Electrical Stimulation of Mesencephalic Noradrenergic Pathway: Effects on Luteinizing Hormone Levels in Blood of Ovariectomized and Ovariectomized, Steroid-Primed Rats*

Abstract

This study examined the effect of electrical stimulation of the dorsal mesencephalic tegmentum (DMT) region on blood LH levels in long term ovariectomized (OVX), pentobarbital-anesthetized rats, with the aim of activating the principal ascending noradrenergic (NE) bundle. In OVX unprimed rats, electrical stimulation (with parameters of 100 Hz, 0.5-msec effective biphasic pulses, 150-200 microA, and 15 sec on/off for up to 1.5 h) of the DMT region inside the ascending NE bundle either completely or partially inhibited the pulsatile pattern of blood LH levels characteristic of OVX animals; stimulation outside the NE bundle was ineffective. Pretreatment of OVX rats with a serotonin synthesis inhibitor, p-chlorophenylalanine (320 mg/kg, ip) 71 h before electrical stimulation of the DMT did not affect the stimulation-induced inhibition of pulsatile LH release. On the other hand, pretreatment of OVX rats with a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine (250 mg/kg, ip) 4.5 h before electrical stimulation of the DMT was effective in preventing the stimulation-induced inhibition of pulsatile LH release, thereby supporting a NE-mediated mechanism. In OVX rats primed with estradiol benzoate alone (5 micrograms/100 g BW for 2 days) or with 50 micrograms estradiol benzoate and 25 mg progesterone, electrical stimulation in the DMT was ineffective in altering the low, nonpulsatile blood levels of LH. The results in OVX unprimed rats suggest that activation of the ascending NE system can inhibit pulsatile LH release, thus indicating a possible functional importance of inhibitory (in addition to well-documented stimulatory) NE synapses in the modulation of LH release.

Estradiol Enhances Prostaglandin E2Receptor Gene Expression in Luteinizing Hormone-Releasing Hormone (LHRH) Neurons and Facilitates the LHRH Response to PGE2by Activating a Glia-to-Neuron Signaling Pathway

“…Surprisingly, central administration of NE to ovariectomized rats or stimulation of a mesencephalic noradrenergic pathway in these animals suppresses LH release, in contrast to the increase seen in estrogen-primed rats (Gallo and Drouva, 1979;Leung et al, 1981Leung et al, , 1982. It is possible that in the absence of estrogen, NE no longer sets in motion stimulatory mechanisms but instead activates pathways inhibitory to LHRH secretion.…”

Medial Preoptic Area Involvement in Norepinephrine-Induced Suppression of Pulsatile Luteinizing Hormone Release in Ovariectomized Rats

“…Therefore, these studies demonstrate that NF. acting at the level of the MPOA can suppress pulsatile LH release solely by decreasing LH pulse frequency.The noradrenergic system, in addition to its well-known stimulatory role on luteinizing hormone (LH) secretion [7, 9, 10, 14-17, 20, 31,38, 39], has been shown to exert inhibi tory effects on pulsatile LH release in the rat [13,14,17,21, 22]. Intraventricular infusions of norepinephrine (NE) [13,14, 22] or electrical stimulation of the ascending noradren ergic pathway [21] suppressed pulsatile LH release in ovar iectomized rats.…”

“…Intraventricular infusions of norepinephrine (NE) [13,14, 22] or electrical stimulation of the ascending noradren ergic pathway [21] suppressed pulsatile LH release in ovar iectomized rats. Recently this laboratory demonstrated that intraventricular infusion of NE decreased pulsatile LH se cretion solely by suppressing LH pulse frequency [13].…”

Suppression of Progesterone-Induced Gonadotropin Surge by Adrenergic Agonists in Estrogen-Primed Ovariectomized Rats

“…However, I h after administra tion of methoxamine to the third ventricle, LH levels had declined to about 30% of those seen in control rats (p < 0.05) and remained significantly suppressed during the re mainder of the bleeding session (p < 0.01). [10,11,18,19]. It has also been shown that intraventricular infusion of a p-adrenergic agonist can block the increase in LH levels produced by stimulation of the medial preoptic area [3].…”