Estrous Cycle Delay and Inhibition of Gonadotropin and Prolactin Release during Sympathetic Nerve Degeneration after Superior Cervical Ganglionectomy of Rats

Abstract

The changes in the activity of the pituitary-gonadal axis during sympathetic nerve degeneration after superior cervical ganglionectomy (SCGx) were examined in female rats. In a first experiment SCGx performed at 24.00 h of diestrus II, 17 h in advance to the critical period for gonadotropin and prolactin (PRL) release, caused a delay of 1 day or more in estrous cyclicity, while SCGx at 24.00 h on estrus did not modify the estrous cycle. In a second experiment ovariectomized rats injected subcuta-neously with estradiol-progesterone or vehicle were subjected to SCGx 17 h before the expected maxima in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and PRL serum levels. A significant decrease of serum gonadotropin and PRL concentration was found in SCGx, steroid-treated rats. In a third experiment groups of rats injected with estradiol-progesterone and killed at 15.00, 16.00, 17.00, or 18.00 h at or around the time of maximal FSH, LH, and PRL release were used. SCGx performed 17 h before killing caused a generally depressive effect of LH, FSH, and PRL release. In a fourth experiment ovariectomized rats were subjected to pinealectomy and, 1 week later, to estradiol-progesterone treatment and SCGx as in experiment 2. Pinealectomy did not modify the depression of steroid-induced LH, FSH, and PRL release found during wallerian degeneration of sympathetic nerves after SCGx. In a fifth experiment the effect of α₁- and/or β-adrenoceptor blockade on SCGx-induced inhibition of hormone release was assessed in estradiol-progesterone treated, spayed rats. During anterograde degeneration (i.e., 17 h after SCGx) injection of the α₁-adrenergic blocker prazosin counteracted the impaired release of LH, FSH, and PRL, while β-adrenoceptor blockade by giving propranolol did not modify hormone secretion. In a sixth experiment groups of rats injected with estradiol-progesterone and killed at 16.00, 17.00, or 18.00 h were subjected to SCGx 17 h before killing, the rats received prazosin or the α₁/α₂-adrenoceptor blocker phentolamine 45 min before sacrifice. Both drugs were found to be equipotent in counteracting the SCGx effect on gonadotropin and PRL release. These results demonstrate that the coincidence of anterograde degeneration of sympathetic terminals in the superior cervical ganglion field of projection with the spontaneous or induced gonadotropin and PRL release in female rats (1) disrupts temporarily estrous cyclicity and (2) decreases estradiol-progesterone-induced LH, FSH, and PRL release through a pineal gland independent mechanism. Noradrenergic transmitter release from degenerating sympathetic nerves acts via α₁-adrenoceptors to decrease gonadotropin and PRL secretion.

Increase in Adrenocorticotropin Release during Wallerian Degeneration of Peripheral Sympathetic Neurons after Superior Cervical Ganglionectomy of Rats

“…The possi bility that the increase in ACTH could be consequence of the stress response induced by disturbed homeostasis after SCGx should be considered. However, in a recent study the basal lev els of another stress hormone, prolactin, were not augmented in estradiol-progesterone-treated spayed rats 17 h after SCGx [7], while the ether-induced prolactin release increased after SCGx at an early phase of wallerian degeneration (i.e. 14 h after SCGx) but not at a later phase (i.e.…”

“…Summarizing, the present results underline a role of periph eral sympathetic projections to the hypothalamic adenohypo physial axis in ACTH release mechanisms. PRL and ACTH are the only two adenohypophysial hormones so far examined that showed increased release during wallerian degeneration of sym pathetic nerves in the SCG territory, acute SCGx decreasing TSH, GH, LH, and FSH release in a number of paradigms [2,4,[6][7][8]. Although further experiments are needed to establish in a more detailed way the participation of SCG neurons in stress reaction, it is tempting to postulate that parallel central and pe ripheral noradrenergic channels convey information to the neu roendocrine system to allow the full response of the stress hor mones ACTH and PRL.…”

“…In female rats, SCGx performed 17 h in advance of the critical period delayed estrous cycle and impaired estradiol-induced gonadotropin and prolactin (PRL) release [7]. Growth hormone (GH) release is decreased, while ether-induced PRL increase is amplified, at the time of walle rian degeneration after SCGx in rats [8].…”

Neuroimmunoendocrinology of the cervical autonomic nervous system

“…its preovulatory surge, to disrupt estrous cyclicity. The inhibitory effect of peripheral Wallerian degeneration on gonadotropin and PRL release was also found in Px rats (31), indicating that the effect observed was independent of the melatonin release taking place during Wallerian degeneration. In confirmation of the cycling in rats mentioned above.…”

“…about 16-18 hours in advance of the critical period of gonadotropin and PRL release, caused 14 days delay of cycle, as shown by leukocytic diestrous vaginal smears, at the end of which the estrous cycle resumed. SCGx at 24:00 h on the day of estrus did not modify estrous cyclicity (31). The results indicated that sympathetic nerve degeneration after SCGx must coincide with the stimulus for gonadotropin release, e.g.…”