The roles of hypothalamic norepinephrine (NE) and dopamine (DA) in the regulation of LH and PRL are controversial. In the present studies, we used HPLC and push-pull perfusion to measure NE and DA releases in the medial preoptic area (MPA) of conscious, freely moving rats. Serum LH and PRL were determined in separate groups of rats with indwelling venous cannulas. In young (4- to 5-month-old) rats, concomitant with proestrous surges of serum LH and PRL, NE release in the MPA increased gradually to reach a peak at 1800 h, whereas DA release decreased gradually to its lowest level at 2000 h. Compared to the young animals, in middle-aged (8- to 10-month-old) animals, the proestrous surge of PRL was unaltered, but the LH surge was delayed and attenuated. The pattern of DA release in the middle-aged animals was also unaltered, but the peak in NE release was markedly attenuated, although the average NE release was increased compared to that in the young proestrous animals. In young diestrous rats and old (22- to 24-month-old), persistently diestrous rats, in which serum LH and PRL are known to be stable, both NE and DA releases were devoid of fluctuations. However, in the young diestrous animals, the average NE and DA releases were significantly increased compared to those in the young proestrous animals, whereas in the old, persistently diestrous animals, NE and DA releases were markedly reduced compared to those in the young diestrous animals. These data lead us to conclude that NE, through its stimulatory action, may be the primary regulator of LH release, and that it is the pattern, rather than the level, of NE release that appears to be critical in determining the pattern of LH release. DA, through its inhibitory action, appears to control PRL only and probably has no association with LH release. By tracing NE and DA activities from adulthood through middle-age to senescence, these studies revealed that the marked reductions in catecholamines in old age are preceded by a transitory increase in NE activity in middle-age, and that the cyclic increase in NE activity associated with the LH surge begins to diminish in middle age and disappears completely in old age.

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Lipopolysaccharide (LPS) is known to produce several central and neuroendocrine effects and some of these effects are believed to be mediated through cytokines and other proteins. One such protein, leptin, produced by adipose tissue has been shown to cause anorexia, a central effect associated with LPS treatment. This raised the possibility that LPS-induced effects on feeding behavior may be mediated through leptin. This study was done to investigate the effects of systemic administration of LPS on plasma leptin levels in rats and the possible involvement of interleukin-1 (IL-1) in this mechanism. Adult male rats were implanted with indwelling jugular catheters and after collecting two pretreatment blood samples, the animals were injected (i.p.) with saline, 5 microg, 10 microg, or 25 microg/kg BW of LPS, or treated with 25 microg of soluble IL-1 receptor (sIL-1R) 5 min before and 90 min after 25 microg/kg BW of LPS. Posttreatment blood samples were collected at 30 min intervals for a period of 6 h. Plasma leptin concentrations were measured by radioimmunoassay. Treatment with saline did not produce any change in plasma leptin levels. In contrast, each of the three doses of LPS produced a dose-dependent increase in plasma leptin levels within 120 min. Leptin levels remained elevated for the next 4 h. Treatment with sIL-1 R completely blocked the LPS-induced increase in leptin levels, indicating that this effect is in fact mediated through IL-1. These results indicate that leptin could be a possible mediator of LPS-induced effects on feeding.

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