Further Studies on Norepinephrine-Induced Suppression of Pulsatile Luteinizing Hormone Release in Ovariectomized Rats

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Abstract
The present study examined three aspects of the inhibitory effects of continuous intraventricular infusion of norepinephrine (NE) on pulsatile luteinizing hormone (LH) release in ovariectomized, nonsteroid-primed rats: (1) whether the inhibitory effects of NE infusion were exerted on LH pulse frequency and/or amplitude; (2) whether central nervous system desensitization occurred in response to the inhibitory effects of continuous NE infusion on pulsatile LH secretion, and (3) whether dopamine of serotonin were involved as possible interneuronal transmitter mediators of NE-induced suppression of pulsatile LH release. Unanesthetized rats with external jugular cannulae were bled continuously at a rate of 50 µl whole blood/7 min for 2 h prior to infusion and for 2–3 h during continuous intraventricular infusion of artificial cerebrospinal fluid or NE. Infusion of cerebrospinal fluid had no effect on pulsatile LH release, while continuous infusion of 0.3 or 1.8 µg NE/h for 2–3 h produced suppression of pulsatile LH secretion. Although desensitization to the stimulatory effects of NE on LH release in ovariectomized, steroid-primed rats had been observed to occur rapidly within 90 min after the onset of infusion, desensitization to the inhibitory effect of NE on pulsatile LH release did not occur even after continuous infusion of NE for periods up to 20 h. Mean blood LH levels were as low in rats bled 17–20 h after the onset of NE infusion as in those bled at 0–3 h. The suppressive effect of NE on pulsatile LH release was not prevented by prior blockade of dopamine or serotonin receptors with pimozide or metergoline, respectively. Lastly, in all groups infused with NE, the decrease in mean blood LH levels was due solely to a suppression in LH pulse frequency, as no decrease occurred in pulse amplitude. These experiments demonstrate that (1) the inhibitory effect of NE is exerted solely on LH pulse frequency and suggest that NE suppresses only the firing rate of the presumed luteinizing hormone releasing hormone pulse generator in regulating pulsatile LH secretion; (2) whereas desensitization is rapidly established in the neuronal receptors excitatory to LH release, this phenomenon is not observed when pulsatile LH release is suppressed by NE for much longer periods of time, and (3) dopamine and serotonin are not involved as possible interneuronal transmitter mediators of the inhibitory effects of NE upon pulsatile LH and presumably pulsatile luteinizing hormone releasing hormone secretion.