Evidence for reorganization of the neuroendocrine centres regulating pulsatile LH secretion in rats receiving neonatal monosodium-l-glutamate treatment

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Abstract
Previous research has shown that the combination of anterior hypothalamic deafferentation (AHD) and electrolytic lesions of the anterior part of the arcuate nuclei blocks pulsatile LH secretion in ovariectomized rats, but that neither lesion alone was effective. Furthermore, the combination of AHD with arcuate lesions produced by neonatal treatment with monosodium-l-glutamate (MSG) does not block pulsatile LH release. To distinguish between the various possible reasons for this result, AHD and electrolytic lesions of the arcuate nuclei were combined in rats which had been treated neonatally with MSG or saline of equal osmolarity. One week after brain surgery, venous catheters were installed and blood samples taken at 5-min intervals for up to 3 h for assay of plasma LH. Rats treated with MSG and bearing AHD and electrolytic lesions of the arcuate nuclei continued to show pulsatile secretion of LH. Where the electrolytic lesions were posterior and dorsal to the anterior arcuate nuclei, however, LH release was blocked whether AHD was performed or not, but only in rats treated with MSG. None of the lesion combinations blocked pulsatile LH secretion in rats treated with saline. These results suggest that neonatal MSG treatment leads to a reorganization of the hypothalamus such that the role normally played by the arcuate nuclei in the regulation of pulsatile LH secretion is taken over by other hypothalamic structures. J. Endocr. (1987) 113, 261–269

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