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L Baran

Publications and source records attributed to L Baran.

At least 19 recordsLinked to original sources
PubMed1994

The role of nitric oxide in the kainate-induced seizures in mice.

The effect of L-arginine (L-Arg), D-arginine (D-Arg), N-nitro-L-arginine methyl ester (L-NAME) and N-monomethyl-L-arginine (L-NMMA) on the kainate-induced seizures was studied in mice. It was found that the precursor of nitric oxide (NO) L-Arg (150-600 mg/kg i.p.) increased dose-dependently the dose of kinate necessary to produce clonic convulsions in 50% of the animals (CD50). Such an anticonvulsant effect was not observed in mice pretreated with D-Arg (150-600 mg/kg i.p.), the latter drug not being a substrate for NO formation. The inhibitors of NO synthase L-NAME and L-NMMA, both administered in doses of 30-30 mg/kg i.p., reduced the convulsive threshold by decreasing the CD50 of kainate. Moreover, L-NAME (3 mg/kg) antagonized the anticonvulsant effect of L-Arg (300 mg/kg). These results indicate that NO may play a role of an endogenous anticonvulsant substance in mice.

Amino Acid Oxidoreductases↗
PubMed1990

[The agonists of I-A serotoninergic receptors restore in rats behavior impaired by L-dihydroxyphenylalanine].

The ability of selective and nonselective 5-HT1A agonists, nondirect 5-HT agonists and 5-HT2 antagonists influence on the L-DOPA-disturbed rats behaviour were studied. The results indicate that agonists 5-HT1A like receptors largely than 5-HT2,3 agonists, 5-HT2 antagonists and nondirect 5-HT agonists promote restoration of the L-DOPA disturbed escape behaviour in acute stress situation.

Animals↗
PubMed1989

The effect of repeated treatment with antidepressant drugs on the thyrotropin-releasing hormone (TRH)-induced hyperthermia in mice.

The effect of acute (single dose) or repeated (twice daily, for 14 days) administration of 10 mg kg-1 p.o. of imipramine, amitriptyline, citalopram or mianserin has been examined on the hyperthermia induced by thyrotropin-releasing hormone (TRH) (40 mg kg-1 i.p., 2, or 2 and 72 h after single or last dose of antidepressants, respectively) in mice. Both imipramine and amitriptyline, given repeatedly, potentiated the TRH response, though the effect was observed 2 but not 72 h after the last dose of those drugs. Potentiation was also found after the single dose of imipramine or amitriptyline. On the other hand, citalopram and mianserin, administered either acutely or repeatedly, did not affect the TRH-induced hyperthermia.

Amitriptyline↗
PubMed1985

Chronic treatment with the potential antidepressant drug rolipram: the effect on the behavioural responses to adrenergic and dopaminergic receptor agonists with some biochemical correlates.

We studied the effect of acute and chronic treatment with rolipram, a potential antidepressant drug, on the behavioural responses induced by adrenergic and dopaminergic receptor agonists in mice and rats, and on (3H)prazosin and (3H)dihydroalprenolol binding to cortical membranes and whole brain noradrenaline and dopamine utilization in rats. Chronic, but not acute, administration of rolipram potentiated a behavioural response mediated through central alpha 1-adrenoceptors, attenuated an alpha 2-adrenoceptor-mediated response and inhibited a beta-adrenoceptor-mediated response. Neither treatment affected the behavioural responses to dopaminergic stimulants. Repeated treatment with rolipram decreased the density of cortical (3H)dihydroalprenolol, but not (3H)prazosin bindings sites, and reduced brain noradrenaline, but not dopamine utilization. These results suggest that chronic administration of rolipram induces the down-regulation of the central beta- and alpha 2-adrenoceptors and enhances the responsiveness of the central alpha 1-adrenoceptors with no apparent changes in the alpha 1-adrenoceptor density.

Aggression↗
PubMed1984

Opposite action of m-chlorophenylpiperazine on avoidance depression induced by trazodone and pimozide in CD-1 mice.

m-Chlorophenylpiperazine (CPP) given in doses up to 2 mg/kg did not affect conditioned avoidance responses (CAR) of CD-1 mice pre-trained in a shuttle box. It reversed the inhibitory action of trazodone (10 mg/kg) on CAR, but dose-dependently potentiated the inhibitory effect of pimozide (0.2 and 0.5 mg/kg). Apparently, dopaminergic transmission is important for the attenuating effect of CPP on CAR inhibition.

Animals↗
PubMed1984

Repeated treatment with antidepressant drugs prevents salbutamol-induced hypoactivity in rats.

We have found earlier that a number of antidepressant drugs, administered repeatedly, prevent the salbutamol-induced hypoactivity in rats. Our further experiments show that a similar effect is produced by repeated, but not acute, treatment with other antidepressants: clomipramine, mianserin and nialamide. Two non-antidepressant psychotropic drugs, haloperidol and diazepam, were inactive after repeated administration. These results seem to support our earlier hypothesis that prevention of the salbutamol-induced hypoactivity may be regarded as functional evidence at the behavioral level for the subsitivity of beta-adrenoceptors.

Albuterol↗
PubMed1984

Chronic treatment with electroconvulsive shock prevents the salbutamol-induced hypoactivity in rats.

Several lines of evidence (binding studies, reduced responsiveness of brain adenylate cyclase to noradrenergic stimulation) indicate that chronic treatment with electroconvulsive shock (ECS) induces down-regulation of central beta-adrenoceptors. The effect of acute and chronic (10 days) treatment with ECS on salbutamol-induced suppression of exploratory activity in rats has been examined. This effect was prevented by chronic but not by acute treatment with ECS. Chronic treatment with ECS did not affect exploratory activity. The salbutamol-induced hypoactivity is mediated through central beta-adrenoceptors (antagonistic effect of (-)-propranolol but not (+)-propranolol or practolol), so the results may be regarded as functional evidence at the behavioral level for the down-regulation of beta-adrenoceptors produced by chronic treatment with ECS.

Albuterol↗
PubMed1983

The effect of chronic treatment with antidepressant drugs on salbutamol-induced hypoactivity in rats.

Several lines of evidence (binding studies, reduced responsiveness of brain adenylate cyclase to noradrenergic stimulation, electrophysiological data) indicate that chronic treatment with antidepressant drugs induces subsensitivity of central beta-adrenergic receptors. We studied the effect of acute (single dose) and chronic (14 days, twice daily) treatment with imipramine, desmethylimipramine, amitriptyline, fluvoxamine and citalopram (10 mg/kg, orally) on salbutamol-induced suppression of exploratory activity in rats. This effect of salbutamol was antagonized by chronic, but not acute treatment with antidepressants. Chronic treatment with antidepressants as a rule did not significantly affect exploratory activity. Our results may be regarded as functional evidence at the behavioural level for the subsensitivity of beta-adrenergic receptors.

Albuterol↗
PubMed1983

Antagonism by tricyclic antidepressants of reserpine-induced hypothermia in mice. Involvement of postsynaptic alpha 2-adrenoceptors.

The effects of adrenoceptor blocking agents and cyproheptadine on the antagonism by the antidepressants imipramine, desipramine and maprotiline, of reserpine-induced hypothermia in mice were studied. The anti-reserpine effect of the antidepressants was reduced by phenoxybenzamine, prazosin, yohimbine and d,1-propranolol, the two latter drugs exhibiting the strongest effect. Practolol was ineffective, while cyproheptadine potentiated the effect of maprotiline and was inactive towards imipramine and desipramine. Furthermore, the anti-reserpine effect of desipramine (the other antidepressants not being studied) was also reduced by piperoxan and l-propranolol, but not by d-propranolol. The reserpine-induced hypothermia was antagonized by clonidine and this effect was completely blocked by yohimbine and partly reduced by prazosin. These results confirm that the antagonism by tricyclic antidepressants of reserpine-induced hypothermia depends on the activation of noradrenergic mechanisms and indicate that this effect is mediated not only by alpha 1- and beta-, but also by postsynaptic alpha 2-adrenoceptors.

Animals↗
PubMed1981

Psychopharmacological profile of mesterolone.

A psychopharmacological profile of mesterolone, an androgen and potential antidepressant drug, was tested in mice and rats. Given in a dose of 80 mg/kg ip, mesterolone potentiated the action of L-DOPA in mice and in doses 40 and 80 mg/kg ip potentiated the amphetamine stereotypy in rats. On the other hand, in doses of 20--80 mg/kg ip mesterolone did not affect the reserpine induced hypothermia and ptosis, did not antagonize the apomorphine induced hypothermia in mice, did not change the motor stimulation produced by amphetamine and did not affect the spiperone induced catalepsy in rats. Mesterolone did not affect the head twitch response after 5-hydroxytryptophan in mice and was inactive in the behavioral despair test in rats. The results indicate that the psychopharmacological profile of mesterolone only slightly resembles the profile of classical imipramine-like anti-depressants.

Animals↗
PubMed1980

[Giant aneurysm of the internal carotid artery, stimulating parasellar tumor].

The authors report a case of a giant aneurysm of the internal carotid artery filling from the left internal carotid artery below the site of branching-off of the posterior communicating artery. The initial neurological, and ophthalmological signs and plain films of the skull suggested presence of an Erdheim's tumour. It is worth stressing that the onset of the clinical manifestations was at the age of 15 years, particularly in the form of progressing binasal hemianopsia with sparing of the lower temporal quadrant. The efficiency of the cerebral circulation was tested using Mathas' test, electroencephalography, ophthalmodynamometry and angiography. It was decided to ligate the left carotid artery although Mathas' test during angiography was not as positive. The boy tolerated the operation well. Ophthalmological examination demonstrated after 18 months normal visual fields and normal visual acuity. Further follow-up during 8 years demonstrated normal psychosomatic development of the boy.

Adolescent↗
PubMed1979

The central action of pizotifen.

The central action of the potential antidepressant drug pizotifen (Sandomigran) was studied in mice, rats and rabbits. Pizotifen in doses up to 10 mg/kg i.p. was ineffective in classic tests for antidepressant activity. It neither antagonized the effects of reserpine in rats (hypothermia, ptosis) nor potentiated the effects of amphetamine (in mice and rats), nialamide or L-dopa (in mice) on locomotor activity. However, its antidepressant activitiy was found in the 'despair test' in rats. On the other hand, pizotifen inhibited the head twitch reaction induced by L-5-hydroxytryptophan in mice (ED50 = 0.009 mg/kg, i.p.) and by 5-methoxytryptamine (+ tranylcypromine) in rats (ED50 = 0.45 mg/kg, i.p.). It also antagonized tryptamine-induced clonic convulsions of fore-paws in rats (ED50 = 0.35 mg/kg, i.p.), and in doses of 5--10 mg/kg s.c. inhibited hyperthermia produced by LSD in rabbits. Finally, pizotifen (0.1--0.3 mg/kg, i.v.) inhibited or abolished LSD- or quipazine-induced stimulation of the hind limb flexor reflex of spinal rats; the above effect was not due to noradrenolytic action of the drug. These results suggest that pizotifen strongly blocks the central postsynaptic serotonin receptors.

Amphetamine↗