PubMed Health⌕ Search

Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 19 recordsLinked to original sources
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↗
PubMed1994

CGRP prevents electroconvulsive shock-induced amnesia in rats.

The effects of calcitonin gene-related peptide (CGRP) on electroconvulsive shock (ECS)-induced amnesia and the possible involvement of neurotransmitters in this action were studied in rats. ECS-induced amnesia was elicited in a passive avoidance paradigm. The possible roles of different transmitters involved in mediating CGRP action were followed by pretreating the animals with different receptor blockers in doses which themselves could not influence the paradigm. CGRP facilitated learning in the passive avoidance paradigm and prevented ECS-induced amnesia in a dose-dependent manner. Pretreatment with atropine, naloxone, phenoxybenzamine, or propranolol blocked the antiamnesic action of CGRP. Other receptor blockers, such as bicuculline, methysergide, and haloperidol, were ineffective. The results support our previous findings that CGRP facilitates passive avoidance learning and prevents ECS-induced amnesia. In the antiamnesic action of CGRP, cholinergic, opiate, and alpha- and beta-adrenergic mediators are involved.

Amnesia↗
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

Behavioural impairment induced by calcitonin gene-related peptide (CGRP) antiserum in passive avoidance reflex in rats.

The effects of CGRP antiserum on passive avoidance behaviour were tested in rats. Intracerebroventricular (i.c.v.) administration of CGRP antiserum immediately after a single learning trial attenuated the passive avoidance responses when the animals were tested for 24 h retention. Significant decreases in avoidance latency were found at CGRP antiserum dilutions of 1:20 and 1:40. The data supported the assumption that endogenous brain CGRP may be a modulator in learning-associated memory processes.

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↗
PubMed1994

Modulation of active avoidance behavior of rats by ICV administration of CGRP antiserum.

The effects of ICV administration of CGRP antiserum on active avoidance behavior were studied in rats. CGRP antiserum dilutions of 1:5, 1:10, 1:20, and 1:40 facilitated the extinction of active avoidance responses in a platform-jumping situation in the 3- and 6-h tests. In the 24-h test, only the CGRP antiserum dilution of 1:5 was effective. The present findings suggest that the endogenous CGRP of the brain may be a physiological modulator in extinction processes of active avoidance behavior.

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

The effects of brain natriuretic peptide-32 on electroconvulsive shock-induced amenesia in rats. The role of neurotransmitters.

Partial amnesia was induced in rats by electroconvulsive shock (ECS) immediately after passive avoidance learning. This partial amnesia could be prevented by administering porcine brain natriuretic peptide-32 (pBNP-32) into the lateral brain ventricle. The effects of pretreatment with different receptor blockers (haloperidol, atropine, phenoxybenzamine, propranolol, naloxone, bicuculline and methysergide) on the pBNP-32-induced antiamnesia were investigated. In the doses selected, the blockers had no influence on the ECS-induced amnesia. Haloperidol, atropine, phenoxybenzamine and propranolol blocked the antiamnesic action of the peptide, while naloxone, bicuculline and methysergide were ineffective. These results suggest that pBNP-32 may influence learning processes and that the antiamnesic action of this peptide is mediated by dopaminergic, cholinergic alpha- and beta-adrenergic mediator systems.

Amnesia↗
PubMed1993

The effects of atrial natriuretic peptide on food-reinforced conditioning in rats. Interactions with neurotransmitters.

The effects of two doses of rat atrial natriuretic peptide (TANP-1-28), 200 and 500 ng, on 6-day acquisition and extinction of food-reinforced conditional learning (conditional stimulus: light) were studied in rats following administration into the lateral cerebroventricle. With the higher dose, there was a tendency for facilitated acquisition and significantly delayed extinction of the positively reinforced learning task. In order to clarify whether the effect of the peptide is obtained through the involvement of neurotransmitters, the experimental animals were pretreated with different receptor blockers in selected doses that did not influence the behavioral test. Haloperidol, atropine, phenoxybenzamine, and propranolol blocked the action of ANP on extinction of the food-reinforced conditioning, whereas naloxone, bicuculline, and methysergide were ineffective. The results suggest that ANP might be considered a modulating agent in a positively reinforced conditional learning task, and that its action might involve dopaminergic, cholinergic, and alpha- and beta-adrenergic mechanisms.

Animals↗
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

Anticonvulsive effects of galanin administered into the central nervous system upon the picrotoxin-kindled seizure syndrome in rats.

Galanin (2000, 1000 ng) administered into the lateral brain ventricle decreased the severity of picrotoxin-kindled convulsions in rats. The bilateral injection (200, 100 and 50 ng) of galanin into the hippocampus also evoked an anticonvulsive effect. When administered into the caudate nuclei or substantia nigra reticulata, galanin exerted anticonvulsive action only in a high dose (200 ng), whereas in the nucleus accumbens it did so in a low dose (50 ng). When administered into the ventral tegmental area in a dose of 50, 100 or 200 ng galanin failed to reduce the manifestations of picrotoxin-kindled seizures.

Animals↗
PubMed1992

Effect of atrial natriuretic peptide on apomorphine-induced stereotyped cage-climbing behavior in mice.

In previous experiments, it was observed that rat atrial natriuretic peptide-(1-28) (ANP-(1-28)) participated in fear-induced learning and memory processes via dopaminergic and cholinergic mediation. Since cage-climbing behavior is described as a simple test for studying dopaminergic activity in the central nervous system, a systemic study was carried out with ANP-(1-28) in order to confirm or to exclude the possible involvement of dopamine in the ANP-induced action in the brain. The present study demonstrate that ANP-(1-28) facilitated cage-climbing behavior in mice in a dose-dependent manner. When combined with apomorphine, the peptide potentiated the effect of the dopamine agonist. The effect of ANP-(1-28) in combination with apomorphine could be antagonized by a selected dose of haloperidol. These data suggest that ANP might be regarded as a dopamine agonist-modulating agent and that a dopaminergic mechanism is a possible mode of action of ANP in the fear-induced learning studied earlier.

Animals↗
PubMed1992

Dietary manipulation with high marine fish oil intake of fatty acid composition and arachidonic acid metabolism in rat cerebral microvessels.

Male weanling Wistar rats were maintained on one of two semisynthetic diets, differing only in the type of oil used: (i) 10% by weight marine fish oil (MFO group) containing 20% eicosapentaenoic acid (EPA) and 17% docosahexaenoic acid (DHA), or (ii) 10% by weight sunflower oil (SFO group). The control group was kept on standard diet for 4 weeks. Blood-free microvessels were isolated from brain cortex by a rapid micromethod, and their fatty acid composition was determined by gas chromatography. It was found that the proportion of n-3 fatty acids (including EPA and DHA) increased significantly in the microvessels of the MFO group, accompanied by a decrease of the n-6 fatty acid series. The changes in fatty acid composition of endothelial cells were not significant in the SFO group in comparison to the control. The amounts of lipoxygenase and cyclooxygenase metabolites were determined. Dietary fish oil decreased the percentage of total products of arachidonate by 50%, while the SFO diet had no effect on it. The amount of lipoxygenase products in the MFO group decreased significantly from 16931 +/- 3131 dpm to 6399 +/- 357 dpm/300 mg wet weight of brain. Significantly less PGF-1 alpha, PGF-2 alpha and 12-hydroxyheptadecatrienoic acid (HHT) were found in the capillaries of MFO treated animals, in comparison to the SFO group. The ratios of vasoconstrictor and vasodilator metabolites of arachidonate cascade were not modified by the diets. Our results suggest that fish oil diet reduces the arachidonate cascade in cerebral microvessels. This effect may explain for the efficiency of n-3 fatty acids in vascular diseases.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of somatostatin and anti-somatostatin serum on picrotoxin-kindled seizures.

The effects of somatostatin, administered into different areas of the brain were studied in preliminary picrotoxin-kindled rats. The injection of somatostatin into the lateral ventrical of the brain (i.c.v.) (1.8 nmol), the hippocampus (0.6 nmol) or the amygdala (0.6 nmol), resulted in a decrease in the severity of the picrotoxin-induced convulsions. Application of the peptide into the caudate-putamen or the substantia nigra reticulata did not alter the behavioural manifestations of the kindled seizures. The local injection of anti-somatostatin serum (1:5) into the hippocampus increased the severity of the kindled convulsions and blocked the anticonvulsive effect of somatostatin, given intraventricularly. Local administration of anti-somatostatin serum into the amygdala did not alter the kindled seizures and did not abolish the anticonvulsive action of somatostatin given intraventricularly. It is concluded that somatostatin could take part in endogenous control of seizures through a suppressant influence on limbic structures; the hippocampus could be a specific site for the antiepileptic action of somatostatin.

Animals↗
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

Behavioral effects of centrally administered LH-RH agonist in rats.

The neuropharmacological actions of the agonist analog D-Trp-6-LH-RH were investigated in several tests after intracerebroventricular (ICV) administrations to male rats. The doses applied were 10, 100 and 1000 ng/animal. In the open field the 1000 ng ICV dose of the peptide D-Trp-6-LH-RH suppressed the ambulation, rearing and grooming. In a combined catalepsy test, the 10 ng and 1000 ng dose of D-Trp-6-LH-RH increased the total duration of immobility. The LH-RH agonist inhibited stereotyped behavior induced by both apomorphine and amphetamine, and the effects of 100 and 1000 ng D-Trp-6-LH-RH were significant. Naloxone in a dose of 0.5 mg/kg IP totally abolished the inhibition of apomorphine-induced stereotypy by 1000 ng D-Trp-6-LH-RH, but the opiate antagonist did not influence amphetamine-induced stereotypy but significantly potentiated the inhibitory effect of 100 ng D-Trp-6-LH-RH. In the tail-flick test the latencies were significantly increased after D-Trp-6-LH-RH ICV, both 20 or 40 min after the injections. The peptide-induced analgesia was totally naloxone reversible. The results indicate that the agonist analog of LH-RH exert potent actions on the central nervous system, and the mechanism of effects may involve dopaminergic transmission and/or endogenous opiates.

Animals↗