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. 1981 Sep;109(3):720-8.
doi: 10.1210/endo-109-3-720.

Electrical stimulation of mesencephalic noradrenergic pathway: effects on luteinizing hormone levels in blood of ovariectomized and ovariectomized, steroid-primed rats

Electrical stimulation of mesencephalic noradrenergic pathway: effects on luteinizing hormone levels in blood of ovariectomized and ovariectomized, steroid-primed rats

P C Leung et al. Endocrinology. 1981 Sep.

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.

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