Effects of hypothalamic arcuate nucleus lesions on pulsatile luteinizing hormone concentration in ovariectomized rats.

Abstract

We investigated the effects of hypothalamic arcuate nuclei destruction on the postovariectomy rise in plasma luteinizing hormone (LH) concentration and the pulsatile LH release mechanism in ovariectomized rats. Rats were injected with 1, 2, or 4 mg/g body wt of L-monosodium glutamate (MSG) on Days 1, 3, 5, 7, and 9 of life to lesion the arcuate nuclei. They were then ovariectomized as adults and used 2 or 4-8 weeks later. Serial blood sampling at 10-min intervals and measurement of plasma LH concentration revealed elevated plasma LH levels which fluctuated in a pulsatile fashion in all control and 1 and 2 mg/g/MSG-treated rats. In 4 mg/g MSG-treated rats, plasma LH levels were lower than in controls of both time periods after ovariectomy due to a decrease in the amplitude and/or frequency of LH pulses. Phenobarbital was administered to all 4- to 8-week ovariectomized rats to block endogenous pulsatile LH release. In phenobarbital-blocked rats, three sequential iv injections of LH releasing hormone (LHRH) caused substantial elevations in plasma LH concentrations even in the 4 mg/g MSG-treated animals which had low plasma LH concentrations during control bleedings prior to the injection of phenobarbital. The results indicate that the postovariectomy rise in plasma LH concentration and the associated pulsatile LH release mechanism are functional in rats with extensive arcuate nucleus lesions. The diminution in the rise in plasma LH levels and the decreased amplitude and/or frequency of LH pulses in the MSG-treated rats is likely due to a diminution in hypothalamic LHRH release.