Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 109 records · Page 6Linked to original sources

PubMed1991

Central effects of antiserum against human atrial natriuretic polypeptide on water and electrolyte metabolism and plasma arginine-8-vasopressin level in conscious rats.

Although synthetic atrial natriuretic polypeptide (ANP) is known to influence the water and electrolyte metabolism and arginine-8-vasopressin (AVP) secretion, the physiological role of endogenous ANP in the rat brain is still unclear. Accordingly, an investigation was made of the effects of intracerebroventricular (icv) administration of human h-ANP antiserum, which can neutralize endogenous ANP, on the water intake, urine output, urinary excretion of potassium and sodium, and plasma AVP level in normally hydrated rats. Apart from the water intake, all the parameters were also determined in 48-h water-deprived rats after h-ANP antiserum treatment. The icv administration of the h-ANP antiserum significantly increased the spontaneous water intake, urine output and urinary potassium excretion in rats given water ad libitum. These effects developed by 24 h after icv treatment. The h-ANP antiserum had no effect on the urine volume in 48-h water-deprived rats, suggesting a primary effect of endogenous ANP in the brain on the spontaneous water intake in rats given water ad libitum. These results suggest that ANP may have a physiologically important role in the central regulation of the water and electrolyte metabolism. The h-ANP antiserum did not alter the basal and dehydration-induced AVP release. This raises the possibility that the endogenous ANP in the brain may not participate in the control of AVP secretion.

Animals↗

PubMed1991

The effects of atrial natriuretic peptide on the open-field activity of rats. The role of neurotransmitters.

In the present study, four doses (50, 100, 200 or 500 ng per animal) of rat atrial natriuretic peptide (rANP1-28) were tested on the open-field activity of rats following i.c.v. application of the peptide. ANP in doses of 200 ng or 500 ng/rat significantly increased the ambulation activity 15 min after the treatment. However, the effect was transitory; 30 min after application it was no longer observed. When the experimental animals were pretreated with different receptor blockers in doses which per se could not affect the behavioral paradigm, the effect of ANP was completely blocked by haloperidol (a dopaminergic blocking agent), phenoxybenzamine (an alpha-adrenergic blocker) and propranolol (a beta-adrenergic blocker). Atropine, naloxone, bicuculline and methysergide were ineffective. These results suggest that dopaminergic and adrenergic transmitter systems are involved in the ANP-induced locomotor activity of rats.

Animals↗

PubMed1991

The effects of atrial natriuretic peptide on electroconvulsive shock-induced amnesia in rats. Transmitter-mediated action.

Electroconvulsive shock (ECS) applied immediately after passive avoidance learning in rats caused partial amnesia. This could be prevented by administering r-ANP into the lateral brain ventricle. The effects of pre-treatment with different receptor blockers: (haloperidol, atropine, phenoxybenzamine, propranolol, naloxone, bicuculline and methysergide) on the ANP-induced antiamnesia were investigated. The receptor blockers per se in the doses selected had no influence on the ECS-induced amnesia. Haloperidol, atropine and propranolol blocked the antiamnestic action of the peptide, while phenoxybenzamine, naloxone, bicuculline and methysergide were ineffective. The results confirm our previous observations that ANP might play a role in learning and memory processes and also suggest that the antiamnestic action of the peptide is mediated by dopaminergic, cholinergic and beta-adrenergic mediator systems.

Amnesia↗

PubMed1991

The effects of atrial natriuretic peptide on passive avoidance behaviour in rats.

The effects of rat atrial natriuretic peptide (ANP 1-28) on passive avoidance behaviour were tested following its administration into the lateral brain ventricle in rats. Different doses of ANP 1-28 were administered immediately after the learning trial of passive avoidance behaviour and the effects on the consolidation of learning were tested 24 h later. ANP 1-28, in doses in the range 50-2000 ng/rat, caused a dose-dependent increase in passive avoidance latency. Selected doses (100, 200 and 500 ng/animal) were given 30 min before the learning trial. These doses lengthened the passive avoidance latency in a dose-dependent manner. When the peptide was given 30 min before the retention trial, there was no significant alteration in passive avoidance response. The data suggest that ANP 1-28 is able to facilitate the learning and consolidation of fear-motivated passive avoidance behaviour.

Animals↗

PubMed1991

Bimodal effect of neuropeptide Y on feeding, and its antagonism by receptor blocking agents in rats.

Satiated rats received intracerebroventricular (icv.) injections of several doses of neuropeptide Y (NPY) and the food intake was measured in the following 4 h. The peptide exerted a dose-dependent biphasic effect; the 100 dose significantly suppressed the food intake, but doses of 1 microgram and 5 micrograms stimulated feeding. After the injection of 2 microliters NPY-antiserum (icv., 1:50 dilution), the cumulative food intake decreased significantly in the first 24 h. From the drugs tested the alpha-1-antagonist prazosine (4 micrograms icv.) and the opiate antagonist naloxone (NX, 0.5 micrograms, icv.) selectively inhibited the feeding-stimulatory effect a high icv. dose of NPY. The alpha-2-antagonist yohimbine (4 micrograms icv.) and the non-selective beta-antagonist propranolol (5 micrograms icv.) did not influence either effect of NPY on feeding. The results suggest the involvement of alpha-1-adrenergic and opiate receptors in the food intake-stimulatory effect of a large icv. dose of NPY. The food intake-inhibitory effect of a low icv. peptide dose was not selectively antagonized by the receptor blocking agents used.

Animals↗

PubMed1990

Partial reversal of behavioral action of the agonist D-Trp-6-LH-RH by naloxone in mice.

The effects of the superactive agonist analog D-Trp-6-LH-RH were investigated in several neuropharmacological tests: inhibition of picrotoxin-induced seizures, open-field behavior, hot-plate and tail-flick tests, assessment of catalepsy and apomorphine-induced cage-climbing. In most tests, D-Trp-6-LH-RH was administered subcutaneously (sc.) at the dose of 100 micrograms/kg. The opiate involvement in the peptide action was checked by using naloxone HCl (NX) in a dose of 1 mg/kg intraperitoneally (ip.), with the exception of the analgesic tests where the dose was 0.5 mg/kg. The analog significantly suppressed the open-field parameters of ambulation, rearing and grooming; except for grooming, these actions were fully antagonized by NX. Similarly, NX pretreatment restored to the control levels the latencies of seizure parameters increased by D-Trp-6-LH-RH. The hot-plate latencies did not change after pretreatment with NX but the opiate antagonist was fully able to antagonize the analgesic effect of the peptide in the tail-flick test. The cataleptogenic effect and the inhibition of apomorphine-induced cage-climbing demonstrated after D-Trp-LH-RH were not antagonized by NX.

Animals↗

PubMed1990

The role of oxytocin-dopamine interactions in cocaine-induced locomotor hyperactivity.

Cocaine is a widely used drug of abuse. One of the characteristic effects of this stimulant drug in the CNS of mice is the induction of motor hyperactivity. It was demonstrated that cocaine-induced motor hyperactivity could be blocked by pimozide, a dopamine receptor blocker, suggesting that dopamine was involved in cocaine-induced hyperactivity. Oxytocin, a neurohypophyseal neuropeptide, also partially antagonized cocaine-induced motor hyperactivity. Moreover, oxytocin antagonized the increased utilization of dopamine, elicited by cocaine in the nucleus accumbens. The data suggest that oxytocin may influence the behavioural effects of cocaine by affecting dopaminergic neurotransmission in some regions of the brain.

Animals↗

PubMed1990

The effects of somatostatin and somatostatin antiserum on the retention of passive avoidance behavior after neofrontal decortication in rats.

Rats were tested for passive avoidance behavior in a one-trial step-through learning paradigm. After the learning trial, the animals underwent neofrontal decortication or sham operation. On the 8th day after operation, the lesioned or sham-operated rats received intracerebroventricular (ICV) injections of somatostatin (SST; 4 micrograms/2 microliters) or somatostatin antiserum (SST-AB; 2 microliters) 1 hr before the retention test. Decortication alone decreased the latency in comparison to that in the sham-operated group, and ICV treatment did not influence this impairment. After treatment with SST-AB the latency decreased, indicating that endogenous SST may play a role in the maintenance of normal memory processes.

Animals↗

PubMed1990

Neuropharmacological actions of the superactive agonist analog D-TRP-6-LH-RH after peripheral injection into mice.

The neuropharmacological actions of the agonist analog D-Trp-6-LH-RH were investigated in several tests after subcutaneous administrations to male mice. The doses applied were in the range 1-1000 micrograms/kg. D-Trp-6-LH-RH doses of 10 micrograms/kg and higher induced significant analgesic effects in the hot-plate and tail-flick tests, and decreased the open-field parameters (ambulation, rearing, grooming). The 100 and 1000 micrograms/kg doses increased the latencies of picrotoxin-induced seizures, significantly inhibited apomorphine-induced cage climbing and also exerted a cataleptogenic effect. The results indicate that this agonist analog of LH-RH has an inhibitory effect on the central nervous system, and the mechanism of its action may involve dopaminergic transmission and/or endogenous opiates.

Analgesia↗

PubMed1990