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Biomedical subjects

R Lasek

Publications and source records attributed to R Lasek.

17 recordsLinked to original sources

Category-order effects in memory span.

When Ss are required to recall lists containing both words and digits, memory span is higher when the digits precede the words than when the words precede the digits. In Experiment 1, both forward and backward recall were tested; it was demonstrated that this category-order effect reflects the input position, and not the output position, of the items. Experiment 2 revealed that this effect was not eliminated by a filled retention interval. Experiment 3 showed that the effect was eliminated when lists were presented at a fast presentation rate. In Experiment 4, the effect was eliminated when Ss engaged in articulatory suppression. A 5th experiment extended the findings of Experiment 4 to the case in which lists are composed of semantically related or unrelated words. These results suggest that category-order effects reflect mnemonic activity that Ss engage in during list presentation and do not arise from structural characteristics of the memory system.

Humans

[The influence of central monoaminergic systems on the anticonvulsive action of propranolol].

The influence of substances modulating the activity of central monaminergic systems on the anticonvulsant effect of propranolol was investigated with the maximal electroshock test in mice. The results demonstrated that especial the noradrenergic system plays an important role in modulating the efficacy of propranolol. Pharmacological stimulation of the noradrenergic system (e. g. with desipramine, pargyline, yohimbine) resulted in an enhanced anticonvulsant effect of propranolol. Compounds that suppress the noradrenergic transmission reduced this action. On the other hand manipulations of serotonergic (with 5,7-DHT, 5-HTP, PCPA) or dopaminergic (with 6-OHDA + desipramine, apomorphine) mechanisms seems to be without marked influence on the protective effect of propranolol in maximal electroshock.

5-Hydroxytryptophan

[The neuropharmacology of beta adrenolytics].

The paper provides a survey of neuropharmacological fundamentals for the use of beta-adrenolytics in the treatment of psychiatric and neurological diseases. In particular there are discussed results of animal- and clinical-pharmacological experiments carried out in order to assess the influence of betaadrenolytics in disorders and diseases such as anxiety, psychoses, tremor, some kinds of addiction, migraine and epilepsy. The conclusion is that in spite of some ascertained clinical indications on the one hand and a variety of neuropharmacological results on the other the mode of action of betaadrenolytics at the level of the CNS remains still insufficiently explainable.

Adrenergic beta-Agonists

[Effect of stimulation of the locus coeruleus on cobalt-induced epileptiform activity in the rat].

The effects of a short-time serial stimulation of the locus coeruleus (LC) on cobalt-induced focal epileptiform activity were investigated in unrestrained rats with chronically implanted electrodes. The results show a marked reduction of the spike-wave activity immediately after stimulation. The characteristic groups of "cobalt-spikes" are completely suppressed within 30 s and significantly reduced up to 120 s. This suppression was partly antagonized by pretreatment with the beta-receptor antagonist propranolol (2-5 mg/kg i.p.). On the other hand, the stimulation of other areas, lateral or medial of the LC (n. parabrachialis; stratum griseum centrale), reduced the spike-discharges only insignificantly. These data support the hypothesis that the noradrenergic system play an important inhibitory role in epileptiform activity.

Animals

[Effect of drugs on laboratory diagnosis--effect of propranolol on selected laboratory values].

In the accessible literature the influence of beta-blockers on laboratory methods is estimated only little systematically and nearly exclusively on parameters of the glucose and lipometabolism. The influence on several methods in vitro is without relevance to practice. Own examinations showed that in 32 patients with essential hypertension of stage I (after Baumann and Nitschkoff) under therapeutic doses of 50--80 mg propranolol a day in none of the 18 chemical parameters tested after a four weeks' treatment significant deviations relevant to practice appeared in comparison to the parameters before treatment.

Adolescent

Anticonvulsant effects of propranolol and their pharmacological modulation.

The anticonvulsant activity of propranolol was investigated in mice and rats using the electroshock seizure test (MES) and in special cases the electrically evoked hippocampal afterdischarges as a model. The results show that racemic propranolol as well as the two enantiomers were effective against MES. (+)-propranolol, the isomer with negligible beta-adrenoceptor blocking capacity revealed the stronger effect, its efficacy was comparable with the potency of phenobarbital, an overadditive synergism could be demonstrated. Subchronic administration of the two enantiomers led to a significantly reduced ED50 value of (-)-propranolol 24 h after the last application, the (-)-isomer became more effective. The (+)-propranolol did not reveal significant differences. In unrestrained rats with chronically implanted electrodes propranolol increased the stimulation threshold and reduced the duration of electrically evoked hippocampal afterdischarges. Investigations with drugs affecting monoaminergic systems in the CNS demonstrated that the noradrenergic system might play a predominant role in modulating the anticonvulsant effectiveness of propranolol. Pharmacological suppression (6-hydroxydopamine, reserpine, phenoxybenzamine) or stimulation (maprotiline, yohimbine, clenbuterol) reduced or enhanced the activity of propranolol against MES. On the other hand, manipulation of the serotonergic or dopaminergic system seemed to be less effective. In general, the findings confirm the results of previous studies that the membrane stabilizing property and not the blocking action on beta adrenergic (or serotonergic) receptors accounts for the anticonvulsant activity of propranolol.

Animals