Biomedical subjects

I Bollók

Publications and source records attributed to I Bollók.

At least 19 recordsLinked to original sources

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↗

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

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

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↗

PubMedDate not supplied

Amnesic action of FMRFamide in rats.

The effects of FMRFamide on passive avoidance behaviour and electroshock-induced amnesia following intracerebroventricular administration were studied in rats. FMRFamide given immediately after the learning trial, or 20 min before the retention trial, attenuated the avoidance response, thereby impairing the consolidation and retrieval processes. Electroshock induced amnesia when applied immediately after the learning trial. Treatment with FMRFamide facilitated the amnesia of the passive avoidance response. The results indicate that FMRFamide peptide belongs in the class of neuropeptide which are amnesic.

Amnesia↗

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↗