Biomedical subjects

M Dikova

Publications and source records attributed to M Dikova.

9 recordsLinked to original sources

PubMed1993

Learning performance at different time periods after hypoxia in infant rats.

Infant rats were exposed to hypoxia. At different time periods after the hypoxic aggression the animals were subjected to a one-way active avoidance task consisting of 3 daily training sessions. Learning performance of hypoxic rats, expressed as the number of avoidances per 10 trials, was significantly decreased in all the sessions at posthypoxic day 35 (P < 0.001). The rate to which learning behaviour was affected by hypoxia was comparable among all 3 sessions in both groups. Histological evaluation of hippocampus and cortex at day 7 and day 35 after hypoxic exposure, did not reveal detectable structural changes. It can be concluded from this study that hypoxia, induced in 21 day old rats leads to learning performance deficits in the adult animal.

Animals↗

PubMed1992

Synaptic plasticity in rat hippocampus associated with learning.

Rats subjected to a one-way active avoidance task consisting of 3 daily training sessions, showed obvious shape changes in dendritic spines of the hippocampal supragranular molecular layer. Performance, expressed as the number of avoidances per 10 trials, significantly improved in the second and third session (P < 0.001). In trained animals, at the end of the third session, the amount of perforated concave synapses significantly increased as compared to untrained controls (P < 0.05). When compared with a group of sham-shocked rats, the increase was less pronounced. The length of the postsynaptic density in both, perforated and non-perforated synapses, significantly increased in comparison with untrained control and sham-shocked animals (perforated: P < 0.005; non-perforated: P < 0.05). The results are indicative for the existence of synaptic remodeling and turnover in rats subjected to one-way active avoidance training.

Animals↗

PubMed1990

Rheoencephalographic and electroencephalographic studies on nicergoline.

The effect of nicergoline on the rheoencephalogram (REG) and on spontaneous electroencephalographic activity (EEG) was studied in acute experiments in cats. The following REG parameters were assayed: amplitude, anacrotic section of the curve and its relative part and dicrotic index. EEG spectra were derived from 10-sec samples of ECoG and the relative amplitude was estimated at 2 Hz-intervals from 0-44 Hz. The REG study showed that nicergoline (0.05 mg/kg i.v.) caused an increase of the amplitude, and a decrease of the anacrote, of the relative part of the anacrote and the dicrotic index - changes indicating a lowering of cerebrovascular resistance. EEG study showed a decrease of the slow activities (theta and delta), and an increase of the fast activities (alpha and beta-1).

Animals↗

PubMed1989

Effects of nicergoline in experimental models related to pathogenesis of migraine.

The effect of nicergoline on cerebral blood flow (CBF), cerebrovascular resistance, the constriction of cerebral vessels caused reflectorily or by 5-hydroxytryptamine (5-HT) and on the transport of 5-HT in rat brain synaptosomes was studied using different experimental models. Nicergoline reduced cerebrovascular resistance in the carotid and vertebrobasilar system. The drug decreased carotid blood flow and local cortical CBF, preceded in some experiments by short-lasting CBF increase. Nicergoline almost completely inhibited brain vessels responses in the carotid and vertebrobasilar systems after tibial nerve stimulation. Simultaneously, inhibition of reflectory discharges of the sympathetic nerves was observed. Nicergoline showed an antiserotonin action by antagonizing the 5-HT effect on the cerebral circulation and inhibiting 5-HT-induced constriction of isolated rabbit basilar artery. The inhibition of uptake and enhancement of the release of 5-HT from brain synaptosomes indicates its ability to affect neuronal transmission in serotoninergic neurons. The effects of nicergoline are probably involved in the realization of its antimigraine action.

Animals↗

PubMed1989

Quantitative EEG analysis of the effects of nicergoline in some brain structures after asphyxic anoxia in cats.

A beneficial stabilizing effect of nicergoline on EEG recorded from cortex and some subcortical structures was established in cats under acute normal and anoxic conditions.

Acute Disease↗

PubMed1989

[Assessment of local cerebral blood flow by the hydrogen clearance method. I].

The effects of flunarizine and fezam on the local cerebral blood flow (LCBT) were examined by the hydrogen clearance with inhalation of hydrogen. The experiments were carried out on male nonbred cats under cetamine narcosis. The results showed that flunarizine (1 mg/kg i.v.) induced apparent enhancement of LCBF with 58% in comparison with the control values. The effect was read up to 60 min. The combined preparation fezam (100 mg/kg i.v.) caused considerable improvement of LCBF 30 min after inhalation with 63% in comparison with the control values. It is suggested that the observed effects are due to Ca-blocking action on cerebral vessels after flunarizine treatment as well as a reduction of cerebral-vascular resistance and influence on the metabolism after the combination fezam.

Animals↗

PubMed1988

Effect of nicergoline on learning and memory.

The anti-amnestic action of nicergoline was studied using the following experimental methods for learning and memory impairment, based on passive avoidance response: amnesia induced by maximal electroshock in mice, scopolamine-induced amnesia in mice and amnesia by paradoxical sleep deprivation in rats. Piracetam, meclofenoxate, pyritinol, deanol and phenazepam were used as reference drugs. The results show that nicergoline demonstrates well-expressed anti-amnestic effect manifested by reducing the amnestic effect of maximal electroshock, scopolamine or paradoxical sleep deprivation, its effect being equal to or more pronounced than piracetam, meclofenoxate, pyritinol, deanol and phenazepam.

Amnesia↗

PubMed1987

Cerebroprotective effect of nicergoline and interference with the anti-hypoxic effect of prostacyclin.

The cerebroprotective effect of nicergoline was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice, incomplete ischemia by bilateral carotid ligation in rats, hemic hypoxia in rats and asphyxic anoxia in cats. Xanthinol nicotinate, vincamine, vinpocetine and cinnarizine were used as reference drugs. In hypobaric hypoxia and complete ischemia by decapitation the interaction of nicergoline with the effect of prostacyclin (PGI2) was investigated. Nicergoline showed cerebroprotective effect of varying potency in all the methods used except asphyxic anoxia. Nicergoline manifested a synergic effect with PGI2 shifting its anti-hypoxic dose-response curve to the left.

Animals↗

PubMedDate not supplied

Cerebroprotective effect of flunarizine.

The cerebroprotective effect of flunarizine was studied using the following methods: hypobaric hypoxia in mice, complete ischemia by decapitation in mice, anoxic hypoxia in mice, hemic hypoxia in rats, incomplete ischemia by bilateral carotid ligation in rats and asphyxic hypoxia in cats. Piracetam, meclofenoxate, nicergoline, naftidrofuryl, cinnarizine and nifedipine were studied as reference drugs. Flunarizine increased the survival time in all survival models. Its effect was most pronounced in complete ischemia model, and considerably higher than that of reference drugs. In asphyxic hypoxia flunarizine increased cortical resistance and shortened cortical recovery. The EEG frequency-amplitude analysis during asphyxic hypoxia showed a significant decrease of the slow-waves amplitudes of delta and theta range, and an increase of the fast-waves amplitudes of beta-2 range, changes indicating protective action.

Animals↗