The superior ovarian nerve (SON) arrives at the ovary through the suspensory ligament and innervates mainly the ovarian stroma. Most neurones from which the SON fibres originate are located in the complex coeliac and mesenteric ganglia. Taking into account that other ganglia have been shown to have alpha- and
beta-adrenergic receptors, and that the coeliac
ganglion receives
adrenergic fibres from other sympathetic paravertebral and preaortic ganglia, we utilised
adrenergic agonists and antagonists specific to the
ganglion, to analyse the role of the alpha and beta receptors in ovarian physiology. To that end, it was necessary to develop and standardise an in vitro coeliac
ganglion-SON-ovary (coeliac
ganglion-SON-O) experimental system that would enable study of the release of
steroids in the ovary in the absence of humoral factors. We investigated the effect of
adrenergic agents on the liberation of
progesterone in the different stages of the oestrous cycle. To this end we placed the coeliac
ganglion and the ovary in different compartments, connected through the SON, to produce a system being studied as a whole. Combined neural and hormonal (luteinising
hormone (LH)) effects were also examined. Non-specific stimulation with KCl in the
ganglion compartment evoked different responses in terms of release of
progesterone, depending on the physiological conditions of the cycle; this demonstrated the sensitivity and viability of the system. During pro-oestrus, stimulation of the
ganglion compartment with
adrenergic agents such as the agonist
noradrenaline or the
beta-adrenergic antagonist propranolol, did not modify the release of
progesterone. In contrast, the alpha-
adrenergic antagonist,
phentolamine, induced a strong inhibitory response. During the oestrous stage,
noradrenaline was inactive, but
phentolamine and
propranolol exerted a strong stimulus throughout the experiment. On dioestrus day 1 (D1), both
noradrenaline and
propranolol increased the release of ovarian
progesterone, whereas
phentolamine had the opposite effect. Finally, on dioestrus day 2 (D2), what was noteworthy was the pronounced inhibitory effect of
noradrenaline, whereas
phentolamine was inactive and
propranolol showed its greatest stimulatory effect. In order to compare the combined neural and endocrine effects on the ovarian release of
progesterone, the experiment was carried out during stages D1 and D2, when the corpora lutea are at their peak of activity.
Adrenergic agents were added to the
ganglion and LH in a final concentration of 50 ng/ml was added to the ovarian comparment. Different effects were observed indicating a differential response to these agents in stimulated and basal conditions. We conclude that the in vitro coeliac
ganglion-SON-ovary system is a functional entity because it possesses its own autonomic tone. This is verified because different basal values of
progesterone appear in the different stages of the oestrous cycle. In similar fashion, variations of
progesterone induced via the neural pathway were observed under different experimental conditions. In contrast, on D2,
noradrenaline added to the
ganglion compartment had an inhibitory effect on the liberation of ovarian
progesterone. This would indicate that, during this phase,
noradrenaline may not be the
neurotransmitter released in the ovarian compartment, but that other inhibitory molecules might participate in the observed effects. Finally, during D2, the neural input would condition the ovarian response to LH, facilitating the decrease in
progesterone necessary to start a new cycle. The experimental scheme is, in our opinion, a valuable tool for the study of peripheral neural participation in ovarian physiology.