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Biomedical subjects

I Zebrowska-Lupina

Publications and source records attributed to I Zebrowska-Lupina.

At least 37 records · Page 2Linked to original sources
PubMed1975

Central action of drugs acting on the cholinergic muscarinic receptor. III. Influence of atropine and scopolamine injected intraventricularly on behavior and levels of biogenic amines in the rat brain.

Atropine (At) and scopolamine (Sc) in low doses intensify basic activity, increase amphetamine stereotypy, and suppress catalepsy induced by injection of haloperidol. High doses lower body temperature, antagonize amphetamine stereotypy, and intensify the hypnotic action of chloral hydrate. Doses of about 1/2 LD50 induce narcotic sleep. Both At and Sc in a wide range of dosage protect against the tonic phase of convulsions produced by electroshock. Sc depresses content of acetylcholine in the brain proportionally to its dosage; At had a similar effect only at the lower of the two doses that were used. Both compounds had no effect on levels of noradrenaline and dopamine in the brain. The results indicate that low doses of blockers of the cholinergic muscarinic receptor, injected intraventricularly, produce strong central stimulation, whereas high doses produce depression of the central nervous system.

Acetylcholine↗
PubMed1975

The effect of alpha-adrenolytics on the levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in rat's brain.

Alpha-Adrenolytics (ABA)-phenoxybenzamine, phentolamine and aceperone-increase 5-hydroxyindoleacetic (5-HIAA) acid content in rat's brain. At the same time, these compounds either increase or do not affect 5-hydroxytryptamine (5-HT) level. Moreover, they potentiate L-dopa and reserpine-induced increase in 5-HIAA level and antagonized clonidine-induced decrease in 5-HIAA content. The experiments with probenecid indicate that the observed increase in 5-HIAA does not result from the deficient elimination of the metabolite from brain. The increase in 5-HT turnover in brain, due to ABA, is suggested.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Reversal of stress-induced deficit in aggression by monoamine oxidase inhibitors.

In the present study we investigated the effect of two monoamine oxidase (MAO) inhibitors: moclobemide (selective, reversible inhibitor of MAO-type A) or selegiline (selective irreversible inhibitor of MAO-type B) on electric footshock-induced fighting behavior in normal (unstressed) and chronically stressed (14 various stressors over 16 days) rats. In rats exposed to chronic stress the number of fighting attacks was reduced by about 75%. Prolonged (once a day, for 14 days) treatment with moclobemide (50 mg/kg/day) or selegiline (2 mg/kg/day) counteracted the deficit in aggression induced by chronic stress. The findings of the present study demonstrate that the selective MAO inhibitors, moclobemide and selegiline, protect against "behavioral depression" induced by the chronic stress similarly to other classes of antidepressant drugs.

Aggression↗
PubMedDate not supplied

Influence of antiepileptics on efficacy of antidepressant drugs in forced swimming test.

Antidepressant medications are indicated in a variety of sustained mood disorders, including depression, and in epileptic patients. On the other hand, some antiepileptics are also used in the treatment of affective disorders. Therefore, some interactions may appear between antiepileptics and antidepressant drugs. The aim of the present study was to investigate the influence of the treatment with antiepileptic drugs on the antidepressants' activity in mice (forced swimming test or assessment of locomotor activity). The animals received intraperitoneally (ip) antiepileptics: phenytoin (PHT) at 6 or 12 mg/kg, valproate (VAL) at 50, 100, 200 or 300 mg/kg, carbamazepine (CBZ) at 4, 6 or 9 mg/kg, vigabatrin (VGB) at 50, 100, 200 or 300 mg/kg or lamotrigine (LTG) at 12.5 or 25 mg/kg, 30, 60 or 90 min before the injection of antidepressants: imipramine (IMI, 20 mg/kg) amitriptyline (AMI, 10 mg/kg), maprotiline (MAP, 10 mg/kg), mianserin (MIA, 15 mg/kg), fluoxetine (FLX, 40 mg/kg) or fluvoxamine (FLV, 20 mg/kg). It was shown that the acute administration of antidepressant drugs significantly reduced the immobility time in forced swimming test in mice. Antiepileptics, given in a single dose, caused did not change the behavior of mice in this test, however, they abolished the characteristic effect of antidepressant drugs. Each antidepressant, given at a single dose, shortening the immobility time in forced swimming test and reduced the locomotor activity of mice. This sedative effect of antidepressants was intensified by antiepileptics. The present results suggest that antiepileptics can reduce the activating effect of antidepressant drugs of different groups.

Animals↗
PubMedDate not supplied

Comparison of central effects of noradrenaline and dopamine injected into the lateral brain ventricle in rats.

Noradrenaline and dopamine injected into the lateral brain ventricle exerted a significant effect on the behavior of rats. Both amines caused a slight rise in the basic locomotor activity which was significantly increased in the animals with inhibited monoamine oxidase activity. Besides that, they suppressed the behavior of rats in the open-field test, inhibited the conditioned avoidance response, decreased body temperature and increased amphetamine-induced motor hyperactivity. Noradrenaline, in contrast to dopamine, changed the intensity of amphetamine-induced stereotypy and prolonged the action of hypnotics. The central action of both catecholamines (in higher doses especially) seemed to have a biphasic course: in the first phase after administration depression was observed which was more pronounced after noradrenaline administration, in the second phase a stimulating effect b

Amphetamine↗
PubMedDate not supplied

The influence of antidepressants on aggressive behavior in stressed rats: the role of dopamine.

The influence of dopamine (DA) receptor blockers (haloperidol, sulpiride) on electric footshock-induced fighting behavior and on the effect of antidepressants (imipramine, clomipramine, nomifensine, mianserine) was investigated in chronically stressed male Wistar rats. Exploratory activity in an open field was measured in the same groups of animals. The effect of chronic stress and antidepressants on DA utilization in the brain was also investigated. It was shown that 48 h after the last session of repeated stress (various unpredictable stressors over 16 days) the number of fighting attacks was significantly reduced. However in stressed rats treated chronically (for 14 days) with antidepressants the intensity of fighting was restored to control value. On the contrary, when the stressed rats, receiving antidepressants chronically, were pretreated with DA receptor blockers: haloperidol (0.5 mg/kg) or sulpiride (50 mg/kg) but also alpha 1-adrenergic receptor blocker - prazosin (3 mg/kg) the effect of antidepressants was abolished. Exploratory activity was not significantly reduced under influence of stress. Neither antidepressants nor sulpiride modified exploratory activity of stressed rats. Haloperidol and prazosin but not sulpiride decreased this activity of normal, stressed and antidepressant-treated rats. It is concluded that prolonged treatment with antidepressants counteracts the decrease in aggression induced by chronic stress and that DA mechanism participate in this effect of antidepressant drugs.

Aggression↗
PubMedDate not supplied

The effect of noradrenergic receptor blocking agents on 5-hydroxytryptamine turnover in the brain of rats.

Phenoxybenzamine (PB), phentolamine (PT) and aceperone (AC) in doses of 25 and 50 mg/kg increased cerebral noradrenaline (NA) turnover so these doses were regarded as blocking brain NA receptors. PB (50 mg/kg), PT (50 mg/kg) and AC (25 and 50 mg/kg) accelerated also the turnover of brain 5-HT. PT in a dose of 25 mg/kg counteracted deceleration of 5-HT turnover induced by clonidine but not by quipazine. Almost the same extent of decrease in 5-HIAA concentration after quipazine was observed in controls as in the rats pretreated with NA blockers in a dose of 25 mg/kg. On the contrary PT given in a dose of 50 mg/kg antagonized significantly the effect of quipazine. The results indicate that NA blockig agents given in lower doses do not affect the 5-HT system, however after higher doses such effect is possible.

Animals↗
PubMedDate not supplied

Synthesis and some central pharmacological properties of new derivatives of 2,3-dihydroimidazo[1,2-a]pyrimidine-6-carboxylic acid.

Twenty one derivatives of 2,3-dihydroimidazo[1,2-a]pyrimidine-6-carboxylic acid (6 n-butyl amides and 15 free acids) bearing the aromatic ring in position 1 or 2 were obtained. They were synthesized by aminolysis or hydrolysis of respective ethyl esters. Pharmacological studies on the central action of eight compounds 1, 2, 4, 5, 7, 8, 9 and 10 were carried out on mice and rats. The most active compounds, producing sedation and hypothermia, and 1, 2 and 5. The compounds decreased amphetamine-induced hyperactivity. Besides, compound 2 exerted analgesic effect in mice.

Animals↗
PubMedDate not supplied

Analgesic action of alpha-adrenolytics in albino mice.

The effect of alpha-adrenolytics: phenoxybenzamine, phentolamine, aceperone, dihydroegotamine, and yohimbine, was tested on reactivity to pain, and on the analgesic action of morphine and pethidine in albino mice. The compounds exert an analgesic effect by themselves, and potentiate the analgesic action of threshold doses of morphine and pethidine. The results seem to provide another proof that the cerbral noradrenaline neurons participate in central mechanisms of pain perception.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

The effect of alpha-adrenolytics on central action of agonists and antagonists of dopaminergic system.

alpha-Adrenoceptor blocking agents: phenoxybenzamine, phentolamine and aceperone, potentiated and prolonged amphetamine and apomorphine stereotypy in the rat, but inhibited the amphetamine hypermotility. The hypermotility produced by apomorphine was antagonized only by aceperone. Cataleptogenic action of haloperidol and fluphenazine was inhibited by the alpha-adrenoceptor blocking agents. Phenoxybenzamine and phentolamine, and to a smaller degree aceperone, inhibited the depletion of dopamine following pretreatment of rats with alpha-methyltyrosine. The results indicate that the blockade of central alpha-adrenergic receptors changes the reactivity of dopaminergic system on the action of its agonists and antagonists.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Stress-induced depression of basal motility: effects of antidepressant drugs.

Behavioral and biochemical effects of repeated immobilization stress were determined in male Wistar rats. The influence of acute or repeated administration of antidepressant drugs on these effects of stress were also evaluated. It was found that repeated stress (immobilization 3 h/2 degrees C/4 days or various stressors/8 days) reduced basal locomotor activity of rats and prolonged immobility time in Porsolt's despair test. Antidepressant drugs (desmethylimipramine, imipramine, amitriptyline, clomipramine, mianserine), given acutely, restored basal locomotor activity of stressed rats to control level. Desmethylimipramine, imipramine and amitriptyline reduced immobility time in Porsolt's test similarly in control as in stressed rats. However clomipramine, mianserine and trazodone were effective in this test only in stressed rats. Imipramine given for 4 or 8 days (1 h before the stressor) normalized basal locomotor activity. Repeated (for 8 days) various stressors decelerated utilization of noradrenaline (NA) and dopamine (DA) in the brain. Imipramine given once a day for 8 days (1 h before the stressor) normalized brain utilization of catecholamines (CA). It was proposed that depression of basal motility and reduction of CA utilization in the brain induced by repeated stress may be counter acted by antidepressant drugs.

Animals↗
PubMedDate not supplied

5-Methoxytryptamine-induced head twitches in rats.

In rats pretreated with pargyline ip injection of 5-methoxytryptamine (5-MT), but not of 5-HT, produced characteristic head twitches. 5-HT receptor blocking agents (cyproheptadine, methergoline, mianserine, WA-335-BS, and methsergide) reduced the effect of 5-MT. These substances in doses 20-160 times higher than their ED50 in head twitch test did not antagonize the pinna reflex. 5-MT-induced head twitches were also inhibited by imipramine, morphine, phenoxybenzamine and aceperone. However, their ED50 were only 3-8 times below the doses necessary to inhibit the pinna reflex. Reserpine, phentolamine, spiroperidol, pimozide and LiCl did not modify head twitches produced by 5-MT, while PCPA even potentiated them. Our results suggest the 5-MT-induced head twitches are due to the activation of the central 5-HT mechanisms probably as a result of direct stimulation of 5-HT receptors by 5-MT. Antagonism of 5-MT-induced head twitches and the dissociation of doses effective in this test from those inhibiting the pinna reflex may be of value in the prediction of central 5-HT receptor blocking properties.

5-Methoxytryptamine↗