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Biomedical subjects

C Nyakas

Publications and source records attributed to C Nyakas.

At least 91 records · Page 5Linked to original sources
PubMed1984

The behavioural depression of hippocampal kindled rats is attenuated by subcutaneous and intracerebroventricular naltrexone.

Two questions were asked: Does naltrexone attenuate the behavioural depression (BD) in other models of limbic epilepsy besides amygdala kindling? Does intracerebroventricular (ICV) administration produce the same effects as subcutaneous injection, i.e., attenuation of the BD. Male wistar rats with bipolar electrodes implanted bilaterally in the dorsal hippocampus and a metal cannula in the lateral ventricle were kindled through 1 electrode and EEG recorded through the contralateral electrode. Subcutaneous (sc) and ICV naltrexone administration attenuated the BD of hippocampal kindled rats. These results further implicate the brain opioid system in the postictal phase of kindling and possibly epilepsy.

Amygdala↗
PubMed1984

Footshock sensitivity of rats after adrenalectomy and glucocorticoid treatments.

The threshold of flinch-jump response to electric footshock was measured after adrenalectomy (ADX) in male albino rats. The ADX-rats showed higher threshold from the 2nd to 6th postoperative days than the sham-operated animals. Daily subcutaneous administration of 100 micrograms/100 g b.w. corticosterone (CS) led to restoration of the footshock sensitivity of ADX-rats. The same effect was observed following dexamethasone (DEX) treatment. DEX but not CS administration resulted in a decrease of the footshock sensitivity in the sham-operated rats. On the 9th and 18th days after adrenalectomy, in contrast to the early postoperative period, the threshold for footshock sensitivity was significantly lower than in sham-operated controls. It is suggested that an excess release of endogenous opiates from the pituitary are involved in the changes of pain threshold under the conditions studied.

Adrenalectomy↗
PubMed1983

Hippocampal corticosterone receptors and novelty-induced behavioral activity: effect of kainic acid lesion in the hippocampus.

Rats were injected bilaterally in the dorsal and ventral hippocampus with kainic acid (KA) or with artificial CSF and their behavior and brain corticosterone (B) receptor systems were studied. The hippocampal KA injection destroyed part of the pyramidal neurons and of the dentate gyrus neurons. These neurons contain a receptor system for B. At 2 weeks after the KA lesion this B receptor system displays an increase in apparent maximal binding capacity (Bmax) of approximately 25%. The compensatory increase in B receptor concentration is reflected in an increased uptake of [3H]B in cell nuclei of hippocampal slices incubated in vitro with saturating concentrations of the steroid. Administration of a tracer dose of [3H]B shows that labelled steroid can enter in vivo the cell nuclear compartment of the KA-lesioned lobe. The role of B was investigated on novelty-induced behavioral activities of KA-lesioned and sham-lesioned animals in a large open and a small closed field at 10 days after bilateral adrenalectomy (ADX) or sham-ADX which is 14 days after the (sham) lesion. B (300 micrograms/kg rat) was administered s.c. 1 h prior to the test. KA lesion resulted in an increase in exploratory activity and a reduction in grooming and immobility. After ADX the effect of KA on exploration was reduced in the 5 min open field and abolished in the 30 min closed field. ADX animals displayed more grooming behavior (closed-field). B replacement of ADX rats reinstated the exploratory hyperactivity of KA-lesioned rats. On some components of the behavior such as ambulation in open-field and locomotion in closed field, there was even a larger responsiveness to B in the KA-lesioned rats than in the control animals. It is concluded that (1) after KA lesion of receptor containing neurons, the remaining tissue displays a compensatory increase in number of B receptor sites; (2) B is required for full expression of exploratory activity of rats with or without KA lesions; (3) the KA-lesioned rats display a larger responsiveness to B; and (4) the increased number of B receptor sites may underlie the larger responsiveness to B.

Adrenalectomy↗
PubMed1982

Effect of mazindol on feeding behaviour and on noradrenergic function of various parts of the rat brain.

The effect of mazindol on feeding behaviour was investigated in rats fasted for 24 hours. They were then given mazindol i.p. and placed in a new environment. The effect of the drug on the disappearance of 3H-noradrenaline (3H-NA) from various parts of the brain after injection into the cerebral ventricles was also investigated. Mazindol was more potent in suppressing feeding behaviour than in reducing food intake, indicating that a number of aspects of feeding behaviour may be more sensitive indices of the anorectic effect of a drug than food intake per se. Mazindol, in a dose of 30 mg/kg, accelerated the disappearance of 3H-NA from the medial hypothalamus but not from other areas of the brain, suggesting that the drug has a locus-specific action on cerebral noradrenaline metabolism.

Animals↗
PubMed1981

Corticosterone binding capacity increases in contralateral hippocampus after partial unilateral hippocampectomy.

After unilateral dorsal hippocampectomy the binding of [3H]corticosterone to cytosol receptors in contralateral hippocampus was measured. For estimation of binding capacity the adrenals were removed bilaterally 24 h prior to sacrifice. The apparent maximal binding capacity (Bmax) for corticosterone in the contralateral hippocampus lobe was increased by 74 and 41%, respectively, 10 and 20 days after surgery. The data reveal a novel aspect of steroid receptor capacity control. It is suggested that compensation of altered amounts of receptor sites is an intrinsic property of the hippocampal corticosterone receptor system.

Adrenalectomy↗
PubMed1981

Effects of neonatal ACTH4-10 administration on adult adaptive behavior and brain tyrosine hydroxylase activity.

The effects of daily injection of ACTH4-10 in postnatal days 2-8 were studied on adult adaptive behavior and brain TH activity in male rats. Four groups were used: (1,2) 10 and 2 nmol ACTH4-10 injected, (3) saline injected, and (4) intact, unhandled. The peptide did not influence acquisition but delayed extinction of CAR in the shuttle-box and facilitated passive avoidance behavior against saline control. The experimental manipulation in the saline control group (neonatal stress) also significantly influenced these behavioral variables and motility during conditioning but in the opposite direction as did ACTH4-10 treatment. It was concluded that ACTH4-10 interfered with the action of neonatal stress on the development of adaptive behavior. A similar kind of interaction could also be observed in TH activity of striatum and locus ceruleus but not in all brain areas investigated.

Adrenocorticotropic Hormone↗
PubMed1981

Corticosterone binding in myocardial tissue of rats after chronic stress and adrenalectomy.

Male rats were trained to swim for 9-10 days to assess the effect of chronic stress on the capacity and affinity of specific glucocorticoid binding in the cytosol fraction of myocardial tissue. A significant decrease in the binding capacity for corticosterone (Cpd B) was found 24 hours after the last swimming test, while the affinity constant remained unchanged. Contrary to Cpd B binding, there was no change in the capacity of dexamethasone binding, and there was no decrease in the Cpd B binding capacity in rats which had been adrenalectomized 2 days prior to the training period. We conclude that daily swimming for 9-10 days alters the numbers of cytoplasmic Cpd B binding sites in the face of increased adrenocortical activity, while not affecting dexamethasone binding in the cytosol fraction of myocardial tissue.

Adrenalectomy↗
PubMed1980

Changes in the pituitary-adrenocortical function after intracerebral administration of di-isopropyl-fluorophosphate and physostigmine in the rat.

Local administration of di-isopropyl-fluorophosphate (DFP) and physostigmine into the preoptic area produced a marked elevation of plasma corticosterone level in male albino rats. The drugs failed to change the pituitary-adrenocortical function if they were administered into the septum, hippocampus and posterior hypothalamus. The injections were performed through chronically implanted cannulas and the plasma corticosterone level was measured by competitive protein-binding assay. Atropine pretreatment inhibited the physostigmine-induced increase of plasma corticosterone level but it did not prevent the changes induced by DFP administration. Dexamethasone pretreatment blocked the plasma corticosterone response level evoked by local application of acetylcholineesterase inhibitors into preoptic area.

Adrenal Cortex↗
PubMed1979

Hippocampal function and putative corticosterone receptors. Effect of septal lesions.

In order to investigate the relation between septohippocampal function and hippocampal corticosterone (B) receptors, discrete septal areas were destroyed by electrolytic lesions; the effects of the lesions on cytosol receptor binding of B in the hippocampus were determined 10 or 30 days after lesioning in male rats adrenalectomized 12 h prior to sacrifice. The septal lesions were also characterized functionally by endocrine, neurophysiological and behavioral parameters in the same group of animals. Hippocampal B receptor activity was increased 30 days after lesioning the lateral septal area. The same lesions impaired the acquisition of a conditioned avoidance response. The increase was not due to a behavioral deficiency per se as lesions in the parafascicular nucleus did impair acquisition behavior without affecting B receptors. There was no change in B receptor activity 30 days after destruction of the medial septal nucleus, although such a lesion completely abolished the hippocampal theta activity measured at 10 days. In another group of animals hippocampal B receptors were not affected at 10 days after any of the lesions, while a transient increase in basal plasma levels of B was noted at that time. It appears that the hippocampal receptor activity for B depends on the integrity of the efferents from the hippocampus and/or the dorsolateral septal B receptor system rather than on the septal afferents to the hippocampus.

Adrenalectomy↗
PubMed1977

Role of brain catecholaminergic system in hypothalamic obesity in rats.

Distribution of labelled catecholamines (CA) was studied after intraventricular injection of 3H-norepinephrine (NE) and 3H-dihydrozyphenylalanine (DOPA) in several brain regions of ventromedial hypothalamic lesioned female rats. After intraventricular infection of 3H-NE a decrease in endogenous NE content and a marked increase in labelled NE concentration were observed in the preoptic-basal cortical area and lateral hypothalamus, while no change was found in these parameters in brain areas caudal to the lesion. The 3H-DOPA uptake of preoptic-basal cortical area and also the lateral hypothalamus was lower. No change was found in the uptake of 3H-DOPA in the corpus striatum. These results support the hypothesis that the decreased function of noradrenergic pathways in the medial forebrain bundle plays a role in the development of hypothalamic obesity without any concomitant functional changes in the striatal dopaminergic system.

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↗