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E Bíró

Publications and source records attributed to E Bíró.

18 recordsLinked to original sources
PubMed1997

The effects of brain and C-type natriuretic peptides on corticotropin-releasing factor in brain of rats.

The central corticotropin-releasing factor (CRF)-ergic system plays a critical role in anxiety and other behavioral stress responses. It has been shown that atrial (ANP), brain (BNP) and C-type (CNP) natriuretic peptides exert anxiolytic-like effects in behavioral studies. Our previous findings demonstrated that various doses of centrally administered ANP selectively altered the CRF content in different brain areas. In the present study, CRF immunoreactivity was determined in hypothalamic and extrahypothalamic brain regions after central injection of BNP or CNP in rats. A high dose (400 ng) of BNP significantly increased the CRF-like immunoreactivity (CRF-LI) in the hypothalamus and amygdala, while only a tendency towards an increase was found in the hippocampus. In the hypothalamus, the CRF-LI decreased after a high dose (400 ng) of CNP. The CRF-LI increased in the basal forebrain after a low dose (100 ng) of CNP. These results suggest that CRF may be involved in the mediation of some neuroendocrine and behavioral responses to BNP and CNP.

Animals↗
PubMed1997

Time-dependent alterations in corticotropin-releasing factor-like immunoreactivity in different brain regions after acute cocaine administration to rats.

Recent data from various laboratories suggest that the activation of endogenous corticotropin-releasing factor (CRF) may contribute to the behavioral and neuroendocrine effects of cocaine. In the present study, the time-dependent variations in CRF-like immunoreactivity (CRF-LI) in the hypothalamus and several extrahypothalamic brain regions were determined after acute cocaine administration to handled rats. The intraperitoneal injection of 7.5 mg/kg cocaine led to a significantly decreased CRF-LI level in the basal forebrain and to a significantly increased CRF-LI level in the amygdala 60 min after administration, while the CRF-LI content was decreased in the hypothalamus and in the hippocampus 180 min after cocaine treatment. These results suggest that the durations of the effects of cocaine on CRF-LI are in the brain region-specific, which might contribute to the mediation of the diverse behavioral and neuroendocrine effects of cocaine.

Amygdala↗
PubMed1996

Effect of receptor blockers on brain natriuretic peptide and C-type natriuretic peptide caused anxiolytic state in rats.

Effect of different doses of centrally administered brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were examined in rats with respect to anxiolytic properties in an elevated plus-maze model. BNP in doses of 100, 200 and 400 ng, and CNP in doses of 100 and 200 ng abolished the normal preference for the closed arms of the maze, and increased the percentage time spent in the open arms; this is consistent with an 'anxiolytic-like' effect. Doses of 50 and 1000 ng BNP, and of 25, 50, 400 and 1000 ng CNP produced no behavioural effects in the elevated plus-maze model. Pretreatment with an alpha-adrenoreceptor antagonist or a muscarinergic cholinergic blocker, antagonized the effect of 200 ng BNP in the elevated plus-maze test. The 'anxiolytic-like' effects of a BNP were not modulated by a dopaminergic blocker, an alpha-adrenoreceptor antagonist, a GABA receptor antagonist, a 5-HT receptor antagonist or an opiate antagonist. The 'anxiolytic-like' effect of CNP was prevented by a dopamine receptor antagonist, or an alpha- or beta-adrenoreceptor blocker but not by a muscarinergic cholinergic blocker, a GABA receptor, a 5-HT receptor antagonist or an opiate receptor antagonist. These results suggest that multiple neurotransmitter system activation might be responsible for the BNP and CNP-induced 'anxiolytic-like' activity.

Animals↗
PubMed1995

Brain corticotropin-releasing factor mediates 'anxiety-like' behavior induced by cocaine withdrawal in rats.

Anxiety is a key symptom of the cocaine withdrawal syndrome in human addicts, and it is considered to be one of the major factors in precipitating relapse to chronic cocaine abuse. Corticotropin-releasing factor (CRF) plays an important role in the pathophysiology of anxiety and depression, and it may also be involved in the acute behavioral and neuroendocrine actions of cocaine. The role of endogenous CRF in cocaine withdrawal-induced anxiety was investigated in the present study. Animals were subjected to chronic cocaine (20 mg/kg, intraperitoneally, once a day for 14 days) administration. Rats tested 30 min after the last cocaine injection did not show withdrawal anxiety on the elevated plus maze or any alterations in brain CRF levels. Withdrawal (48 h) from chronic cocaine administration produced an intense anxiety-like behavior characterized by decreased open arm exploration. Immunoreactive CRF (CRF-LI) levels were selectively altered in the hypothalamus, in the amygdala and in the basal forebrain structures at the time of the behavioral anxiety, reflecting an increased activity of brain CRF systems. Daily intracerebroventricular (i.c.v.) pretreatment with an immunoserum raised against CRF completely prevented the development of anxiety induced by cocaine withdrawal. These data suggest that extrahypothalamic-limbic CRF hypersecretion may be involved in the development of anxiety related to cocaine withdrawal and that the CRF system may be a useful target for new pharmacotherapies for cocaine withdrawal and relapse.

Animals↗
PubMed1995

Involvement of neurotransmitters in the 'anxiolytic-like' action of atrial natriuretic peptide in rats.

Effects of centrally administered rat atrial natriuretic peptide (ANP1-28) in different doses (50, 100, 150, 200, 500 or 1000 ng) were examined in rats with respect to anxiolytic properties in an elevated plus-maze model. In doses of 100, 150 and 200 ng, ANP1-28 abolished the normal preference for the closed arms of the maze, and increased the percentage of time spent on the open arms; this is consistent with an 'anxiolytic-like' effect. Doses of 50, 500 and 1000 ng of rANP1-28 produced no behavioral effects in the elevated plus-maze model. Pretreatment with a dopaminergic blocker, an alpha-adrenoreceptor or a beta-adrenoreceptor antagonist antagonized the effect of 200 ng ANP1-28 in the elevated plus-maze test. A muscarinergic cholinergic blocker, a GABA receptor antagonist, a 5-HT receptor antagonist and an opiate antagonist were not able to modulate the 'anxiolytic-like' effects of ANP1-28. These results suggest that a multiple neurotransmitter system activation might be responsible for the ANP1-28-induced 'anxiolytic-like' activity.

Animals↗
PubMed1994

The role of central corticoliberin in the hyperosmosis-induced secretion of neurohypophysial hormones and corticosterone in the rat.

Although synthetic corticotropin-releasing hormone (CRH) is known to influence the secretion of the neurohypophysial hormones, the role of endogenous CRH in the rat brain is still unclear in this respect. Accordingly, experiments were scheduled to study the effects of intracerebroventricularly (i.c.v.) administered CRH-antiserum (AS) on the hyperosmosis-induced secretion of arginine-8-vasopressin (AVP), oxytocin (OXT) and corticosterone in Wistar male rats. A 2 microliters CRH-AS injection was given, and repeated 24 h later, 30 min prior to intraperitoneal administration of hypertonic saline (HS; 2.5% NaCl, 2 ml/100 g body weight) followed by decapitation in 15 min. Plasma AVP and OXT were measured by radioimmunoassay and corticosterone by fluorimetry. HS increased the levels of AVP, OXT and corticosterone. CRH-AS did not change the plasma concentrations of these hormones in 0.9% NaCl-treated animals. CRH-AS pretreatment prevented the corticosterone-releasing action of HS, and significantly moderated the HS-induced AVP and OXT increase. These findings suggest that the central CRH system may participate in the regulation of corticosterone and neurohypophysial hormone secretion evoked by acute osmotic challenge.

Animals↗
PubMed1994

The role of central corticoliberin in the ether stress-induced secretion of neurohypophyseal hormones and corticosterone in the rat.

As corticotropin-releasing factor (CRF) and oxytocin (OXT) are released in response to various stressors and a role of CRF in stress-induced OXT secretion has been proposed by previous authors, the present experiments were scheduled to investigate the participation of the brain CRF system in the stress-evoked release of OXT, arginine-8-vasopressin (AVP) and corticosterone. CRF-antiserum (AS) was given into the lateral ventricle of the brain of Wistar male rats, and 24 h later, the injection was repeated 30 min prior to ether stress followed by decapitation in 5 min. Plasma OXT and AVP were measured by radioimmunoassay and corticosterone by fluorimetry. Ether stress increased the levels of corticosterone and OXT, but not that of AVP. CRF-AS alone did not change the secretion of these hormones. CRF-AS pretreatment blocked the corticosterone-releasing action of ether stress, whereas it exerted no influence on the stress-induced OXT secretion into the circulation. There was no effect of a combined application of CRF-AS and stress on the plasma AVP level. These results suggest that the central CRF system is involved in the ether stress-elicited corticosterone response, however CRF is unlikely to be connected with the regulation of OXT secretion under these experimental conditions.

Animals↗
PubMed1993

Alterations of corticotropin-releasing factor-like immunoreactivity in different brain regions after acute cocaine administration in rats.

Corticotropin-releasing factor (CRF) may mediate some of the neuroendocrine and behavioral responses to cocaine. In this study, the distribution of CRF-like immunoreactivity (CRF-LI) was determined in the hypothalamus and in several extrahypothalamic brain regions after acute cocaine administration in handled rats. CRF-LI decreased dose-dependently with cocaine administration in the hypothalamus and in the basal-forebrain structures. A small dose of cocaine (7.5 mg/kg) decreased CRF-LI in the hippocampus and in the frontal cortex. A significant, selective, dose-dependent increase in CRF-LI was found in the amygdala after cocaine injection. None of the investigated doses of cocaine altered CRF-LI in the striatum. These results suggest that acute cocaine administration alters brain CRF systems to contribute behavioral and neuroendocrine responses to cocaine.

Analysis of Variance↗
PubMed1993

[Amanita phalloides poisoning in a 15-year case load of a pediatric intensive care unit].

The clinical course of eight patients with Amanita phalloides poisoning is reviewed. Early diagnosis was based on the history, characteristic clinical features and non-specific laboratory data. A complex supportive therapy with gastric lavage, bowel irrigation, correction of volume and electrolyte abnormalities, and penicillin-G (Penicillin, Biogal), silibinin (Legalon SIL, Madaus), thioctacid (Thioctacid, Asta), corticosteroid (Di-Adreson-F aquosum, Organon) administration was commenced in every cases before identification of the mushroom. Haemoperfusion was performed in six cases, and in one patient plasmapheresis was applied as well. Seven children recovered completely. Unfortunately, a girl of 12 years died. According to the authors' experience, the use of non-invasive and invasive methods of the non-specific detoxication is proposed in case of severe Amanita phalloides poisoning.

Adrenal Cortex Hormones↗
PubMed1993

Cocaine-induced elevation of plasma corticosterone is mediated by different neurotransmitter systems in rats.

It has previously been demonstrated that cocaine stimulates the hypothalamic-pituitary-adrenal (HPA) axis through hypothalamic corticotropin-releasing factor (CRF) secretion. The role of different neurotransmitters in mediation of the cocaine-induced elevation of plasma corticosterone (CORT) were investigated in rats by using transmitter antagonists. Peripheral (IP) pretreatment with a dopaminergic antagonist, pimozide (0.01-1.0 mg/kg, IP), a noradrenergic blocker, phenoxybenzamine (1.0-4.0 mg/kg, IP), a beta-adrenergic blocker, propranolol (0.2-10 mg/kg, IP), an opiate antagonist, naloxone (1.0-4.0 mg/kg, IP), and a muscarinic cholinergic antagonist, atropine (1.0-4.0 mg/kg, IP), inhibited the cocaine-induced CORT response dose dependently. A similar dose-dependent inhibition of the plasma CORT response induced by cocaine was observed after the ICV route of administration of these antagonists in microgram quantities. None of the investigated IP or ICV doses of transmitter antagonists altered the basal CORT level. These results suggest that the activation of multiple neurotransmitter systems, including catecholaminergic, opiate, and cholinergic systems, might be responsible for the cocaine-induced HPA axis activation, probably through the specific receptors located in the CNS.

Animals↗
PubMed1992

The cocaine-induced elevation of plasma corticosterone is mediated by endogenous corticotropin-releasing factor (CRF) in rats.

The role of endogenous corticotropin-releasing factor (CRF) in the cocaine-induced corticosterone response was investigated by using the immunoneutralization and receptor blockade of endogenous CRF. Pretreatment with different dilutions (1:5, 1:10 and 1:20, i.c.v.) of CRF antibody and different doses of an antagonist for CRF receptors, alpha-helical CRF9-41 (alpha h-CRF, 0.001-1.0 micrograms, i.c.v.), dose-dependently prevented the cocaine-induced increase in corticosterone level. These results support the hypothesis that the activation of the hypothalamo-pituitary-adrenal (HPA) axis by cocaine is mediated through the release of endogenous CRF.

Animals↗
PubMed1992

[Reasec poisoning in childhood].

Three cases of severe accidental poisoning with "Reasec" in infants and young children are reported. Patients' medical history, the clinical features and ways of antidote administration are described. In severe poisoning in addition to symptomatic intensive care administration of "Narcanti" in continuous infusion is recommended. The necessity of strict observation and ventilation facilities because of the potential respiratory failure is emphasised.

Accidents, Home↗
PubMed1992

Oxytocin modulates behavioural adaptation to repeated treatment with cocaine in rats.

Behavioural adaptation to and the effects of the neurohypophyseal peptide, oxytocin, on repeated treatment with cocaine were investigated in rats. The content of immunoreactive oxytocin in the plasma, hypothalamus and different limbic structures in the brain were also studied after treatment with cocaine, identical to that used in the behavioural experiment. Repeated administration of cocaine (7.5 mg/kg, s.c.) produced a behavioural tolerance to the stereotyped sniffing-inducing effect of the challenge doses (1.875, 3.75 and 7.5 mg/kg, s.c.) of cocaine on the fifth day, which was demonstrated by parallel shifting of the dose-response and time-effect curves of the test doses of cocaine. The development of tolerance was inhibited by pretreatment with oxytocin (0.05 micrograms, (s.c.), administered before each daily injection of cocaine. A smaller dose of oxytocin (0.005 micrograms, s.c.) had no effect in this model. A decreased amount of immunoreactive oxytocin was detected in the plasma, in the hypothalamus and in the hippocampus, after repeated treatment with cocaine. Replacement of oxytocin by local injection (100 pg) into the ventral hippocampus, before each daily administration of cocaine, prevented the development of tolerance to cocaine. These results suggest that endogenous oxytocin, localized in limbic-forebrain areas, may have an important regulatory role in the development of behavioural changes induced by the repeated administration of cocaine.

Analysis of Variance↗
PubMed1992

Effects of cocaine on the contents of neurohypophyseal hormones in the plasma and in different brain structures in rats.

The effects of acute and chronic cocaine treatments on the levels of the neurohypophyseal hormones oxytocin (OXT) and vasopressin (AVP) in the plasma and in different brain structures in rats were measured by radioimmunoassay (RIA). Acute cocaine treatment had no effect on the level of OXT in the plasma or in the amygdala, but increased OXT contents were measured in the hypothalamus and in the hippocampus. The OXT levels in the basal forebrain structures (including the septum and the nucleus accumbens) were decreased by a single dose of cocaine. The acute injection of cocaine increased the level of AVP in the plasma, and decreased contents of OXT were measured in the amygdala and in the basal forebrain. Repeated treatment with cocaine decreased the level of OXT in the plasma, hypothalamus and hippocampus. The AVP contents were decreased in all of the brain structures investigated, but no change was caused in the plasma level of AVP by repeated injections of cocaine. These results demonstrate complex, region-specific interactions between cocaine and the neurohypophyseal hormones in the brain and in the periphery underlying the alteration in behavioral and autonomic functions caused by acute and chronic cocaine exposure.

Amygdala↗