The suprachiasmatic nucleus (SCN) is the major pacemaker in the central nervous system responsible for generating circadian rhythmicity in mammals. Tracer studies show limited projections of the SCN, mainly to the paraventricular nucleus of the thalamus and paraventricular and dorsomedial nuclei of the hypothalamus, suggesting that the latter two areas may be the target areas of the SCN for controlling corticosterone release. The present results show that when infused in the paraventricular/dorsomedial nucleus of the hypothalamus femtomolar concentrations of vasopressin (VP), but not vasoactive intestinal peptide (VIP), are able to suppress elevated levels of corticosterone in SCN-lesioned animals to basal daytime values. On the other hand, infusion of the VP antagonist in the same hypothalamic area induced a sevenfold increase of basal corticosterone levels in intact animals. The SCN origin of this VP input was established in SCN-lesioned animals where no difference between the effect of infusing the antagonist or Ringer could be detected. These results imply that the SCN can influence the daily corticosterone rhythm through its VP-containing projection to the paraventricular/dorsomedial nucleus of the hypothalamus.

The diurnal rhythm of corticosteroid secretion is controlled by the suprachiasmatic nucleus (SCN). In rats, plasma corticosteroid levels rise just before the onset of the activity period during the dark phase. Our previous results indicated that vasopressin as a neurotransmitter from the SCN inhibited corticosteroid secretion in the area of the paraventricular/dorsomedial nucleus of the hypothalamus. We hypothesized that during the day the SCN may serve as an inhibitory system for corticosteroid secretion. To investigate this possibility, intact and SCN-lesioned animals were exposed to mild stress in the morning and evening and their plasma corticosteroid levels were monitored. The results indicate that SCN-lesioned animals have higher morning corticosteroid levels and respond both in the morning and evening with higher corticosteroid levels after stress than do intact control animals. We conclude, therefore, that these results indicate an inhibitory role of the SCN on corticosteroid secretion. The apparent discrepancy with the reported stimulatory role of the SCN on adrenocorticotropic hormone secretion is discussed.

Recently, anatomical evidence was presented that the mammalian circadian clock located in the suprachiasmatic nuclei (SCN) may utilize GABA to transmit diurnal information to the dorsomedial hypothalamus (DMH). The present study provides further physiological evidence for the involvement of this GABAergic projection in the regulation of diurnal rhythms. Infusion of the GABA agonist muscimol in the region of the DMH completely blocked the daily increase of plasma melatonin during darkness and reduced sympathetic output in the pineal gland resulting in lower pineal melatonin production, as measured with transpineal microdialysis. Further experiments in SCN-lesioned animals indicated that the origin of this inhibitory input to the DMH is indeed the SCN. The results of this study imply that the SCN can influence the sympathetic outflow of the hypothalamus through its GABA-containing projection. Furthermore, the present results probably explain the previously reported strong inhibitory effect of benzodiazepines on plasma melatonin in both animals and humans.

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