Biomedical subjects

L Vécsei

Publications and source records attributed to L Vécsei.

At least 91 records · Page 5Linked to original sources

PubMed1988

The effects of different receptor blockers on the H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH induced inhibition of extinction of active avoidance behaviour.

H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH after intracerebroventricular (icv.) administration inhibited the extinction of active avoidance behaviour for a short period. The dopamine receptor blocker haloperidol completely blocked this effect of the heptapeptide, while the muscarinic anticholinergic agent atropine only partly inhibited it. The alpha 1-receptor blocker phenoxybenzamine and the beta-receptor blocker propranolol did not significantly influence the extinction inhibition induced by the peptide. These results suggest that the dopaminergic and, in part the cholinergic system, play important roles in this behavioural action of H-Phe-Ile-Tyr-Ser-Tyr-Lys-OH.

Adrenergic alpha-Antagonists↗

PubMed1987

Correlation between blood pressure and the level of monoamines in the cerebrospinal fluid of patients with cerebral haemorrhage. Case reports.

The correlation between the noradrenalin (NA), dopamine (DA) and serotonin (5-HT) contents of cerebrospinal fluid (CSF) samples obtained from the cerebro-ventricular space and the systolic and diastolic blood pressure (BP) of two patients with cerebral haemorrhage were investigated. Significant correlation was found between CSF NA, CSF DA level and systolic BP in case I. There was no correlation between CSF catecholamine levels and diastolic BP and between serotonin level and BP. Significant correlation was observed in case II between CSF DA level and diastolic BP. There was no correlation between CSF serotonin level and BP. These results suggest that CSF catecholamines might play some role in the regulation of BP.

Adult↗

PubMed1987

The effect of "facteur thymique serique" (FTS) on catecholamine and serotonin neurotransmission in discrete brain regions of mice.

The dose-related effect of Facteur Thymique Serique (FTS) on hypothalamic, mesencephalic and striatal neurotransmission were investigated after intracerebroventricular (icv) administration. FTS pretreatment with dose of 1 microgram (icv) increased the mesencephalic serotonin content, while failed to influence the hypothalamic and striatal serotonin levels. The nonapeptide in a dose of 0.1 microgram (icv) decreased the hypothalamic, while in a dose of 1 microgram the hypothalamic and also the mesencephalic dopamine content, but did not influence the striatal dopamine level. FTS in a dose of 1 microgram (icv) significantly decreased the hypothalamic noradrenaline level, but did not influence the noradrenaline content of the mesencephalon and striatum. These results suggest that FTS is able to modify central neurotransmission.

Animals↗

PubMed1986

Somatostatin and (D-Trp8, D-Cys14)-somatostatin delay extinction and reverse electroconvulsive shock induced amnesia in rats.

In the present study the effects of somatostatin and its analogs on active avoidance behavior, electroconvulsive shock (ECS)-induced retrograde amnesia, and spatial-discrimination learning were compared in rats. (D-Trp8, D-Cys14)-somatostatin (as did the somatostatin molecule itself) delayed the extinction of active avoidance behavior, antagonized ECS-induced amnesia, and did not modify spatial-discrimination learning. Des-Asn5-(D-Trp8, D-Ser13) somatostatin and des-AA1,2,4,5,12,13,-(D-Trp8) somatostatin did not influence these behaviors. The data suggest that certain parts of the somatostatin molecule are important for its behavioral actions.

Amnesia↗

PubMed1986

Correlation between monoamine content and other parameters of cerebrospinal fluid in aneurysmal subarachnoid haemorrhage: a case report.

The monoamine content and other parameters of cerebrospinal fluid (CSF) were studied in aneurysmal subarachnoid haemorrhage (ASH). The blood content of CSF was determined by the protein concentration and cell count, while the haemostatic status of the patient was characterized by the prothrombin level of blood. The serotonin content of CSF was elevated at the beginning of ASH (high protein content and fresh blood cells in CSF, and low level of prothrombin in blood). Later the level of serotonin and protein of CSF decreased, while the prothrombin level of blood increased. During rebleeding on the 20th day after admission, the CSF serotonin and protein content increased again, while the prothrombin level of blood was decreased. The dopamine and noradrenaline levels of CSF markedly decreased on the 11th day after ASH, but in the following days these parameters returned to the control level. The findings suggested that the serotonin content of CSF originated mainly from extravasated blood. The decreased level of dopamine and noradrenaline 11 days after ASH might be connected with increased blood viscosity, decreased peripheral blood pressure or other changes.

Cerebrospinal Fluid Proteins↗

PubMed1985

Effects of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on different behavioral tests of rats.

H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH inhibited the extinction of active avoidance behavior 3 h and 6 h after administration and facilitated the learning of a T-discrimination task. The peptide antagonized ECS-induced amnesia, if the treatment was performed 1 h before the test session. These results suggest that H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH can facilitate learning and memory processes.

Amnesia↗

PubMed1985

The role of central dopaminergic systems in the behavioral effects of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH.

In the present study the role of the central dopaminergic systems in the behavioral action of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH was investigated. The heptapeptide inhibited the extinction of active avoidance behavior if the treatment was performed intracerebroventricularly (icv) in a dose of 1 microgram, but was ineffective in a dose of 0.1 micrograms. If the peptide was injected into the nucleus accumbens septi (NAS) in a dose of 1 microgram, 0.1 micrograms or 0.01 micrograms it inhibited the extinction, but in the latter dose its effect was only a short one. H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH in a dose of 1 microgram, 10 micrograms or 20 micrograms (icv) did not influence the turning activity of unilateral substantia nigra (USN)-lesioned animals. These results suggest that the NAS plays an important role in the behavioral action of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH and the heptapeptide has no direct dopamine receptor stimulatory or dopamine-releasing effect in the striatum.

Animals↗

PubMed1985

The role of the nucleus accumbens septi (NAS) in the behavioral action of beta-(Tyr9)melanotropin-(9-18).

In this study the effects of beta-(Tyr9)MSH-9-18 administered intracerebroventricularly (icv) or into the nucleus accumbens septi (NAS) were investigated on active and passive avoidance behavior of rats. This hypothalamic decapeptide in a dose of 1.0 microgram (icv) inhibited the extinction of active avoidance behavior however, in a dose of 0.1 microgram (icv) it was ineffective. The peptide injected into the NAS in a dose of 0.1 microgram had a same inhibitory effect but in a dose of 0.01 microgram this inhibitory effect was only a short lasting one. In the passive avoidance behavior the peptide in a dose of 1 microgram and 0.1 microgram (icv) significantly increased the passive avoidance latency, but in a dose of 0.01 microgram it was ineffective. If the same doses of the decapeptide were injected into the NAS the peptide was ineffective. These results suggest that the NAS doses not play a role in the memory effect of beta-(Tyr9)MSH9-18 and memory compound does not participate in the NAS mediated effect of the decapeptide on the active avoidance behavior.

Animals↗

PubMed1985

Dose-related effects of cysteamine treatment on hypothalamic and striatal dopamine, noradrenaline and serotonin neurotransmission.

The dose-related effects of cysteamine treatment on hypothalamic and striatal neurotransmission were investigated. Cysteamine pretreatment with a dose of 150 mg/kg slightly increased the dopamine, and markedly decreased the noradrenaline, content of the hypothalamus in a dose-related manner. The serotonin levels of the hypothalamus and striatum were not affected. Cysteamine pretreatment with a higher dose (300 mg/kg sc) slightly increased the uptake of noradrenaline into hypothalamic slices. The drug did not influence dopamine and serotonin uptake into hypothalamus and striatal slices. These results suggest that cysteamine decreases rather selectively the noradrenaline content of the hypothalamus.

Analysis of Variance↗

PubMed1985

Selective decrease of hypothalamic noradrenaline by cysteamine.

In dose studies, cysteamine pretreatment in a dose of 200 mg/kg or 300 mg/kg (subcutaneously, s.c.) markedly decreased the hypothalamic noradenaline content, but did not influence the dopamine and serotonin contents. In time studies, pretreatment with cysteamine in a dose of 300 mg/kg (s.c.) led to markedly decreased hypothalamic noradrenaline contents 4 hr, 8 hr and 12 hr after treatment. These results suggest that cysteamine treatment selectively decreases the hypothalamic noradrenaline content in dose- and time-related manners.

Animals↗

PubMed1984

Phenoxybenzamine antagonizes somatostatin-induced antiamnesia in rats.

The effects of pretreatment with atropine, haloperidol and phenoxybenzamine on somatostatin-induced antiamnesia were investigated. Somatostatin itself blocked electroconvulsive shock (ECS)-induced amnesia. The receptor blockers per se had no influence on the ECS-induced avoidance latency. Atropine and haloperidol did not inhibit somatostatin-induced antiamnesia, whereas phenoxybenzamine blocked it completely. The results suggest that the central noradrenergic system plays an important role in the mediation of the antiamnesic action of somatostatin.

Animals↗

PubMed1984

Effects of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on the in vitro uptake and release of radiolabelled dopamine, noradrenaline and serotonin in rat brain hypothalamic slices.

The effects of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH, a hypothalamic heptapeptide with weak CRF activity were investigated on the in vitro uptake and release of radiolabelled dopamine (DA), noradrenaline (NA) and serotonin (5-HT) in rat brain hypothalamic slices. In a doses of 5 X 10(-6) M and 10(-5) M the heptapeptide significantly increased the 5-HT uptake, whereas it had no effect on the DA and NA uptakes. The same doses (5 X 10(-6) M, 10(-5) M) significantly increased the DA release without affecting the NA and 5-HT release. These results suggest that H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH as a hypothalamic peptide is able to modulate selectively the activity of the serotonergic and dopaminergic transmission without influencing the noradrenergic system in the hypothalamus.

Animals↗

PubMed1984

The effects of somatostatin, its fragments and an analog on electroconvulsive shock-induced amnesia in rats.

In the present study the effects of intracerebroventricularly [icv] administered somatostatin [linear and cyclic], somatostatin3-6, somatostatin7-10 and des AA1,2,4,5,12,13 [D-Trp8] somatostatin [ODT8-SS] were investigated on electroconvulsive shock [ECS]-induced retrograde amnesia in rats. The ECS significantly decreased the foot shock-induced avoidance latency, and thus caused retrograde amnesia. Somatostatin [linear and cyclic] in a dose of 0.6 nM had no action on the ECS-induced retrograde amnesia, while in doses of 3 nM and [cyclic only] 6 nM it significantly prevented it. Somatostatin3-6, somatostatin7-10 and ODT8-SS in doses of 0.6, 3 and 6 nM had no effect on the ECS-induced amnesia. These results indicate that the whole sequence of the original somatostatin molecule is needed to block the ECS-caused retrograde amnesia.

Amnesia↗

PubMed1984

The effect of beta-(Tyr9)melanotropin-(9-18) on the active avoidance and open-field behavior on rats pretreated with atropine or propranolol.

beta-(Tyr9)melanotropin-(9-18) inhibited the extinction of active avoidance behavior. The muscarinic cholinergic blocker atropine did not influence the peptide-induced inhibition, whereas the beta-receptor blocker propranolol decreased it. Furthermore, the peptide increased the ambulation of the animals. Neither the muscarinic blocker nor the beta-blocker had any action on this effect of beta-(Tyr9)melanotropin-(9-18). Atropine markedly decreased the defecation of the animals, and this effect was not influenced by the peptide. The results suggest that the beta-receptors play an important role in the inhibition of extinction induced by the peptide, however, the actions on the open-field activity are mediated by different mechanisms.

Animals↗

PubMed1984

Comparative studies with beta-(Tyr9)melanotropin-(9-18) and amphetamine on open-field behavior and striatal dopamine uptake and release.

The effect of beta-(Tyr9)melanotropin-(9-18) and amphetamine on the open-field behavior and the striatal dopamine uptake and release were compared. beta-(Tyr9)melanotropin-(9-18) at doses of 1 microgram (icv) or 2 micrograms (icv) increased the ambulation of the rats, while in a dose of 5 micrograms (icv), it had no effect. Amphetamine had a similar dose-related effect on ambulation. This peptide also increased the rearing activity, in doses of 2 micrograms or 5 micrograms (icv), while amphetamine was effective only in a dose of 2 micrograms (icv). beta-(Tyr9)melanotropin-(9-18) at doses of 1 microgram, 2 micrograms or 5 micrograms (icv) increased the grooming, while amphetamine at the same doses decrease it. The peptide had no significant influence on the striatal dopamine uptake and release, whereas amphetamine markedly decreased the uptake and facilitated the release in a dose-related manner. These results suggest that although beta-(Tyr9)melanotropin-(9-18) and amphetamine have similar effects on the open-field behavior, the mechanisms of action of the two substances are different.

Amphetamine↗

PubMed1984

Comparative studies with somatostatin and cysteamine in different behavioral tests on rats.

In the present study the effects of somatostatin and cysteamine (a selective decreaser of the somatostatin level in the body) were compared in different behavioral tests on rats. Somatostatin inhibited the extinction of active avoidance behavior 8 hr and 24 hr after intracerebroventricular (ICV) treatment, while cysteamine facilitated it 4 hr and 8 hr after subcutaneous (SC) treatment. Somatostatin did not significantly influence the cysteamine-induced facilitation of the extinction. Somatostatin did not have a significant effect on T-maze spatial discrimination learning and reverse learning, whereas cysteamine markedly attenuated the performance 4 hr (1st day) after treatment. Somatostatin in a dose of 4 micrograms (ICV) increased the locomotor activity 10 min after treatment, while cysteamine markedly decreased all parameters of the open-field test. These effects of the drug had disappeared 24 hr after treatment. If different doses of somatostatin (4 micrograms or 10 micrograms ICV) were administered to cysteamine-pretreated rats, the peptide did not modify the drug-induced changes in the open-field test. The data suggest that the brain somatostatin might have a physiological role in the organization of certain types of behavior.

Animals↗

PubMed1984

Effect of somatostatin and its fragments on turning behaviour induced by unilateral substantia nigra lesion in the rat.

The effect of somatostatin and its two tetrapeptide fragments was investigated on turning activity induced by unilateral substantia nigra lesion in rats. Somatostatin in a dose of 0.6 nM had no action on the turning behavior, while a dose of 6 nM increased slightly while a dose of 12 nM significantly the contralateral turning. Cys-Lys-Asn-Phe and Phe-Trp-Lys-Thr had no action in low or high doses on the turning activity of the animals. The results suggest that somatostatin has a direct postsynaptic dopamine receptor stimulating effect. It seems that for dopamine receptor stimulating action the complete somatostatin molecule is needed.

Amphetamines↗

PubMed1983

The effect of somatostatin on self-stimulation behavior in atropine- and methysergide-pretreated rats.

The effect of somatostatin on lateral hypothalamic self-stimulation was investigated in atropine- and methysergide-pretreated rats. Somatostatin markedly decreased the self-stimulation rate of the animals. Atropine in a dose which had no action on self-stimulation partly antagonized the effect of somatostatin. Methysergide potentiated the somatostatin-induced depression of self-stimulation behavior. These results suggest that the central cholinergic and serotoninergic systems may play a role in the somatostatin-induced inhibition of self-stimulation.

Animals↗