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Thirst stimulation of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) was induced in rats by withholding all fluids during three days. 35S-cysteine was then intraperitoneally administered and the rats were killed at predetermined times and examined by autoradiography, applying the authors' previously described method. This experimental series totalling 51 animals was compared with a control series of 70 rats, similarly treated, who had had free access to water. The kinetic phenomena in SON and PVN were analysed in terms of the two-compartment model previously used, which gives an estimate of the neurosecretory material (NSM) secretion parameters and of those of the lumped structural cell protein turnover in the nuclei. The kinetics of the precursor amino acids after administration of labelled cysteine were also assessed. Determinations of the label uptake at two specific times in the experiment, in the infundibular nucleus, ventromedial nucleus and optic nerve tissue in both series served as a check on the specifity of the structural protein turnover changes observed. Compared with the controls, the turnover rate of the slow compartment was more than tripled in the dehydrated rats, while that of the fast compartment had gone down to about one-third; both effects very nearly equal in SON and PVN. These results are compatible with the concept according to which thirst stimulates the SON and PVN equally. A distinct, and strikingly equal, hump was observed (2 hours after label administration) in all specific activity curves, also in the precursor serum concentration, and it is probably due to recycling of 35s from cysteine to methionine. This and other circumstances render the phenomena rather too complex for a straight-forward evaluation by the two-compartment model. Even so, the observations are believed to furnish good evidence of the biological verity of this model as well as the thirst-induced changes elicited.

The physiological role of the subcommissural organ (SCO) is still unclarified, although numerous hypotheses have been presented (see for references Palkovits 1965). Morphological evidence speaks in favour of a secretory function especially of the sulxommissural ependyma. The cytoplasmic selectively stainable material in the ependymal cells, "secretion", can be demonstrated by the methods which also stain the hypothalamic neurosecretory material. This "secretion" appears to be rich in histochemically demonstrable cystine (Talanti 1958).A correlation between the function of the SCO and the adrenal glands has also been experimentally proved. Palkovits (1965) reported changes in the secretion of aldosterone after destruction of the SCO, and he observed histoquantitative changes in the zona glomerulosa after administration of SCO extract.An attempt has been made to employ the intensity of incorporation of labelled cysteine as an indicator of the secretory, or metabolic, activity of the SCO (Talanti 1971). It is likely that a high proportion of cysteine is incorporated in proteins and at least partly in the "secretion" of the SCO. The present study constitutes a part of the studies concerning the influence of the function of the endocrine glands on the SCO. Its principal aim was to investigate the effect of experimental changes in the function of the adrenal glands on the incorporation of labelled cysteine in the SCO. Changes were induced in the adrenal glands by adrenalectomy and by treatment with hydrocortisone. 54 male adult albino rats were used. All rats received a standard pellet diet and tap water ad libitum. 18 of the animals were adrenalectomized under anesthesia, another 18 rats were treated with hydrocortisone ("Hydro-Adreson", Organon) at 5 mg/daily i.m., and 18 rats served as controls. After 14 days, counted from adrenalectomy or from the beginning of hydrocortisone treatment, all animals received an average dose of 150 pCi of 35S-labelled cysteine ("L-Cysteine-S 35 hydrochloride", The Radiochemical Centre, Amersham, Bucks, England) by i.p. injection. 6 animals from each group were sacrificed by rapid decapitation at each of the times 45 min, 4 h and 24 h after the cysteine injection.

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