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Biomedical subjects

A Hraschek

Publications and source records attributed to A Hraschek.

7 recordsLinked to original sources
PubMed1977

Brain catecholamine metabolism and avoidance conditioning in rats.

Male albino rats were trained in a shuttle-box by presentation of 50 trials and were grouped according to the performance level. The disappearance of labelled catecholamine pool was studied after intraventricular injection of tritiated noradrenaline in the neocortex, brain stem, hypothalamus and hippocampus. Rats with a high performance level showed a greater disappearance rate of the labelled catecholamine pool than low or medium performers. In another experimental series the animals were grouped on the basis of their performance level which was tested 2 days before the intraventricular injection of the tracer. There was no significant difference in disappearance rates between the good and poor performances. It is assumed that integration of the goal-directed motor pattern is mediated through catecholaminergic (noradrenergic) neuronal mechanisms.

Animals↗
PubMed1976

Effect of ACTH and its fragment on brain catecholamines in intact and adrenalectomized rats.

Brain catecholamine metabolism was monitored by distribution of labelled noradrenaline (3H-NA) after intraventricular injection to intact and adrenalectomized rats. The adrenalectomy produced an increased disappearance rate of the labelled pool in the hypothalamus, hippocampus and neocortex. These changes could be prevented by hydrocortisone pretreatment. Painful stimuli resulted in an increased disappearance of the labelled pool in both intact and adrenalectomized rats. The implantation of hydrocortisone into the tuberoinfundibular region prevented the stress-induced changes of the catecholamine metabolism. Intraventricular administration of ACTH1-24 and ACTH4-10 produced a significant increase of the disappearance rate in different brain regions of adrenalectomized rats. The blocking of catecholamine synthesis by intraventricular injection of alpha-methyl-m-tyrosine resulted in a marked decrease of the labelled pool but did not prevent the ACTH-induced decrease of the tracer pool. On the other hand, the blocking of monoamine-oxydase activity by Pargyline led to a marked increase of the labelled pool but intraventricular administration of ACTH led to an increase of the disappearance rate. The mechanism of ACTH action on brain catecholamine metabolism is still obscure, however, an increased release of the NA to ACTH peptides is very likely in the light of the present observations.

Adrenal Glands↗
PubMed1975

Effects of ACTH on the uterine weight response to HCG in mice.

The effects of ACTH and dexamethasone on the uterine weight of immature mice treated with HCG or oestradiol-17 beta were studied. The animals were treated daily for 3 days and wet and dry uterine weights were measured on the 4th day. Low doses of ACTH (1-25 mug/day) raised the sensitivity of the uterine weight response to threshold doses of HCG (0-05 to 0-1 i.u.). By increasing the doses of ACTH or HCG, the stimulation gradually turned into inhibition. By itself, ACTH was ineffective and it had no influence on the increase in uterine weight induced by oestradiol-17 beta. Dexamethasone failed to stimulate the effect of HCG.

Adrenocorticotropic Hormone↗
PubMed1975

Role of sodium and potassium in aldosterone binding of kidney receptors in the rat.

An increase of the sodium concentration produced a diminished binding of labeled aldosterone to kidney receptors in both in vivo and in vitro conditions. The elevation of potassium level did not change the binding capacity of kidney nuclear receptors for aldosterone. Hypernatraemia-induced decrease of aldosterone uptake was significant in the nuclear fraction of both medullary and cortical region of the kidney but did not show remarkable changes in the uptake of cytosol fraction. The transfer of aldosterone from cytosol into the nuclear compartment seems to be changed by the alteration of extracellular sodium concentration.

Aldosterone↗