Biomedical subjects

I Bollók

Publications and source records attributed to I Bollók.

8 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↗

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

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↗