This study examined the alterations in episodic luteinizing hormone (LH) release in response to third ventricle infusions of various α- and β-adrenoceptor agonists in ovariectomized (OVX) rats as well as the effects of steroid priming with 50 µg estradiol benzoate (EB) and 25 mg progesterone (P) on the LH responses to these agonists. Unanesthetized rats with indwelling atrial cannulae were bled at 10-min intervals for 0.5–1.5 h prior to infusion and up to 1.5 h following infusion of equimolar amounts (0.06 or 0.3 µmol in 2 µl saline adjusted to pH 5.5 and infused slowly over a 2-min period) of norepinephrine (NE), phenylephrine (Phen, α₁-agonist), isoproterenol (Iso, β-agonist) or clonidine (Clon, α₂-agonist). In unprimed OVX rats, 0.06 µmol NE induced a significant lengthening (by ∼ 121%) of the episodic interval between the peak LH levels and caused a decrease in mean blood LH levels of ∼ 24%, which began almost immediately and lasted for approximately 1 h after infusion. When administered in the same manner and dosage, both α- and β-adrenergic agonists were similarly effective in suppressing pulsatile LH release in OVX unprimed rats, with the following rank order being apparent:Clon > NE ≈ Phen > Iso. However, in OVX-EBP-primed rats, while 0.06 µmol NE significantly stimulated LH release, none of the other adrenoceptor agonists administered at this dosage was effective in altering the low nonpulsatile levels of blood LH characteristic of the steroid-primed animal. Nevertheless, at a concentration 5 times higher (0.3 µmol) Clon and Phen did induce LH surges while Iso, even at this higher dose, was not stimulatory to LH release. These results suggest that the inhibitory action of NE on LH secretion in OVX rats may be exerted via activation of both α- and β-adrenoceptors, whereas primarily α-adrenoceptors are responsible for mediating the NE-induced stimulation of LH release in OVX steroid-primed animals.

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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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