Previous research has shown that electrolytic lesions of the anterior arcuate nuclei combined with anterior hypothalamic deafferentation (AHD) blocked pulsatile luteinizing hormone (LH) release in the ovariectomized rat, but that neither lesion was sufficient by itself. This led to the hypothesis that two separate neural pathways were capable of effecting pulsatile LH secretion, which was tested in another way in the present study. Newborn rats were injected with monosodium glutamate (MSG), a treatment which damages the arcuate nuclei, or NaCl of the same osmolarity as a control. As adults, the rats were gonadectomized and 2 weeks later, AHD or sham AHD was performed. One week after that, the rats were catheterized, and small blood samples were taken every 5 min for 3 h. Plasma was assayed for LH by radioimmunoassay. Neither MSG alone, AHD alone, nor the combination affected the number of animals with pulsatile LH patterns. In female rats, MSG treatment slightly decreased pulse frequency, while AHD depressed mean LH levels in male rats. No differences were seen in LH pulse amplitude. These results suggest either that MSG spares those neurons of the arcuate nuclei which are important for LH secretion, that electrolytic lesions of the arcuate nuclei destroy fibres of passage which are important for LH release, or that functional reorganization of the systems controlling LH release occurs following neonatal MSG treatment.

Keywords:
Luteinizing hormone, Anterior hypothalamic deafferentation, Monosodium glutamate
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© 1986 S. Karger AG, Basel
1986
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