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M M Winnicka

Publications and source records attributed to M M Winnicka.

30 records · Page 2Linked to original sources

6-OHDA bilateral lesions to the central amygdala do not affect vasopressin improvement of recall in rats.

The influence of vasopressin (AVP) on recall of information in a passive avoidance situation after bilateral 6-OHDA lesions to the central amygdala was tested. AVP given 15 min before the retention testing at the icv dose of 1 microgram significantly prolonged avoidance latencies both in lesioned and in sham-operated rats in comparison with the respective icv saline injected animals. Insignificant increase of spontaneous locomotor activity in rats lesioned to the central amygdala was unlikely to interfere with the cognitive effect of AVP. These results suggest that dopaminergic projection to the central amygdala is not responsible for the facilitatory effect of AVP on retrieval process in a passive avoidance situation.

Amygdala↗

Solcoseryl improves learning and memory in rats.

Our previous experiments have shown that Solcoseryl (S), a protein-free extract of calves' blood stimulates locomotor activity and decreases haloperidol catalepsy in rats. In this study the influence of S on acquisition, consolidation, and recall of both, conditioned avoidance responses (CARs) and passive avoidance behaviour was tested. S at the intraperitoneal (i.p.) dose of 1.25 ml/kg significantly improved acquisition and at the dose of 1.0 ml/kg recall of CARs. In the passive avoidance situation the significant effect on acquisition and recall of information was observed after i.p. injection of 1.0 ml/kg of S, and on consolidation after 0.75 ml/kg. These data indicate that S may positively affect the CNS processes responsible for learning and memory.

Actihaemyl↗

Solcoseryl stimulates behavioural activity of rats.

The influence of Solcoseryl (S), a protein-free extract of calves' blood given intraperitoneally (i.p.) on the behavioural measures of activity of the central nervous system of male Wistar rats was examined. The drug (1.0 ml/kg i.p.) given 60 min before testing the animals in electromagnetic motimeter significantly enhanced overall and vertical motility of rats. S at the doses of 0.5, 1.0 and 2.0 ml/kg did not significantly influence the activity of rats in "open field". 1.0 ml/kg of S given 15, 45 and 60 min before thiopental (30 mg/kg i.p.) did not change the onset and time of sleep following the latter drug, except for the significant shortening of the time of sleep of animals injected with S 15 min before thiopental. S at the dose of 1.0 ml/kg did not change stereotypies produced by apomorphine (2.0 mg/kg i.p.) and amphetamine (6.5 mg/kg i.p.) but decreased intensity of haloperidol (1.0 mg/kg i.p.) catalepsy.

Actihaemyl↗

6-OHDA lesion to the entorhinal cortex does not abolish angiotensin II improvement of recall in rats.

Our recent studies have shown that facilitating effect of angiotensin II (AII) on recall is mediated by dopaminergic systems. In this study the influence of bilateral destruction of dopaminergic endings in the entorhinal cortex on improving recall intracerebroventricular injection of AII was tested. Since this lesion did not abolish the facilitating influence of AII, it may be suggested that the dopaminergic projection to the entorhinal cortex is not responsible for the facilitating effect of AII on recall in a passive avoidance situation.

Angiotensin II↗

Effect of angiotensin II on the passive avoidance performance in rats after bilateral 6-OHDA lesions to the hippocampus and olfactory tubercle.

Our earlier experiments have shown that the facilitating action of angiotensin II (AII) on recall of passive avoidance is mediated by dopaminergic systems. In an attempt to find the site of action of AII on memory in the brain, bilateral lesions of the two structures belonging to the limbic system, receiving efferentation from A 10 dopaminergic neurons, were made in 32 male rats before behavioral testing of the influence of intracerebroventricular AII injection on recall in a passive avoidance situation. 32 additional rats served as sham operated controls. Bilateral lesions to the dentate gyrus of the hippocampus and olfactory tubercle did not significantly change the facilitating effect of AII on recall. The results may suggest that dopaminergic projections from A 10 neurons of the ventral tegmental area to the dentate gyrus and olfactory tubercle are not responsible for the enhancing effect of AII on recall of passive avoidance.

Angiotensin II↗

Lesions of central amygdala abolish angiotensin II improvement of recall in passive avoidance situation.

Our earlier experiments have shown that facilitating action of angiotensin II (AII) on recall of passive avoidance is mediated by dopaminergic systems. In an attempt to evaluate the possible site of action of AII on memory processes, bilateral lesions of the structures belonging to the limbic system, receiving efferentation from A 10 dopaminergic neurons were made before behavioral testing of the influence of intracerebroventricular (icv) AII injection on recall in a passive avoidance situation. Bilateral lesions of the nucleus centralis corporis amygdaloidei totally abolished the facilitating effect of AII on recall, while the lesions of the nucleus septi lateralis were ineffective. These results may suggest that improvement of recall in passive avoidance situation after icv injection of AII is mediated by A 10 dopaminergic neurons projecting to the central amygdala.

Amygdala↗

Effect of angiotensin II on passive avoidance performance after bilateral lesion of the nucleus accumbens septi.

The experiments performed earlier in this Department indicated that facilitatory effect of angiotensin II (AII) on recall is connected with its influence on dopaminergic systems. In an attempt to evaluate the possible site of action of AII on the memory processes, bilateral lesion of the nucleus accumbens septi (NAS, a limbic structure which receives projection from A 10 dopaminergic neurons) was made before behavioral testing of the influence of icv injection of AII on recall in passive avoidance situation. Unexpectedly, bilateral lesion of the NAS improved the recall itself. In such a situation any facilitatory action of AII on recall in this test could not be shown.

Angiotensin II↗

2-amino-3-phosphonopropionic acid (AP3) and its N-methyl analog improve learning and memory in rats.

The influence of 2-amino-3-phosphonopropionic acid (AP3), an antagonist of metabotropic glutamate receptors and its N-methyl analog (N-methyl AP3) on acquisition, consolidation and recall of information in a passive avoidance situation was tested. Both compounds improved three examined parameters. The significant effect of AP3 appeared at the icv dose of 12.5 micrograms per rat when its influence on acquisition and consolidation was tested, and at the icv dose of 100 micrograms when its influence on retrieval process was evaluated. The significant improvement of acquisition of information was observed at the icv dose of 50 micrograms per rat of N-methyl AP3, but significant facilitation of consolidation and retrieval processes appeared at the higher dose of 100 micrograms per rat. Significant improvement of performance in a passive avoidance situation persisted in all experiments to the highest used dose of both compounds, 250 micrograms.

Alanine↗

Central activity of 2-amino-4-phosphonobutyric acid (AP4).

The influence of intracerebroventricular (icv) injections of 2-amino-4-phosphonobutyric acid (AP4) on the activity of central nervous system was examined in rats. The compound (100 and 200 micrograms icv) significantly enhanced apomorphine stereotypy, in doses of 50, 75, and 100 micrograms decreased haloperidol-induced catalepsy and did not change motility of rats estimated in the "open field" test. AP4 significantly improved learning and memory processes in passive and learning in active avoidance situation. The highest significant effect was observed after icv dose of 100 micrograms per rat, when acquisition, consolidation and recall of information was evaluated in the passive avoidance behavior. AP4 significantly improved only acquisition of information in active avoidance situation at the icv dose of 50 micrograms per rat. The mechanism of the positive effect of AP4 on learning and memory is at present unclear, and its explanation needs future investigations.

Aminobutyrates↗

Central activity of 2-amino-3-phosphonopropionic acid (AP3) and its N-methyl analog.

The influence of 2-amino-3-phosphonopropionic acid (AP3) an antagonist of metabotropic glutamate receptors and its N-methyl analog (N-methyl AP3) on locomotor activity in the "open field" test, apomorphine stereotypy and haloperidol catalepsy were tested. Both compounds had not any influence on spontaneous crossings of squares, number of rearings and bar approaches in the "open field" test. AP3 and its N-methyl analog significantly enhanced apomorphine stereotypy at the intracerebroventricular (icv) doses of 100 and 200 micrograms per rat respectively. Although, both compounds significantly diminished haloperidol catalepsy at the icv doses of 50, 100 and 200 micrograms per rat. All observed effects of AP3 and N-methyl AP3 were dose independent. Methyl substitution at the N-position in AP3 did not change pharmacological properties of this compound i.e. its influence on behavior mainly dependent on dopaminergic systems.

Alanine↗

Psychotropic activity of N-methyl-2-amino-4-phosphonobutyric acid (N-methyl AP4).

We have previously reported that 2-amino-4-phosphonobutyric acid (AP4), an agonist of presynaptically located metabotropic glutamate receptors, administrated at a single intracerebroventricular (icv) injection facilitated learning and memory in a passive- and learning in an active avoidance situation, enhanced apomorphine stereotypy, and attenuated haloperidol catalepsy in rats. In the present study the effect of a single icv injection of N-methyl analogue of AP4 (N-methyl AP4), in the same behavioral tests was investigated in rats. The compound at the doses of 100 and 200 micrograms per rat significantly enhanced apomorphine stereotypy, at the dose of 75 micrograms per rat attenuated haloperidol-induced catalepsy, without having any influence on spontaneous locomotor activity estimated in the open field test. N-methyl AP4 at the doses of 75 and 100 micrograms per rat significantly facilitated acquisition of information, consolidation, and retrieval process in a passive avoidance situation. The compound significantly improved only acquisition of conditioned avoidance responses (CARs) at the doses of 50 and 75 micrograms per rat; the positive effect of N-methyl AP4 on consolidation and recall of CARs was insignificant. Methyl-substitution at N-position in AP4 did not change its effects in the performed behavioral tests.

Aminobutyrates↗