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Biomedical subjects

L Vécsei

Publications and source records attributed to L Vécsei.

At least 109 records · Page 6Linked to original sources
PubMed1983

The effects of beta-(Tyr9)melanotropin-(9-18) and H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on the analgesic action of morphine.

beta-(Tyr9)melanotropin-(9-18), which itself has no analgesic action, as measured by the tail-flick and hot-plate methods, decreased morphine-induced analgesia following intracerebroventricular injection. H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH heptapeptide, which has weak CRF-like activity, had no action on analgesia and was not able to modify morphine-induced analgesia. Compared with ACTH1-24, which in a subcutaneous dose of 100 micrograms/rat decreased morphine-induced analgesia, the same dose of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH was ineffective.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of intracerebroventricular administration of beta-/Tyr9/-melanotropin-/9-18/ on rotational behavior induced by substantia nigra lesion in rats.

beta-/Tyr9/melanotropin-/9-18/ administered intracerebroventricularly /icv./ in doses of 1 microgram/rat or 10 micrograms/rat had no influence on the substantia nigra lesion-induced turning activity of rats, however, it was able to potentiate apomorphine-induced contralateral turning. In a dose of 20 micrograms/rat /icv./ the peptide alone induced clear contralateral turning. The results suggest that at lower doses the peptide facilitates apomorphine-induced dopamine receptor stimulation, while in a higher dose the peptide alone can stimulate dopamine receptor activity.

Amphetamine↗
PubMed1983

The effects of interaction between propranolol and somatostatin on the active avoidance behavior, open-field activity and electroconvulsive shock-induced amnesia of rats.

In the present study the role of beta-receptors in the behavioral action of somatostatin was investigated. Somatostatin inhibited extinction of the active avoidance behavior. Propranolol alone had no action on this behavior but significantly inhibited the peptide-induced effect. In the open-field test somatostatin induced locomotor activation; propranolol did not influence this effect of the peptide. Somatostatin inhibited electroconvulsive shock-induced amnesia. Propranolol alone had no action in this test, but significantly decreased the antiamnesic effect of the peptide. These results suggest that the central beta-receptors play an important role in the behavioral action of somatostatin.

Amnesia↗
PubMed1983

Comparative studies with cyclic and linear somatostatin on active avoidance behaviour and open-field activity in rats.

The action of cyclic and linear somatostatin on active avoidance and open-field behaviour was investigated in rats. Both peptides inhibited the extinction of the avoidance behaviour and slightly but not significantly increased the intertrial activity (ITR). Both peptides increased ambulation and rearing activity in a dose related fashion, while the grooming and defecation rates were not changed. Since both peptides are capable of increasing the locomotor performance this action might contribute to the effect exerted on the extinction of active avoidance behaviour.

Animals↗
PubMed1983

The effect of linear somatostatin on the active avoidance behaviour and open-field activity on haloperidol, phenoxybenzamine and atropine pretreated rats.

Somatostatin administered intracerebroventricularly inhibited the extinction of active avoidance behaviour. The dopamine receptor blocking agent haloperidol, the alpha 1-receptor blocker phenoxybenzamine and the muscarinic anticholinergic agent atropine inhibited the behavioural effect of the peptide. Furthermore, somatostatin increased the locomotor activity of the animals. Neither of these drugs influenced the effect of the peptide exerted on locomotor activity. The peptide was ineffective on other parameters of the open-field test while phenoxybenzamine decreased the defecation rate of the animals and this effect was not influenced by somatostatin. The results suggest that the catecholaminergic and the cholinergic system play an important role in the inhibition of extinction produced by somatostatin but these mechanisms to not have a role in the locomotor activity induced by the peptide.

Animals↗
PubMed1982

The interaction between beta-[Tyr9]melanotropin-(9-18), haloperidol and amphetamine in different behavior tests of rats.

The effects of beta-[Tyr9]melanotropin-(9-18) on the extinction of the active avoidance reflex in (dopamine receptor blocker) haloperidol-treated animals, and on the open-field activity in haloperidol and amphetamine-treated rats were studied. It was shown that a systemically given 100 microgram dose of the peptide, which had no action on the ambulation and rearing activity in the open-field test, could still delay the extinction of the active avoidance reflex. Haloperidol treatment was able to partially block the effects of the ICV administered beta-[Tyr9]melanotropin-(9-18) on both the extinction and open-field activity. After intracerebroventricular administration, the effect of the peptide on the open-field test was partially similar to that of amphetamine: it facilitated the ambulation and rearing activity, and (in contrast with amphetamine) was able to facilitate the grooming activity, even in the presence of amphetamine. The results suggest that dopaminergic innervation might play a mediating role in the effect of beta-[Tyr9]melanotropin-(9-18) on the extinction of the active avoidance reflex and open-field activity. The effect on the open-field activity differens in part from that of amphetamine.

Amphetamine↗
PubMed1982

Effects of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on passive and active avoidance behavior and on open-field activity of rats.

The action of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on the passive and active avoidance behavior and open-field activity of rats was studied after peripheral and intracerebroventricular administration. When applied before the test session, intracerebroventricular administration increased the avoidance latency of passive avoidance behavior. Subcutaneous, intraperitoneal and intracerebroventricular administration of the peptide delayed the extinction of active avoidance behavior. Both subcutaneous and intracerebroventricular administration increased the grooming activity of the rats. The data suggest that H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH is able to influence memory, acting mainly on the retrieval processes, and to modify open-field activity.

Animals↗
PubMed1982

Effects of beta-/Tyr9/melanotropin-/9-18/ on apomorphine-induced stereotyped cage-climbing and on striatal dopamine release in mice. Comparative studies with amphetamine.

beta-/Tyr9/melanotropin-/9-18/ significantly increased apomorphine-induced cage-climbing, while only a tendency towards an increase was observed after supersensitization with haloperidol. Amphetamine also enhanced apomorphine-induced climbing behavior. The peptide showed only a tendency to increase dopamine release from striatal slices, while amphetamine elevated this significantly. The results suggest that the striatal dopamine system is involved in the behavioral action of beta-/Tyr9/melanotropin-/9-18/.

Amphetamine↗
PubMed1982

Comparative studies with linear and cyclic somatostatin on the self-stimulation of rats.

In the present study the dose-related effects of linear and cyclic somatostatin were compared on the self-stimulation rate of rats. Twenty micrograms of linear somatostatin administered intracerebroventricularly (icv.) markedly decreased the self-stimulation rate, while 5 micrograms and 10 micrograms was ineffective. Cyclic somatostatin in a dose of 1 microgram caused a transitory but not significant increase in the self-stimulation rate, which later returned to the control level. Five micrograms and 10 micrograms of the peptide decreased the self-stimulation rate. These results indicate that the cyclic somatostatin is more effective in inhibiting the self-stimulation rate than the linear one.

Animals↗
PubMed1981

Effects of beta-(Tyr9)melanotropin-(9-18) decapeptide on passive and active avoidance behavior and on open-field activity of rats.

The effects of the administration of beta-(Tyr9)melanotropin-(9-18) into the lateral ventricle in a dose of 1.0 micrograms in 2 microliters were studied on passive avoidance behavior, extinction of active avoidance behavior, and open-field activity in rats. beta-(Tyr9) melanotropin-(9-18) given 30 min pretrial facilitated the acquisition of passive avoidance behavior; however, it was ineffective on retention when the material was given immediately posttrial or 30 min before retention testing. The extinction of active behavior was delayed. In open-field activity, the ambulation rate and rearing activity were increased 30 min following administration. The data suggest that beta-(Tyr9)melanotropin-(9-18) has distinct neurotropic properties, and is able to modify behavioral reactions.

Animals↗
PubMed1980

Effect on memory processes of anti-vasopressin serum microinjected into the dorsal raphe nucleus: the role of catecholaminergic neurotransmission.

Anti-arginine8-vasopressin serum was microinjected into the mesencephalic dorsal raphe nucleus immediately after the learning trial, in a one-trial learning passive avoidance reaction. The treatment attenuated passive avoidance behavior 24 h after treatment, suggesting a role of the endogenous vasopressin of this area in memory processes. On the other hand, the antiserum did not influence passive avoidance behavior if 6-hydroxydopamine was microinjected into the raphe region. The data suggest that the antiserum may have primarily interacted with catecholaminergic terminals, which enter the dorsal raphe nucleus.

Animals↗
PubMedDate not supplied

Effects of intracerebroventricularly administered somatostatin on passive avoidance, shuttle-box behaviour and open-field activity in rats.

Behavioural effects of somatostatin after intracerebroventricular (icv) administration have been investigated in male rats. In a passive avoidance learning test, somatostatin (1 microgram), given 30 min before the learning session, increased the avoidance latency at 24 h, but not at 48 h, after the injection, when compared to a 10 micrograms treated group. However, compared to a saline treated group, somatostatin (0.01, 0.1, 1, or 10 micrograms) did not significantly influence the avoidance latency. In a shuttle box experiment somatostatin (1 microgram) facilitated the learning process. In an open-field behaviour test, immediately after the 24 h passive avoidance test, 10 micrograms of the peptide decreased the rearing activity without influencing other open field behaviours, like locomotion, grooming and defecation. In a second open-field experiment somatostatin (1 microgram), given 30 min prior to the test, similarly as in the shuttle box learning experiment, increased the locomotion of the animals. These data suggest that somatostatin influences both the passive avoidance and shuttle box behaviours. The peptide-induced motor performance of the animals may play an important role in influencing the responses observed in these behavioural tests.

Animals↗
PubMedDate not supplied

Somatostatin and Alzheimer's disease.

One of the most consistent neurochemical deficits in Alzheimer's disease is a reduction in cortical somatostatin concentrations. The probability of a predominant regulatory change is heightened by the finding that 90% of somatostatin positive nonpyramidal neurons are also positive for NADPH, and NADPH neurons are 'protected' in Alzheimer's disease and do not appear to be lost. The first evidence that somatostatin influences learning and memory processes in experimental animals was published more than a decade ago. These reports of somatostatin effects on cognitive functions in rats were later confirmed by several other studies. The somatostatin depleting substance cysteamine inhibited the learning and memory performance of rats in active and passive avoidance behavior tests. Post-mortem human studies suggest that although somatostatin concentration is reduced, the somatostatin receptors are less affected in the brain in Alzheimer's disease. These findings may be of importance for possible therapeutic approaches using somatostatin-receptor-influencing compounds.

Journal Article↗
PubMedDate not supplied

Intracerebroventricular somatostatin attenuates electroconvulsive shock-induced amnesia in rats.

In the present study the effect of intracerebroventricularly (ICV) administered somatostatin on electroconvulsive shock-(ECS) induced retrograde amnesia was investigated in rats. The ECS significantly decreased foot shock-induced avoidance latency. Somatostatin in a dose of 1 microgram/4 microliter (ICV) had no action on the ECS-induced retrograde amnesia, while in a dose of 4 micrograms/4 microliters it significantly increased the avoidance latency if the treatment was performed immediately, 4 hr, 20 hr or 23 hr after the ECS. The results suggest that ICV administered somatostatin has an antiamnesic effect.

Amnesia↗
PubMedDate not supplied

The effect of beta-(Tyr9)melanotropin-(9-18) on active avoidance behavior, electroconvulsive shock-induced amnesia and T-discrimination learning of rats.

The effect of beta-(Tyr9)melanotropin-(9-18) was investigated on active avoidance behavior, electroconvulsive shock (ECS)-induced amnesia and T-discrimination learning in rats. The decapeptide inhibited the extinction of active avoidance behavior. It was also able to block ECS-induced amnesia if the treatment was performed immediately, or 4 hr or 20 hr after the ECS. In the T-discrimination paradigm the peptide facilitated spatial discrimination learning and reversal learning. These results suggest that beta-(Tyr9)melanotropin-(9-18) can influence learning and memory processes in different behavioral tests.

Amnesia↗
PubMedDate not supplied

Comparative studies of somatostatin-14 and some of its fragments on passive avoidance behavior, open field activity and on barrel rotation phenomenon in rats.

Behavioral effects of somatostatin-14, and some of its fragments [somatostatin(3-8), somatostatin(9-14), somatostatin(7-10)] after intracerebroventricular (ICV) administration have been investigated in male rats. In a passive avoidance learning test, somatostatin-14 (0.6 nM) given immediately after the learning session increased the avoidance latency at 24 hr after the injection, when compared to a somatostatin(3-8) (0.6 nM)-treated group. However, compared to a saline-treated group, the peptides did not significantly influence the avoidance latency. Somatostatin-14 administered in higher dose (6.0 nM) decreased the avoidance latency compared to the saline-treated group, while its fragments did not influence it. In an open field behavioral test, immediately after the 24-hr passive avoidance test, 6 nM of somatostatin-14 decreased the rearing activity, while the fragments did not influence this behavior. Somatostatin-14 produced barrel rotation in a dose-related manner, but after the injection of a high dose of the peptide (12 nM) all of the animals died in cardiorespiratory failure (apnea, pulmonary oedema). The fragments did not produce barrel rotation.

Amino Acid Sequence↗
PubMedDate not supplied

Comparative studies of intracerebroventricularly administered cysteamine and pantethine in different behavioral tests and on brain catecholamines in rats.

In a passive avoidance test, intracerebroventricular administration (post-trial treatment) of the somatostatin-depleting compound cysteamine decreased the avoidance latency of the rats in a dose-related manner, while the effect of pantethine (which is metabolized to cysteamine) was less pronounced. In open-field studies, both compounds decreased the motor activity (ambulation, rearing) of the animals 15 min after the injection followed by a subsequent recuperation of the locomotor depression. Following pantethine, the ambulation increased during the later tests (60 min, 240 min, 24 hr). Cysteamine decreased the noradrenaline and increased the dopamine and dihydroxyphenyl acetic acid content in the hypothalamus, whereas the effects of pantethine were less expressed. Both compounds slightly decreased the striatal noradrenaline and increased the dihydroxyphenyl acetic acid levels at 15 and 60 min after administration. However, contrary to pantethine, 4 hr after treatment with cysteamine, there was a decrease in dihydroxyphenyl acetic acid concentration in this brain region. These findings suggest that both pantethine and cysteamine attenuate passive avoidance latency after intracerebroventricular treatment. The different efficiency of pantethine and its metabolite cysteamine might be connected to the low pantetheinase activity of the brain tissue; however, some direct effects of pantethine cannot be excluded. The different effects of the two compounds on the open-field activity are possibly associated with the diverse effects of the compounds on the striatal dopaminergic neurotransmission.

3,4-Dihydroxyphenylacetic Acid↗