Ibolya Bollók

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.

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.

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.

Phenoxybenzamine antagonizes somatostatin-induced antiamnesi 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.

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.

The effect 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.

The effect of β-(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.

Effect of intracerebroventricular administration of β-/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.

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

SummaryH-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 1h before the test session. These results suggest that H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH can facilitate learning and memory processes.

Comparative studies with β-(TYR)9melanotropin-(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.