Two experiments were undertaken to investigate the way that fasting impairs LH secretion and to assess whether endogenous opioid mechanisms might be responsible for the impairment. In the first experiment, pulsatile LH secretion was measured in a total of 51 chronically ovariectomized female rats. Initially 29 rats were subjected to food withdrawal for 24, 48, 72 or 120 h before the experiment. When compared with data collected from eight unfasted control rats, the 120-h fast was found to reduce significantly the mean peak and trough values of the LH pulses measured. However, in a subsequent study, the inhibition of pulsatile LH secretion by a 120-h fast was prevented in a group of eight rats given the opioid antagonist naloxone hydrochloride before the start of the blood-sampling period. Naloxone was without effect on pulsatile LH secretion in eight unfasted control rats. In the second experiment, plasma LH concentrations were measured before and after unilateral electrical stimulation of the ventral noradrenergic tract (VNAT) in ovariectomized female rats pretreated with oestradiol benzoate. In 17 rats VNAT stimulation caused a significant rise in plasma LH, but after a 72-h fast this rise was significantly less than in unfasted control rats. However, pretreatment of fasted rats with naloxone (n = 9) significantly enhanced the VNAT-stimulated release of LH to the control values. Naloxone did not potentiate VNAT-stimulated LH release in unfasted animals (n = 6) or LH release in control unstimulated rats (n = 12). The experiments indicate that both pulsatile LH secretion, and LH release caused by VNAT stimulation, are impaired by an acute fast.(ABSTRACT TRUNCATED AT 250 WORDS)

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 less than 0.01) greater LH surge than did oestradiol benzoate. In experiment 2 100 ul 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 no significantly influenced by MSG treatment. However the mean pulse height was significantly (P less than 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 less than 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.

The catabolism of neurotensin (NT) was studied in the gastric submucosa of the conscious rat using a novel technique to obtain a dialysate of interstitial fluid. A microdialysis fiber system was surgically implanted into the gastric submucosa, and 2 days later experiments were commenced on conscious animals. Isotope-labeled NT was administered to the tissue, and a dialysate of the submucosal interstitial fluid was collected. In the dialysate, NT and catabolites of NT formed in the interstitial fluid were identified and quantitated by high-pressure liquid chromatography. The catabolism of 125I-NT-(1-13) and [3H]NT-(1-13) was studied as was the further breakdown of the major catabolites. NT-(1-13) was, regardless of the type of label, catabolized mainly into NT-(1-8), NT-(9-13), NT-(1-11), and free tyrosine. None of the catabolites formed is known to possess significant biological activity. NT-(9-13) was rapidly cleared, whereas the amino-terminal fragments NT-(1-8) and NT-(1-11) were more resistant to degradation. The biological half-life of neurotensin in the gastric submucosa of the rat was between 9 and 15 min.

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