Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 91 records · Page 5Linked to original sources

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↗

PubMed1992

Effects of brain natriuretic peptide-32 on the extinction of active avoidance behavior in rats. Transmitter-mediated action.

Three doses of porcine brain natriuretic peptide (pBNP-32) were tested in regards to the extinction of active avoidance behavior following injection into the lateral brain ventricle in rats. This peptide delayed the extinction of the active avoidance reflex in a dose-dependent manner. To clarify the involvement of transmitters in the action of the peptide, the animals were pretreated with different receptor blockers in doses that did not affect the behavior of the animals in this learning paradigm. Dopaminergic, cholinergic, and alpha- and beta-adrenergic blockers effectively blocked the delaying action of pBNP-32, whereas GABAergic, serotoninergic, and opiateergic blockers were ineffective. The data suggest that the delaying action of pBNP-32 on the extinction of active avoidance behavior is mediated via dopaminergic and alpha- and beta-adrenergic neuromediations.

Animals↗

PubMed1992

Opposite actions of oxytocin and vasopressin in the development of cocaine-induced behavioral sensitization in mice.

Subchronic administration of cocaine induces behavioral sensitization (increasing hypermotility) to a challenge dose of the drug administered 72 h after the cessation of treatment. The effects of repeated administration of the neurohypophyseal hormones oxytocin (OXT) and arginine8-vasopressin (AVP) on the development of behavioral sensitization induced by subchronic treatment with cocaine were investigated in mice. Repeated treatment of OXT and AVP did not modify the locomotor stimulatory effect of the challenge dose of cocaine in cocaine-naive control animals. OXT in a dose of 0.5 microgram (sc) augmented the cocaine-induced behavioral sensitization. In contrast, AVP (0.005-0.5 microgram/mouse, sc) dose dependently attenuated the development of sensitization to the hypermotility-inducing effect of cocaine. The results suggest that the behavioral sensitization induced by cocaine can be modulated in opposite directions by neurohypophyseal hormones.

Animals↗

PubMed1992

An LH-RH antagonist inhibits the behavioral effects of the agonist D-TRP-6-LH-RH in mice.

The effects of a potent LH-RH receptor antagonist, [Ac-4-Cl-D-Phe1,2,D-Trp3,D-Arg6,D-Ala10]LH-RH (ORG 30276), on the behavioral actions of the LH-RH agonist, D-Trp-6-LH-RH, were studied in mice. The subcutaneous (SC) administration of 100 micrograms/kg D-Trp-6-LH-RH inhibited ambulation in an open-field, produced analgesia in the hot-plate and tail-flick tests. These effects of the agonist were totally antagonized by pretreatment with ORG 30276 at a dose of 100 micrograms/kg SC. In the apomorphine-induced cage-climbing test, both the agonist and the antagonist alone or together suppressed the duration of stereotyped behavior in dose-dependent manner, but, as there was no additive synergism after combined treatments, it seems that the two substances mutually diminish each other's effects. The results indicate that the behavioral effects of the LH-RH agonist can be antagonized by pretreatments with a potent LH-RH antagonist designed to block pituitary LH-RH receptors, with the exception of the suppression of apomorphine-induced cage-climbing, where special type of receptors and/or mechanisms might be involved.

Analgesia↗

PubMed1992

Oxytocin blocks the development of heroin-enkephalin cross-tolerance in mice.

The development of cross-tolerance to an analgesic effect has been observed between a mu-receptor agonist, heroin, and a delta-receptor agonist, Met2-Pro5-enkephalinamide. Repeated treatments with heroin twice a day for 4 days resulted in a decreased nociceptive effect to enkephalin on day 5. The enkephalin dose-response line was shifted to the right, considered a sign of the development of cross-tolerance. Peripheral treatment with oxytocin blocked the development of heroin-enkephalin cross-tolerance. A similar effect was observed after intracerebroventricular administration of oxytocin, supporting our assumption that oxytocin blocks the development of heroin-enkephalin cross-tolerance via CNS mechanisms.

Analgesics↗

PubMed1992

Effects of atrial natriuretic peptide on acute and chronic effects of morphine.

Atrial natriuretic peptide (ANP) is known to participate in different vegetative functions. The aim of the present study was to investigate the influence of ANP on nociception itself, pain sensitivity to morphine, and the development of acute and chronic tolerance to morphine. Morphine withdrawal signs were also evaluated by injecting naloxone. In adult, male NMRI mice, ANP administered SC or ICV did not affect pain sensitivity itself in a heat-radiant tail-flick test. Peptide treatment, however, depressed the acute nociceptive effect of a single dose of morphine (4 mg/kg, SC) after both SC (20-200 ng/animal) and ICV (5, 10, 20, or 200 ng/animal) ANP administration. ANP given SC and ICV attenuated the development of acute morphine tolerance. Acute morphine tolerance was assessed by giving a bolus injection of morphine (60 mg/kg) 24 h before the pain sensitivity to a challenge dose of morphine (4 mg/kg) was measured. ICV treatment with ANP also blocked the development of chronic morphine tolerance, but did not affect the appearance of naloxone-precipitated withdrawal syndromes. ANP seems to act differently on the development of tolerance to and dependence upon morphine.

Animals↗

PubMed1992

Effects of intracerebroventricular administration of calcitonin gene-related peptide on passive avoidance behaviour in rats.

The effects of different doses of calcitonin gene-related peptide (CGRP) on passive avoidance behaviour were studied in male rats following its intracerebroventricular (i.c.v.) administration. Treatment with doses of 200 ng, 300 ng, 500 ng or 1 microgram was performed prior to learning, immediately and 6 h after the learning session and 30 min before the 24 h retention test. CGRP enhanced the avoidance latency in a dose-dependent manner at each time studied, with the exception of 6 h after the learning session. It is concluded that CGRP might be able to lengthen the passive avoidance latency by facilitating learning and memory formation.

Animals↗

PubMed1992

The effects of receptor blockers on brain natriuretic peptide-32-induced action on passive avoidance behavior in rats.

The effects of several doses of porcine brain natriuretic peptide-32 (pBNP-32) administered into the lateral brain ventricle were tested as regards the consolidation of passive avoidance learning in rats. The peptide was found to increase the passive avoidance latency in a dose-dependent manner. In order to clarify which transmitter systems might be involved in the action of pBNP-32, the experimental animals were pretreated with different receptor blockers in selected doses which did not influence the behavioral paradigm. Four of the receptor blockers (haloperidol, atropine, phenoxybenzamine and propranolol) effectively blocked the action of the peptide on the consolidation of passive avoidance learning. The other three (naloxone, bicuculline and methysergide) were ineffective. The results suggest that dopaminergic, cholinergic and alpha- and beta-adrenergic mediations might be involved in the effects of pBNP-32 on the consolidation of passive avoidance learning in rats.

Animals↗

PubMed1992

Structure-activity studies on the effects of atrial natriuretic peptide, brain natriuretic peptide and their analogs on fear-motivated learning behavior in rats.

Our previous studies have demonstrated that rat atrial natriuretic peptide (rANP 1-28) and porcine brain natriuretic peptide (pBNP 1-32) administered into the lateral brain facilitate the consolidation of a passive avoidance response and delay the extinction of an active avoidance response in fear-motivated learning in rats. To study the structure-activity relationships in the same learning processes, the effects of several fragments related to ANP and BNP were investigated following their intracerebroventricular administration to rats. The following peptides were studied: rANP 1-28, rANP 5-28, rANP 5-27, rANP 7-23 (ring), rANP 17-23, hANP 10-28, hANP 15-28, hANP 20-28, hANP 1-28, pBNP 1-32 and pBNP 7-32. The peptides were used in equimolar concentration. Two of the peptides studied, ANP 20-28 and ANP 17-23, were ineffective on the extinction of active avoidance behavior and on the consolidation of passive avoidance learning. They exhibited similar actions. The results showed that small fragments of ANP and BNP can carry the biological activity of ANP and BNP on the central nervous system (CNS). It is likely that the biological active center for ANP lies between amino acids 15 and 23 and it is suspected that the ring structure is not absolutely important for the CNS activity.

Amino Acid Sequence↗

PubMed1992

Effect of atrial natriuretic peptide on dopa potentiation in mice.

The effect of rat atrial natriuretic peptide (ANP1-28) on the pargyline-DOPA potentiation test was studied following its administration into the lateral brain ventricle in mice. Thirty minutes after pargyline pretreatment, three doses of ANP (200, 500, or 1,000 ng/mouse) were administered simultaneously with DOPA and animals were then observed for 2 h. ANP in doses of 500 and 1,000 ng markedly enhanced the effect of DOPA. The maximum intensity of the effect was registered 30-45 min following administration of the peptide. The data suggest that ANP might be regarded as a dopaminergic-modulating agent in the CNS.

Animals↗

PubMed1992

Behavioral effects of atrial and brain natriuretic peptides in rats.

The effects of intracerebroventricular administration of rat atrial natriuretic peptide (rANP-1-28) and porcine brain natriuretic peptide-32 (pBNP-32) on passive and active avoidance behavior and on electroconvulsive shock-induced amnesia were studied in rats. The dose range for both peptides was selected to lie between 0.016 and 0.32 nmol. The two peptides were found to facilitate consolidation of the passive avoidance response, to delay extinction of the active avoidance response, and to prevent electroconvulsive shock-induced amnesia in a similar way. It is suggested that some modulatory functions in the central nervous system of the rat, so far attributed to ANP, may in fact involve a dual control by both ANP and BNP, and there is no difference in the biological activity of the two peptides as far as fear-motivated learning behavior is concerned.

Amnesia↗

PubMed1992

Effects of cocaine and pimozide on plasma and brain alpha-melanocyte-stimulating hormone levels in rats.

The effects of cocaine on rat plasma and brain alpha-melanocyte-stimulating hormone (alpha-MSH) levels have been studied by means of a specific radioimmunoassay. The selected brain areas were the hypothalamus, septum-nucleus accumbens and hippocampus. Cocaine given subcutaneously decreased the alpha-MSH levels in the peripheral blood. Pimozide, a dopaminergic antagonist, had an opposite effect: it increased the alpha-MSH levels in the peripheral blood. Combined treatment with cocaine + pimozide resulted in a decrease in the pimozide-induced increase in alpha-MSH levels in the blood. Cocaine and pimozide or the combination of cocaine + pimozide were ineffective on the alpha-MSH levels in the hypothalamus and septum-accumbens brain regions. In the hippocampus, cocaine in the dose applied induced a slight but not significant decrease in the alpha-MSH level. Pimozide caused a significant decrease in the hippocampal alpha-MSH level which disappeared at 60 min. Cocaine prevented the pimozide-induced depletion of alpha-MSH. The data indicate that cocaine may act as a dopaminergic agonist in the mechanism of control of alpha-MSH secretion from the intermediate lobe of the pituitary. The alpha-MSH levels in the brain are controlled by different mechanisms. In some brain areas, the dopaminergic system has no action; in others the mechanisms might be similar to but slightly different from that in the pituitary.

Animals↗

PubMed1992

Captopril as a modifier of the arachidonate cascade of rat platelets.

The lipoxygenase pathway of arachidonate cascade in the platelets of spontaneously hypertensive rats has been found to be significantly higher than in normotensive animals. Repeated oral administration of Captopril (in drinking water - 200 mg/100 ml) for 14 days resulted in an elevation in the activity of arachidonate cascade in the platelets of treated rats. At the same time the Captopril treatment induced the formation of 12-hydroxy-heptadecatrienoic acid (12-HHT), which molecule is known to be a potent prostacyclin (PGI2) releaser and/or synthesis inducer. PGI2 is one of the most potent vasodilatator molecule in living organisms. The in vitro experiments in rat platelets suggest, that very low doses of Captopril (10(-12) to 10(-10) M) result in a significantly elevated 12-HHT synthesis. Captopril might act through the 12-HHT--PGI2 mechanism, resulting in blood pressure reduction. The lipoxygenase pathway of platelets, the formation of 12-hydroxyeicosatetraenoic acid (12-HETE), was significantly elevated in vitro in the presence of low dose of Captopril (10(-11) and 10(-10) M).

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1991

The effects of atrial natriuretic peptide on active avoidance behavior in rats. The role of transmitters.

Different doses of rat atrial natriuretic peptide (rANP1-28) were tested as regards the extinction of active avoidance behavior following its injection into the lateral brain ventricle in rats. ANP delayed extinction of the active avoidance reflex in a dose-dependent manner. When the animals were pretreated with different receptor blockers in doses which themselves had no action on the extinction of active avoidance behavior, the action of ANP on this paradigm was completely blocked by haloperidol and atropine, whereas phenoxybenzamine/propranolol, naloxone, bicuculline and methysergide were ineffective. The data suggest that ANP delays the extinction of active avoidance behavior, and that cholinergic and dopaminergic transmitter systems might be involved in this action.

Animals↗

PubMed1991

The effects of receptor blockers on atrial natriuretic peptide-induced action on passive avoidance behavior in rats.

In previous experiments, it was shown that rat atrial natriuretic peptide (rANP1-28) is able to increase the passive avoidance latency in a dose-dependent manner in the learning and consolidation phase (3). In order to clarify whether ANP has a direct action on this behavioral paradigm, or whether the action is mediated by neurotransmitters, rats were pretreated with different receptor blockers. The selected doses of the different receptor blockers could themselves not influence the behavioral paradigms. Haloperidol or atropine blocked the action of ANP on the consolidation of the passive avoidance response. Phenoxybenzamine, propranolol, methysergide, bicuculline and naloxone were ineffective. The data suggest that dopaminergic and cholinergic mediations are involved in the action of ANP on the passive avoidance response.

Animals↗

PubMed1991

Selective attenuation of cocaine-induced stereotyped behaviour by oxytocin: putative role of basal forebrain target sites.

The effects of oxytocin (OXT), arginine- and lysine-vasopressin (AVP and LVP) and an OXT-receptor antagonist on cocaine-induced sniffing behaviour were investigated in rats. OXT, but not AVP or LVP injected subcutaneously (s.c.) attenuated cocaine-induced sniffing. The effect of OXT (s.c.) was inhibited by an OXT-receptor antagonist administered intracerebroventricularly (i.c.v.). I.c.v. administration of different doses of OXT in nanogram quantities caused a dose-dependent attenuation of cocaine-induced sniffing. Local cerebral microinjection of OXT into the accumbens nucleus and olfactory tubercle but not into the olfactory nucleus, central amygdaloid nucleus or caudate nucleus, inhibited the cocaine-induced sniffing behaviour. These results demonstrate that OXT selectively attenuates the cocaine-induced stereotyped behaviour through basal forebrain target sites.

Animals↗