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Biomedical subjects

K Murgas

Publications and source records attributed to K Murgas.

At least 19 recordsLinked to original sources
PubMed1994

Catecholamine overflow within rat striatum: the influence of microstimulation and electroconvulsive stimulation as observed with voltammetry.

Differential pulse voltammetry with a carbon fibre microelectrode was used in chloral hydrate-anaesthetized rats for testing the influence of microstimulation and of electroconvulsive stimulation on the changes in concentration of electro-oxidizable materials (catechol derivates) in the extracellular space of the corpus striatum. Microstimulation applied in the striatum (8 V anodal pulses, 0.1 ms, 100 Hz for 40 s) caused a significant increase of the catechol-oxidative current (Ico); 5 s after microstimulation was stopped Ico ranged from 117 to 141% of the control (all values means +/- S.D. unless otherwise stated; 124 +/- 11%, n = 4, P < or = 0.01, Student's t test). This effect ceased in the third minute after microstimulation. A comparable result was observed when microstimulation was repeated at intervals of 10 min. Electroconvulsive stimulation with a sinusoidal current (50 Hz, approximately 150 mA, 0.2 s) caused a large increase in Ico; 20 s after stimulation ceased, Ico was 987 +/- 90% (n = 3) of the control and it returned to the baseline 2 min later. The mechanisms inducing transmitter overflow are considered and the influence of electroconvulsive stimulation on the striatum is discussed in the context of its beneficial effects in psychopathic patients.

Animals↗
PubMed1994

Effects of electroconvulsive shock on catecholamine release in the corpus striatum of the rat: a voltammetric study.

A voltammetric technique was used (differential pulse voltammetry with a carbon fibre microelectrode) to investigate dynamics of the changes of catecholamine overflow in the corpus striatum following electroconvulsive stimulation (ECS) of chloral hydrate-anaesthetized rats. Application of "maximal" ECS (50 Hz, AC, sine wave, approximately 150 mA, 0.2 s) caused large enhancement of catechol-oxidative current (CA.OC): In the first minute after its arrest, the CA.OC peak raised to 1032 +/- 405% (n = 5, mean +/- S.D.) of the controls (P < or = 0.001, Student's t-test). This large elevation of the extracellular catecholamine content ceased rapidly--the baseline level was attained in the second minute. CA.OC changes evoked by a "minimal" ECS (50 Hz, AC, sine wave, approximately 30 mA, 0.2 s) were equivocal in the first minute (increase, decrease: 145 +/- 56%, P > 0.05, n = 6). Possible mechanisms of the ECS therapeutic effect are discussed.

Animals↗
PubMed1992

Effect of acute alcohol treatment on dopamine concentration in corpus striatum of rats: a voltammetric study.

A voltammetry technique has been used to determine changes in dopamine release in the rat corpus striatum after two doses of ethanol administration. The dopamine oxidation current reached a maximal value at 30 min after the first alcohol dose with a subsequent decrease towards the initial level at 60 min and kept to the basal level with a statistically insignificant oscillation. When a second dose of alcohol was applied at 60 min, it was followed by a decrease of the dopamine oxidation current peak to 50% of the initial value after another 60 min observation. The results resemble the known effect of alcohol on human behaviour (excitation followed by depression).

Animals↗
PubMed1992

Voltammetrically determined differences in changes evoked by KCl microinjections on catecholamine levels in the reticular formation and corpus striatum of the rat.

Using a microelectrode with carbon filaments and the voltammetric technique, changes evoked in the catechol oxidation current (CA.OC) and multiple unit activity (MUA) by microinjection of 3-5 microliters 0.5 mol.l-1 KCl were studied in the reticular formation (RF) of the medulla oblongata of anaesthetized rats; the effect of KCl stimulation of the RF and corpus striatum (S) on the CA.OC in these structures was compared. The microinjection of KCl in the vicinity of the working electrode in the RF caused depression of MUA which began 2-3 s after administration, persisted for up to 6 min after and then diminished, reaching control values within 9 min. The voltammetric signal was first recorded in the 1st min after microinjection, when there was an evident decrease in the CA.OC value (59% of the control value); this effect reached its maximum 7 min after administration (a mean drop to 23% of the control), while at the end of the experiment (i.e. after 24 min) CA.OC values had risen to 45-80% of the control value. The response in the S had a biphasic character, however. Immediately after the microinjection (1st min), the mean CA.OC value rose to 626% of the control, while in the second phase (3-10 min) it was seen to fall below the control values (means 21-63% of the control). The differences in the changes evoked by K+ depolarization in the concentration of catecholamines in the RF and S microenvironment are discussed from the aspect of the existence of different pools of the transmitter and other regional differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Monitoring of potassium-stimulated catecholamine changes in striatal synaptosomal preparations and in corpus striatum of rats: a comparative voltammetric study.

Voltammetric techniques were used to compare the effects of K(+)-induced depolarization on catecholamine levels in in vitro synaptosomal preparations of the corpus striatum with those in the in vivo corpus striatum of anaesthetized animals. In vitro, the catechol-oxidation currents could be recorded only in dopamine-preloaded synaptosomes. In isolated synaptosomes prepared in the presence of elevated concentrations of Ca2+ (1 mmol.l-1) and Na+ (135 mmol.l-1), K(+)-induced depolarization had variable effects on catechol-oxidation current. The stimulatory effect of K(+)-induced depolarization (a short transient increase of catechol-oxidation current lasting for 30 s) could be observed after the addition of dopamine loaded synaptosomes in EGTA into the medium with elevated K+ concentration (90 mmol.l-1) and decreased concentrations of Na+ (75 mmol.l-1) and Ca2+ (0.75 mmol.l-1). These results suggest that experimental procedures and parameters of ionic composition of incubation media have to be carefully controlled, owing to an enhanced in vitro permeability of membranes of isolated synaptosomes for Ca2+ and Na+. In in vivo experiments, microinjection of KCl (3 microliters of 0.5 mol.l-1 KCl in 10 mmol.l-1 HEPES, pH 7.4) resulted in the appearance of several phases of catechol-oxidation current: the current increased (to severalfold of the control values) followed by a decrease or even total disappearance, with a gradual return to control values. Under conditions of depletion of extracellular calcium by EGTA (5 microliters of 0.5 mol.l-1 KCl + 0.25 mol.l-1 EGTA in 10 mmol.l-1 HEPES, pH 7.4) K(+)-induced depolarization confirmed the key role of calcium in the release of catecholamine transmitters as well as that in processes regulating the uptake and metabolism of these transmitters. The voltammetric techniques used in the present study may be a useful tool in extending of our knowledge about the cellular mechanisms of stimulus-response coupling in nerve cells.

Animals↗
PubMed1990

Adrenergic regulation of [3H]ketanserin binding sites during immobilization stress in the rat frontal cortex.

Acute immobilization stress increased serotonin and 5-hydroxyindoleacetic acid levels, the 5-hydroxyindoleacetic/serotonin ratio, and the number of [3H]ketanserin binding sites, representing serotonin-2 type receptors, in the rat frontal cortex. Peripheral administration of propranolol or central administration of 6-hydroxydopamine abolished the stress induced elevation of [3H]ketanserin binding sites. Treatment with 6-hydroxydopamine did not affect the increase in serotonin and 5-hydroxyindoleacetic acid levels, and enhanced the increase in the 5-hydroxyindoleacetic acid/serotonin ratio produced by stress. Conversely, chemical serotoninergic denervation with 5,7-dihydroxytryptamine had no influence on the stress-induced elevation of [3H]ketanserin binding sites, but abolished the serotonin and 5-hydroxyindoleacetic acid increase produced by stress. These results suggest that an intact serotoninergic system is not essential for serotonin-2 type receptor regulation during stress. Instead, the noradrenergic system, most probably through stimulation of beta-adrenoreceptors, may control the regulation of [3H]ketanserin binding sites in the rat frontal cortex during acute stress.

Animals↗
PubMed1988

Stressfree administration of drugs by intraperitoneal cannulation in small laboratory animals.

A simple technique of chronic intraperitoneal cannulation in small laboratory animals has been described. It can be used for repeated i.p. administration of drugs without causing any remarkable disturbance to the animal as demonstrated by significantly less increase of corticosterone level compared to usual i.p. injection procedure. A simple device for producing a fixative ring on the cannula in order to hold the cannula in the proper place is described as well.

Animals↗
PubMed1988

Effect of corticosterone treatment and adrenalectomy on phenylethanolamine N-methyltransferase and catecholamines in brain stem and hypothalamic nuclei and superior cervical ganglion of rats.

The effects of corticosterone treatment and adrenalectomy with or without corticosterone replacement on the activity of phenylethanolamine N-methyltransferase (PNMT) and catecholamine content has been studied in isolated brain stem nuclei containing adrenergic and noradrenergic nerve cell bodies, hypothalamic nuclei and in the superior cervical ganglion (SCG) of adult rats. Changes of PNMT activity were found only in a few brain stem areas. In adrenalectomized rats, PNMT activity was decreased in Cl area and in the locus coeruleus, but after corticosterone replacement it returned to the control values. The treatment of rats with corticosterone resulted in a rise of PNMT activity only in C2 area. No significant changes in PNMT activity were seen in the hypothalamic areas in any experimental group of rats. The observed changes of PNMT activity occurred without any measurable changes of noradrenaline (substrate) or adrenaline (product of the reaction catalysed by PNMT). Our results may suggest the involvement of brain stem adrenaline and noradrenaline producing neurons in the central modulation of the pituitary-adrenal function. The basal PNMT activity in SCG of adult rats was very low, but the treatment of rats with high dose of corticosterone or corticosterone replacement to adrenalectomized rats increased PNMT activity in the SCG to the same extent.

Adrenal Glands↗
PubMed1988

3-H-ketanserin (serotonin type 2) binding in the rat frontal cortex: effect of immobilization stress.

The number of 3H-ketanserin (5-HT2) binding sites in rat frontal cortex was estimated in groups of male rats subjected to a single or repeated immobilization stress (IMO). After an acute IMO for 30 or 120 min the number of 5-HT2 binding sites was significantly increased. Similar increase was found even in a group subjected for 120 min IMO for 6 consecutive days and then allowed 24 h rest (i.e. repeatedly stressed controls). If similarly treated animals were subjected to 30 min IMO after 24 h rest, the number of binding sites was increased compared to repeatedly stressed controls, but this was not the case after 120 min IMO. No significant changes of 5-HT2 receptor affinity to 3H-ketanserin were found. The changes of the ratio of 5-hydroxyindolacetic acid/5-hydroxytryptamine were similar to those of binding sites. It was concluded that the enhanced number of cortical 5-HT2 receptor binding sites may result from accelerated serotonin turnover induced by stress, but the results did not indicate any direct association between the serotonin turnover and 5-HT receptor function in the rat frontal cortex.

Animals↗
PubMed1985

Increase in plasma ACTH after dopaminergic stimulation in rats.

The effects of a dopaminergic agonist, apomorphine, and a dopaminergic antagonist, haloperidol, on plasma ACTH, and corticosterone levels were evaluated in adult male rats. Subcutaneous administration of apomorphine in the dose range of 50-500 micrograms X kg-1 significantly increased plasma corticosterone levels. Acute treatment with apomorphine (250 micrograms X kg-1) resulted in an elevation of plasma ACTH concentration, peak values being reached 15 min after the injection. The apomorphine-induced rise in plasma ACTH levels was completely inhibited by pretreatment with haloperidol (1 mg X kg-1). A stimulatory role for dopamine receptors in the control of pituitary ACTH release in the rat is suggested.

Adrenocorticotropic Hormone↗
PubMed1985

Intravenous thiobarbital anaesthesia for determination of liver glycogen phosphorylase activity in rats subjected to various forms of stress.

Glycogen phosphorylase activity was determined in rat livers obtained by laparotomy in thiobarbital (Inactin, PROMONTA) anaesthesia induced by injection of the drug via a polyethylene catheter into a jugular vein as described previously [Németh et al. 1983a]. Intact rats and animals exposed to open field stress without or after i.p. injection of the alpha blocker phentolamine (Regitine, CIBA; 20 mg kg-1, 90 min before stress) or the beta blocker propranolol (Inderal, ICI; 2 mg kg-1, 30 min before stress) were studied. In stressed animals a net increase of phosphorylase activity was observed. This response was abolished after alpha blockade, while after beta blockade it was potentiated. In a further series on animals subjected to the same type of anaesthesia, the activating effect of immobilization stress on phosphorylase activity was confirmed in both fed and fasted animals, the response of the latter issuing from a lower initial level but being of the same extent as in the fed rats.

Animals↗
PubMed1984

Hypertension induced by repeated stress: possible participation of sympathetic-adrenomedullary catecholamines.

Several groups of male Wistar rats weighing 250-300 g were subjected to immobilization stress (IMO) for various intervals (2.5 h to 19 h daily omitting weekends for a total of 2 to 15 weeks). Blood pressure (BP) was measured with the aid of indirect cuff pressure method under routine conditions once weekly during the whole period of immobilization and in some groups also for 10 weeks after the end of this period. It was found that BP significantly increased after 2 weeks of 2.5 h IMO daily and progressively increased later on. There was an indirect relationship between the duration on individual intervals of IMO and the period which was necessary to develop a significant increase of BP. Adrenal medullectomized animals showed a significantly less increase of BP than normal ones during 16 weeks course of IMO. The level of adrenaline and noradrenaline was significantly increased in animals having 24-hour rest after 39th IMO compared to controls, the blood being taken by chronically implanted cannula in a tail artery.

Adrenal Medulla↗
PubMed1982

Changes of plasma and adrenal catecholamines and corticosterone in stressed rats with septal lesions.

The effect of septal lesions on plasma catecholamine and corticosterone (B) levels has been studied in rats during single and 7 times repeated immobilization stress (IMO). Blood samples were obtained via a catheter in the tail artery or by decapitation. The increased circulating epinephrine (EPI) and norepinephrine (NE) levels observed in the initial phase of acute stress as well as the elevated baseline EPI level after six times repeated IMO are indicative of an enhanced response of the sympathetic adrenomedullary system after lesions of the septum. After decapitation of rats with septal lesions there was a significant increase in plasma NE one day after the sixth IMO and a block of EPI increase after the seventh IMO compared to sham-operated rats. The adrenocortical system was similarly found to be activated after septal lesions, exhibiting increased baseline plasma B levels. It has been suggested that the septal region affects the studied systems by exerting an inhibitory tonus. The removal of this inhibitory system results in an increase of adrenocortical and sympathetic-adrenomedullary activities.

Adrenal Glands↗