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PL
Padaczka jest zespołem chorobowym manifestującym się zaburzeniami czynności mózgu, często występującymi u chorego w formie napadów drgawek i zaburzeń świadomości w różnych odstępach czasu. Znane są różne jej postacie kliniczne. Istotnym czynnikiem w patogenezie padaczki jest zwiększona, nienormalna pobudliwość neuronów mózgu powodująca wystąpienie nieprawidłowych, synchronicznych wyładowań elektrycznych określonych grup neuronów mózgu. Występowanie padaczki w populacji ludzkiej jest oceniane na 0,5 – 1%. W Polsce liczba chorych na padaczkę jest szacowana na 300 – 400 tys. osób, co uzasadnia uznanie jej za chorobę społeczną. Sytuacja społeczna chorych na padaczkę w różnych krajach, także w Polsce jest gorsza niż chorych na inne choroby przewlekle. Na ogół w krajach o niskim poziomie rozwoju cywilizacyjnego jest gorsza w porównaniu z krajami rozwiniętymi. Farmakoterapia stanowi istotną część leczenia padaczki. Stosowane leki przeciwpadaczkowe są lekami objawowymi, hamującymi drgawki, główny objaw choroby. Poważnym problemem farmakoterapii padaczki jest oporność na leki przeciwpadaczkowe, występująca u 30% chorych na padaczkę. Koszt leczenia chorego na padaczkę zarówno w Polsce jak i w innych krajach jest wyższy w porównaniu z przeciętnym kosztem leczenia osoby z ogólnej populacji społeczeństwa.
EN
Elepsies have been present thoroughout recorded history. The essential factor in pathogenesis of epilepsy is abnormal neuronal excitability in the brain, which results in excessive and uncontrolled discharge of group of neurons which spreads to other neurons and parts of the brain. These neuronal disturbances may induce seizures and unconsciousness of the patient. This syndrome consists of several, different clinical entities. The incidence of epilepsy occurs in about 0,5 – 1% of human population. The number of epileptic patients in Poland is valuated on 300 – 400 thousand people. Social situation of epileptics is worse than other non-epileptic patients. It is much worse in an undeveloped countries in comparison to well- developed societies. Pharmacotherapy plays an essential role in the treatment of epilepsy. Antiepileptic drugs prevent or decrease, high – frequency, repetitive neuronal firing and inhibit transmission epileptiform activity from epileptic focus to other parts of the brain. About 30% of epileptic patients is resistant to antiepileptic drugs in spite of proper therapy. This phenomenon is of great importance from the therapeutical and economical point of view. The cost of epileptic patient in Poland as well as in other countries is much higher in comparison to other non-epileptic patients.
EN
The aim of present study was to evaluate mechanisms involved in thermomodulatory effect LPK in rats.Experiments were performed on adult Wistar male rats. LPK was applied either intracerebroventricularly (icv), or intraperitoneally (ip) using the similar program and technique of experiments as in our previous study. We confirmed in this paper the results of our previous reports that icv administration LPK at the dose of 20 nmol induced evident significant rectal hypothermia, while lower dose LPK of 1 nmol icv exerted significant hyperthermic effect. Peripherally applied LPK at the range of doses 10-100 nmol/100 g ip displayed slight bimodal (hyperthermic and hypothermic) effect on rectal temperature. Prior administration of haloperidol, an antagonist of central dopamine receptors blocked both effects LPK applied either icv or ip. Obtained results indicate that both hypothermic and hyperthermic effects LPK are also modulated by central dopaminergic receptors.
EN
In this report we present effect of pizotifen, an antagonist of serotonin (5-hydroxytryptamine; 5-HT) receptors, on P-induced convulsions in mice. Experiments were conducted on male mice Balby. Convulsive effect P was determined using the following measures: percentage of mice with seizures, the number of seizure episodes/2 h, the latency time of the beginning P-induced seizure activity in mice and P-induced seizure activity of mice determined by score of Racine. Pretreatment mice with pizotifen (0.5 mg/kg ip) did not prevent convulsive effect P, applied ip at the dose of 50 μmol/kg ip (59.3 mg/kg) but significantly shortened the latency time of the beginning of P-induced seizure activity of mice. We conclude that central serotonin receptors are involved in the mechanism of P-induced convulsions.
EN
Neurotoxic effects of copper ions after intraperitoneal (ip) and intracerebroventricular (icv) injections of CuSO4 • 5H2O and Cu(CH,COO) 2 • H2O at doses of 1-100 nmols icv and 0.1-100 pmols/kg ip was deter­mined in rats using two behavioural methods: exploratory and locomotor activity in an open field test and spatial memory in a water maze test. It has been found that higher doses of copper salts (100 nmols icv and 100 ^mols/kg ip) significantly decreased spatial memory of rats.
18
Content available Antinociceptive effect of poneratoxin [PoTX] in rats
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EN
Poneratoxin (molecular weight 2932) is a 25 amino acid neuropeptide, isolated from an ant venom. It affects excitability of nerve and muscle fibres by changing the kinetics of the voltage-dependent sodium channel. The aim of the study was to investigate the analgetic effect of synthetic poneratoxin (PoTX) in adult female Wistar rats. In the first part of the study the animals received PoTX intracerebroventricularly. The analgetic effect was evaluated by a tail immersion test. In the second part of the experiment the analgetic effect of PoTX was blocked with naloxone, an opioid receptors antagonist. The study showed that poneratoxin exerts the analgetic effect in rats and this effect is not mediated by central opioid system. Therefore it was concluded that other mechanism is resposible for the effect of PoTX.
20
Content available Antinociceptive effect of MAS MT in rats
45%
EN
MAS MT is a myotropic decapeptide isolated from Manduca sexta. This peptide exerts stimulatory effect on insects heart-beat frequency. The present study was undertaken in order to determine a probable antinociceptive effect in rats of native synthetic decapeptide, MAS MT-I and its two analogs, heptapeptides MAS MT-II and MAS MT-III. All these peptides were applied directly into the lateral brain ventricle (icv) at three doses: 10, 25 and 50 nmol. The analgesic (antinociceptive) effect was evaluated by a tail immersion test. It was found that two doses of MAS MT-I: 25 and 50 nmol induced significant antinociceptive effect, while MAS MT-II and MAS MT-III exert a less antinociceptive effect in comparison with native MAS MT-I. Prior icv administration of naloxone, an opioid antagonist weakly blocked MAS MT-I effect. We conclude that antinociceptive effect of MAS MT-I in rats is not mediated by central opioid system.
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