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Biomedical subjects

L Baran

Publications and source records attributed to L Baran.

84 records · Page 5Linked to original sources
PubMedDate not supplied

On the central antiserotonin action of trazodone.

Trazodone, an antidepressant drug with an unknown mechanism of action, has been examined in order to demonstrate its central antiserotonin action. Trazodone antagonizes the head twitch response induced by 5-hydroxytryptophan in rats and mice, or by-5-methoxytryptamine in rats (the ED50 values are 9.3, 5.2, and 10.8 mg/kg respectively). It counteracts convulsions induced by tryptamine in rats (ED50=3.75 mg/kg). Trazodone abolishes hyperthermia induced by serotoninomimetics (LSD, quipazine, fenfluramine) in rabbits. It does not affect ptosis induced by reserpine, and diminishes stimulation of the locomotor activity induced by amphetamine. Our findings demonstrate that trazodone has a central antiserotonin action, similarly as three other antidepressant drugs: mianserin, danitracen and doxepin, whose central antiserotonin action has been found previously.

Animals↗
PubMedDate not supplied

On the central antiserotonin activity of benzoctamine and opipramol.

Benzoctamine inhibited the head twitch reaction induced by L-5-hydroxytryptophan (5-HTP) in mice and by 5-methoxytryptamine (5-MT) in rats pretreated with tranylcypromine. It also antagonized tryptamine (TRP)-induced clonic convulsions of forepaws in rats. Opipramol had no effect in the 5-MT test and appeared to be a weak antagonist in the 5-HTP and TRP tests. Both drugs, of which benzoctamine was a more potent antagonist, inhibited hyperthermia induced by LSD in rabbits. Benzoctamine abolished also LSD-or quipazine-induced stimulation of the flexor reflex in spinal rats; the above effect did not depend on noradrenolytic action of the drug. Opipramol was ineffective as an LSD or quipazine antagonist in this test. These results suggest that benzoctamine blocks the central postsynaptic serotonin receptors. This effect may contribute to the anxiolytic effect of the drug.

Animals↗
PubMedDate not supplied

The central action of salbutamol, a beta-agonist with a potential antidepressant activity.

The pharmacological profile of salbutamol, an agonist of beta-adrenergic receptors and a potential antidepressant drug, and its effect on the central serotonin system were studied. It was found that salbutamol either had no effect, or, at higher doses, inhibited the spontaneous activity of mice and rats; it did not influence significantly either the produced by amphetamine locomotor stimulation (in mice and rats) or amphetamine stereotype (in rats). Salbutamol while not affecting body temperature of normal mice reversed hypothermia but not ptosis induced by reserpine, and counteracted the hypothermic action of apomorphine in mice. It neither affected the spiperone-induced catalepsy nor was active in the behavioural despair test in rats. Salbutamol had no effect either, on the fenfluramine-induced hyperthermia in rabbits, on the 5-hydroxytryptophan-induced head twitch reaction in mice, on the tryptamine-induced clonic convulsions of forepaw in rats on the flexor reflex in spinal rats, or on the quipazine- or fenfluramine-induced stimulation of this reflex. The above findings indicate that the pharmacological profile of salbutamol resembles that of classical imipramine-like antidepressant drugs to a very small extent and it does not affect the central serotonergic transmission.

Albuterol↗
PubMedDate not supplied

Opiate-like peptides. Part IV. Kyotorphin and its analogues: synthesis and analgesic activity.

L-Tyrosyl-L-arginine ( kyotorphin ) and its 8 analogues were synthesized using EEDQ method. Analgesic activity and neurotoxic effect of all dipeptides were examined. Three of analogues investigated display weak analgesic activity occurring on the administration of doses which exert neurotoxic effect. For three other analogues the neurotoxic effect precedes the possible analgesic effect. The remaining two analogues were biologically inactive.

Analgesics↗
PubMedDate not supplied

Central action of Craviten (M-71).

Craviten (M-71) or 2S, 2'S) N, N'-dimethyl-N, N'-bis [1-(3', 4', 5' -trimethoxy-benzoyloxy)-butyl-2]-ethylenediamine dihydrochloride an agent with a strong antiarrhythmic action has practically no effect on the central nervous system of rats and mice. It exerts no effect on the spontaneous motor activity, on amphetamine-stimulated hyperactivity, on rota-red performance, it has no analgesic and anticonvulsant action and does not change the hexobarbital sleeping time. No effects of Craviten were observed on the body temperature in rats and mice. It decreased the arterial blood pressure in rats and stimulated slightly respiration. The hypotensive effect was dose-dependent. The LD50 of the preparation is: rats: 142 mg/kg ip, 15 x 8 mg/kg iv; mice: 550 mg/kg ip; rabbits: 5 x 1 mg/kg iv.

Amphetamine↗
PubMedDate not supplied

Effect of nitric oxide synthase inhibitors and molsidomine on the anticonvulsant activity of some antiepileptic drugs.

The present study examined effects of the two nitric oxide synthase (NOS) inhibitors, N-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), as well as of the NO donor molsidomine on the anticonvulsant activity of conventional antiepileptic drugs (diphenylhydantoin and carbamazepine) and competitive (CGP 37,849) and non-competitive (dizocilpine) NMDA receptor antagonists against the maximal electroshock in mice. It was found that L-NAME (25 and 50 mg/kg) did not affect the anticonvulsant activity of either drug, having had no influence on their anticonvulsive ED50 values. 7-NI (50 and 100 mg/kg) reduced the anticonvulsive ED50 (augmentation of the anticonvulsant activity) of CGP 37,849 and dizocilpine, raised the anticonvulsive ED50 (attenuation of the anticonvulsant activity) of diphenylhydantoin and had no influence on the anticonvulsant effect of carbamazepine. At the same time, augmentation of the anticonvulsant activity (reduction of the ED50 values) of diphenylhydantoin, carbamazepine and CGP 37,849, but not of dizocilpine, was observed after molsidomine (100-150 mg/kg). Moreover, 7-NI (100 mg/kg) and molsidomine (100 and 150 mg/kg), but not L-NAME (25 and 50 mg/kg), raised the threshold for electroconvulsions. The obtained results indicate that alterations in the anticonvulsant activity of the investigated drugs evoked by 7-NI and mosidomine, may result from non-specific effects of the NOS inhibitor and the NO donor, having no connection with the brain NO pathway.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase in the mouse brain.

The present study examined ex vivo effect of kainic acid and pentetrazole administration on the activity of nitric oxide synthase (NOS) in the mouse brain. NOS activity was assayed by measuring the formation of [3H] citrulline from [3H]arginine in the homogenates of mouse hippocampus, neocortex and cerebellum. The highest basal activity of the enzyme was found in this latter brain region. Administration of kainic acid (30 mg/kg) increased the NOS activity in all brain regions examined. On the other hand, pentetrazole (60 mg/kg) did not evoke any significant changes in the NOS activity at 5 min after the administration. Only in cerebellum, at 10 min after administration of pentetrazole, the increase in the activity of the enzyme was observed. The obtained results indicate that the two particular convulsants used in this study differ not only in respect of behavioral signs of seizures which they evoke, but also in respect of the effect on mouse brain NOS activity.

Animals↗