvascular ovarian tissue is the superior ovarian nerve (SON). To determine the influence of the SON on prepubertal ovarian function and, hence, on the time of puberty, several experiments were conducted. Transection of the SON in early juvenile rats (day 24) led to more than 60% depletion in ovarian norepinephrine (NE) content, but affected neither the timing of vaginal opening nor that of first ovulation. SON section, however, produced a 2-fold increase in β-adrenergic receptor density, with no change in affinity, suggesting that hypersensitivity by denervation had developed. Removal of all adrenergic influences from ovarian granulosa cells by culturing the isolated cells in vitro produced a striking increase in β-adrenergic receptor number, which was maximal at 72 h. In spite of this elevated receptor content, the β-adrenergic agonist Zinterol did not induce progesterone release unless the cells were previously exposed for 48 h to a physiological concentration of FSH. Both NE and epinephrine down-regulated the receptors in a dose-related manner, without affecting receptor affinity. To test the hypothesis that denervation of the ovary results in greater steroidal sensitivity to adrenergic stimulation, a model was constructed in which cells were simultaneously exposed to FSH and NE or epinephrine (innervated cells) or exposed only to FSH (denervated cells) for 48 h. The response to adrenergic stimulation was subsequently measured by incubating the cells with Zinterol for 24 h. Zinterol was highly effective in eliciting progesterone release from the denervated cells, but failed to do so in innervated cells. Additionally, the agonist increased cAMP in the former cells, but it was ineffective in the latter, indicating that prior exposure to catecholamines desensitized the adenyl cyclase enzyme coupled to β-adrenergic receptor sites. The results suggest that during prepubertal maturation, noradrenergic fibers reaching the ovary via the SON may modify ovarian steroidogenic sensitivity to catecholamines, by regulating the number of functional β-adrenergic receptors in the gland. They also indicate that the apparent failure of SON denervation to alter the maturation of ovarian steroidogenesis and the time of puberty may be due to development of compensatory hypersensitivity after the denervation.

Original languageEnglish (US)
Pages (from-to)1845-1853
Number of pages9
JournalEndocrinology
Volume114
Issue number5
StatePublished - 1984
Externally publishedYes

Fingerprint

Adrenergic Agents
Denervation
Adrenergic Receptors
Norepinephrine
Puberty
Epinephrine
Catecholamines
Progesterone
Ovary
Hypersensitivity
Gonadotrophs
Adrenergic Fibers
Adrenergic Agonists
Granulosa Cells
Ovulation
Adenylyl Cyclases
Enzymes
zinterol

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Prepubertal ovarian function is finely regulated by direct adrenergic influences. Role of noradrenergic innervation. / Aguado, L. I.; Ojeda, Sergio.

In: Endocrinology, Vol. 114, No. 5, 1984, p. 1845-1853.

Research output: Contribution to journalArticle

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