Effect of lesions in the ventral noradrenergic tract produced by microinjection of 6-hydroxydopamine on gonadotropin release in the rat.

Noradrenergic innervation to the hypothalamus is provided principally by the ventral noradrenergic tract (VNAT) which carries the axons of noradrenergic neurons whose cell bodies lie in the brain stem. To determine the importance of the VNAT in the stimulation of LH release induced by progesterone in ovariectomized, estrogen-primed rats, 6-hydroxydopamine (6-OHDA), an agent which selectively destroys catecholaninergic neurons, was microinjected bilaterally into this tract, 2 days after priming of the ovariectomized animals with 5 mug of estradiol benzoate, sc. Following microinjection, 2 mg of progesterone was injected sc to provoke LH release. A surge of FSH and LH release occurred 6 h after progesterone in control animals and those injected with the ascorbic acid diluent into the VNAT. Injections of 6-OHDA into the tract completely blocked both the LHP AND FSH surge. Control injections of 6-OHDA into the superior colliculus, the caudate-putamen or the frontal cortex did not alter the release of FSH and LH induced by progesterone. Twenty-four hours after injection of 6-OHDA into the VNAT, there was a slight reduction in norepinephrine content in the anterior hypothalamic area and a significant reduction in the region of the arcuate nucleus and median eminence. In this experiment, 6-OHDA injections into the VNAT blocked not only the FSH and LH release induced by progesterone but also the increase in serum prolactin which was present in control animals. In normal females, injections of 6-OHDA into the VNAT blocked the proestrous discharge of LH and partially blocked that of FSH. It is concluded that acute interruption of the VNAT induced by a 6-OHDA can block not only the stimulation of FSH and LH induced by progesterone, but also the preovulatory discharge of gonadotropins. The results suggest that increased impulse traffic in the VNAT on the afternoon of proestrus may be involved in induction of the proestrous gonadotropin surge.