No abstract

The role of brain noradrenaline in the regulation of pituitary-adrenocortical function is controversial. Ganong (1972) suggested that the central noradrenergic system inhibits the secretion of adrenocorticotrophin, but it has also been shown (Kumeda, Uchimura, Kawabata, Maeda, Okamota, Kawa & Kanehisa, 1974) that a drastic reduction in the hypothalamic noradrenaline content, resulting from intraventricular administration of 6-hydroxydopamine, has no effect on the basal levels of corticosterone in rat plasma and adrenal tissue. The stress response is also not affected, nor is the suppressive effect of dexamethasone on the plasma and adrenal concentrations of corticosterone. Almost identical results have been reported by Cuello, Shoemaker & Ganong (1974) and Kaplanski, van Delft, Nyakas, Stoof & Smelik (1974), and Cuello et al. (1974) suggested the possibility of denervation hypersensitivity developing as a result of intraventricular administration of 6-hydroxydopamine. We have therefore investigated whether denervation hypersensitivity develops in order to compensate for the reduced hypothalamic noradrenaline content and we present results concerning the effect of intraventricular administration of 6-hydroxydopamine on the concentration of corticosterone in the plasma of the rat.Male Wistar rats (300-350 g) were implanted stereotaxically with a permanent cannula in the right lateral ventricle. The rats were divided into two groups: one group was pre¬ treated with 6-hydroxydopamine (250 µg in 25 µ 0-9% saline containing 0-1% ascorbic acid, administered intraventricularly; this dose was shown by Kumeda et al. 1974, to cause a drastic reduction in the noradrenahne content of the brain) ; the other group acted as controls and received vehicle only. Noradrenaline (1-0 µg) was administered through the cannula 14 days after the operation and the rats were decapitated after a further 40 min; in suppression experiments, dexamethasone (20 µg/rat) was administered i.p. as two injections 9 and 5 h before decapitation. Experiments were carried out at 08.00 and 15.00 h. Trunk blood was collected, centrifuged and stored deep-frozen until required for fluorometric determination of the corticosterone content as described by Guillemin, Clayton, Lipscomb & Smith (1959).The results are shown in Table 1. In experiments performed at 08.00 h, when the basal level of corticosterone in the plasma was low, injection of noradrenaline into rats pre¬ treated with 6-hydroxydopamine caused a significant increase in the concentration of corticosterone compared with the effect in pretreated rats injected with saline. Injection of the same dose of noradrenaline into control rats (no pretreatment) had no significant effect.

The thermodynamics and kinetics of the dimerization of Acridine Orange (AO, 3,6-bis(dimethylamino)acridinium chloride) and its 10-alkyl derivatives in 0.1 M NaCl solution have been studied by spectrophotometry and temperature-jump method. Dimerization constants, which were determined spectrophotometrically, become large with an increase in the length of the introduced alkyl chain; this behavior is the same as that in water and a dilute HCl solution. The association and dissociation rate constants determined from the temperature-jump measurements also depend on the length of the alkyl chain. Especially, the rate constants for methyl–AO are unexpectedly small. Both the effect of added salt on the thermodynamic parameters and the kinetic results are discussed in view of the structure of hydration water surrounding dye molecules. 1H NMR data for AO and methyl–AO suggest that the planes of two component molecules in a dimer are parallel to each other. This result is consistent with the spectrophotometric and kinetic data.

No abstract

Microinjections of 0.4 microgram of carbachol into the amygdala caused a rise of corticosterone (CS) in the morning when the prestimulating level of CS was lower. But the same procedure with a larger dose had no effect in the afternoon, when the prestimulating level of CS was higher.