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W Turski

Publications and source records attributed to W Turski.

34 records · Page 2Linked to original sources
PubMed1981

Effects of some antiepileptic drugs in pentetrazol-induced convulsions in mice lesioned with kainic acid.

Mice were injected with intracerebroventricular (i.c.v.) kainic acid (KA; 0.1 micrograms per animal) and the pentetrazol test was carried out on the fifth day after the administration of the amino acid. The following antiepileptic drugs were tested for anticonvulsant activity in mice lesioned with KA: diazepam (0.4 mg/kg), phenobarbital (12.5 and 25 mg/kg), trimethadione (200 and 400 mg/kg), depakine (200 and 400 mg/kg), carbamazepine (10 and 20 mg/kg), lefadol (bromophenylsuccinimide; 20 mg/kg), and acetazolamide (320 mg/kg). All drugs were given intraperitoneally, except for carbamazepine, which was also given orally in doses of 100 and 200 mg/kg. Pentetrazol was administered subcutaneously in a dose of 110 mg/kg, and the animals were subsequently observed for the occurrence of clonic and tonic convulsions within 30 min. The protective effects of diazepam and phenobarbital were significantly reduced in the KA-lesioned animals, while the actions of the remaining anticonvulsants were unaltered. Moreover, a substantial loss of pyramidal cells in the CA 3 field of the hippocampus was noted after i.c.v. injection of KA. It may therefore be concluded that the mechanism of the action of diazepam and phenobarbital are partially dependent on the intact functions of the hippocampal formation.

Acetazolamide↗
PubMed1981

The effect of intraventricular phenylethylamine and octopamine on the central effects of tremorine and pilocarpine and the acetylcholine level in the rat brain.

Phenylethylamine (PEA, 50 and 100 microgram ivc) and octopamine (OCT, 50 and 250 microgram ivc) potentiated the tremorine (10 mg/kg ip) induced hypothermia in the rat. This effect was partially antagonized by atropine (10 mg/kg ip). PEA and OCT significantly prolonged the duration of pilocarpine (100 mg/kg iv) induced catalepsy in rats. PEA (100 microgram ivc) and OCT (250 microgram ivc) depressed the acetylcholine (ACh) level in the cerebral cortex and striatum but did not affect it in the hippocampus. In addition, these amines enhanced the synthesis of ACh in the cerebral cortex, and PEA also in the rat striatum.

Acetylcholine↗
PubMed1977

The effect of chloramphenicol and cycloheximide on the activity of enzyme "markers" of mitochondrial substructures of the rat liver.

Chloramphenicol and cycloheximide exert in vivo inhibitory effects on the synthesis of mitochondrial enzymes. Choloramphenicol action results in a significant decrease of the activity of enzymes being the "markers" of all submitochondrial structures including that of the outer membrane. This suggests that chloramphenicol affects biosynthesis of of "assembly protein" on mitochondrial ribosomes and thus affects incorporation of proteins, wherever they are synthesized, into the structure of the mitochondrion as a functional entity. The effect of cycloheximide depends markedly on the concentration of the inhibitor and on the time of its administration. The differences in sensitivity of examined enzymes to the drug are probably related to their differential turnover.

Animals↗
PubMed1975

Investigation of localization of monoamine oxidase (EC 1.4.3.4) in subfraction of rat liver mitochondria.

Subfractionation of the purified preparations of mitochondria was performed according to Schnaitman's digitonin method. In some experiments, polyvinyl sulphate (PVS) was added to the medium during the preparation and subfractionation of mitochondria. The formation of the "fluffy layer" was not observed in the presence of PVS. The "fluffy layer" was either removed or left within the pellet during the separation of the subfraction of mitoplasts from the supernate containing the outer membrane as well as the inter-membrane space. The monoamine oxidase (MAO) activity was determined by means of our own modification of Tabor's method. In this way the influence of aldehyde oxidase upon the obtained results could be eliminated. A part of MAO activity was found in the subfraction of mitoplasts both in the presence and absence of PVS in the medium. The obtained results suggest double localization of MAO both in the outer and inner membrane. The influence of the method of determination of MAO activity on the evaluation of its intra-mitochondrial activity has been discussed.

Aconitate Hydratase↗
PubMed1975

Studies on the latency of rat liver fumarate hydratase.

A hypotonic medium and nonionic detergents Triton X-100 and digitonin have no influence on the activity of fumarase in the homogenate or in the mitochondrial fraction either. Ionic detergents of deoxycholate, cholate and sodium dodecyl sulphate exert an inhibiting influence. The activity of enzyme was determined in an L-malate-fumarate system. 1 h of incubation and the original Racker's method gave similar results. The lack of 'latency', found for the mitochondrial fumarase, was discussed basing on the data concerned with the penetration of metabolites through the inner mitochondrial membrane.

Animals↗
PubMed1972

[Microbodies].

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Animals↗
PubMedDate not supplied

Effect of aminophylline on the protective action of common antiepileptic drugs against electroconvulsions in mice.

The increasing amount of data tends to suggest that adenosine-mediated inhibition may play a role in the anticonvulsant activity of a number of antiepileptic drugs. Consequently, we tried to reverse the protective action of acetazolamide [(40 and 80 mg/kg) i.p.; 60 min before the test]; carbamazepine (20 and 30 mg/kg i.p., 60 min); diazepam (5 and 10 mg/kg i.p., 60 min); diphenylhydantoin (8 and 12 mg/kg i.p., 120 min), phenobarbital (20 and 30 mg/kg i.p., 120 min) and valproate (200 and 300 mg/kg i.p., 30 min) with aminophylline (50 and 100 mg/kg i.p., 30 min) against electroconvulsions in mice. Aminophylline markedly decreased the anticonvulsant efficacy of almost all drugs studied, acetazolamide (40 and 80 mg/kg) and carbamazepine (30 mg/kg) being the only exceptions. The ethylenediamine component of aminophylline did not modify the anticonvulsant activity at all. These results seem to support the suggestion that aminophylline-induced blockade of adenosine receptors might be involved in the reversal of the protective action of at least some drugs studied. Regardless of the nature of the aminophylline-induced impairment in the anticonvulsant efficacy of a number of antiepileptic drugs, the use of methylxanthines in epileptic patients for the treatment of obstructive lung diseases should be avoided.

Aminophylline↗
PubMedDate not supplied

Shuttle behavior in rats after lesion of hippocampal pyramidal cells with kainic acid.

Rats with bilateral lesions of hippocampal pyramidal cells in the subfield CA 3 with intracerebroventricular kainic acid (0.1 microgram/2 microliter) made more shuttle responses to a buzzer in Pavlovian paradigm, classical conditioning and two-way active avoidance but did not differ remarkably in pseudoconditioning and avoidance conditioning without stimulus pairing, than sham-operated and intact control rats. Animals with unilateral lesion in the CA 3 hippocampal subfield showed no differences in these shuttle situations. The results suggest that CA 3 hippocampal pyramidal cells are of particular importance to the establishment of the stimulus-stimulus relations in the brain.

Animals↗