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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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ABSTRACT
The LH surge was induced in ovariectomized rats by sequential treatment with oestradiol benzoate and progesterone. Vasoactive intestinal peptide (VIP) or saline was infused into the third cerebral ventricle from 13.30 to 16.30 h on the afternoon of the anticipated LH surge. Two blood samples were taken by jugular puncture from each animal, one at 12.00 h as a control sample and the other at 16.00, 18.00, 20.00 or 22.00 h. Saline-infused animals showed a normal LH surge, with mean plasma LH concentrations reaching a peak at 18.00 h, declining by 20.00 h and reaching control (12.00 h) levels by 22.00 h. Plasma LH in animals infused with VIP was not significantly higher than control levels at 16.00 or 18.00 h. By 20.00 h, mean LH levels in VIP-infused rats had risen to the levels seen at that time in saline-infused rats, and by 22.00 h LH had returned to control levels in VIP-infused animals. We interpret these findings to mean that VIP inhibits LH secretion during the LH surge. It does not block the surge completely, as pentobarbital during the critical period would have done; nor does VIP appear to affect the timing of the LH surge. Rather, VIP inhibits the increased LH secretion rates of the LH surge only during the period of VIP treatment and for a short time afterward.
Journal of Endocrinology (1992) 133, 433–437
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We have studied the possible effects of monosodium glutamate (MSG) on LH secretion in ovariectomized rats.
In experiment 1 MSG-treated and control rats were given oestradiol benzoate at noon and 72 h later half the rats in each group were given a second injection of oestradiol benzoate or progesterone. Blood samples were taken immediately before and 6 h after these i.m. injections. At 78 h there were no significant differences in plasma LH concentration measured in the two groups of rats given progesterone or in the two groups given a second injection of oestradiol benzoate although for both MSG-treated and control rats progesterone produced a significantly (P < 0·01) greater LH surge than did oestradiol benzoate.
In experiment 2 100 μl blood samples were collected at 5-min intervals for up to 3 h from MSG-treated and control rats. For rats showing more than one pulsatile discharge of LH, peak and trough values for plasma LH concentrations were not significantly influenced by MSG treatment. However the mean pulse height was significantly (P < 0·001) greater in the MSG-treated group than in control rats. Pulsatile release stopped more quickly in the MSG-treated rats and their mean plasma LH concentration after 120 min of blood sampling was significantly (P < 0·05) lower than that obtained in the control animals.
Thus, although some aspects of LH secretion seem to be significantly different in MSG-treated rats, these effects may result from the greater sensitivity of the MSG-treated animals to experimental manipulation.
