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Biomedical subjects

W Kostowski

Publications and source records attributed to W Kostowski.

At least 217 records · Page 12Linked to original sources
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Activity of diltiazem and nifedipine in some animal models of depression.

The effect of two calcium channel inhibitors, diltiazem and nifedipine in animal models of depression: a) behavioral despair test and b) behavioral deficit produced by uncontrollable footshock was investigated. Additionally, the influence of both drugs on mouse killing (muricide) behavior induced by chronic isolation was studied. Both drugs given in single doses increased the active behavior of rats in behavioral despair test. Nifedipine but not diltiazem was partially effective in the test when administered chronically (14 days). Both drugs also attenuated stress-induced behavioral depression in the open field and forced swim test. Diltiazem was markedly more active in the former whereas nifedipine in the latter test. Neither compound influenced killing behavior in muricidal rats. Our data support the notion that calcium channel inhibitors may possess antidepressant activity, although there appear to exist certain differences in their scope of action depending on the model applied.

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Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study.

Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study. W. DANYSZ , W. KOSTOWSKI, M. HAUPTMANN, A. BIDZINSKI. Pol. J. Pharmacol. Pharm., 1989, 41, 15-22. Influence of chemical lesions to the noradrenergic locus coeruleus (intracerebral 6-OHDA injection, systemic administration of DSP-4) and serotonergic raphe system (intracerebral 5,7-DHT) on some effects produced by electroconvulsive shock (ECS) was studied. Administration of ECS slightly but significantly attenuated clonidine (CLO)-induced hypothermia and reduced rats immobility in forced swim test. DSP-4 reduced ECS action on CLO hypothermia remaining without effect upon ECS action in the second test. Other lesions were ineffective in both tests. This finding is in contrast to results obtained previously in animals receiving desipramine. The possible difference between ECS and antidepressant drugs action is discussed.

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The effect of microinjections of clonidine into the locus coeruleus on cortical EEG in rats.

Microinjections of clonidine into the locus coeruleus (LC) area synchronized rat cortical EEG. This effect of clonidine was attenuated by local pretreatment of rats with idazoxan, an alpha-2 adrenoceptor antagonist. The data indicate functional role of alpha-2 adrenoceptors within LC area in regulation of ceruleocortical activity, and point at the LC as one of brain targets for the sedative action of clonidine.

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Chronic administration of desipramine and imipramine but not zimelidine attenuates clonidine-induced depression of avoidance behavior in rats.

Clonidine (CLO) given intraperitoneally in a dose of 0.05 mg/kg decreased the open-field behavior in rats and completely abolished avoidance acquisition. Short term (4 days) administration of desipramine (DMI) and imipramine (IMI) practically failed to change the depressive effects of CLO whilst chronic (21 days) treatment significantly reduced the CLO action on both avoidance and open-field behavior. Contrary to tricyclic antidepressants, zimelidine (ZIM) given either acutely or chronically did not affect the avoidance deficit but given chronically attenuated the CLO-induced sedation in the open field. The results suggest that "classic" tricyclic antidepressants acting strongly upon noradrenaline uptake are more potent in preventing avoidance deficit induced by the alpha 2-adrenoceptor agonist, CLO than drugs acting more selectively upon serotonin uptake.

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Comparative studies on antidepressant action of alprazolam in different animal models.

Alprazolam, a new benzodiazepine from triazolobenzodiazepine group, produced anxiolytic action in the conflict test with potency similar to that of diazepam. The myorelaxant activity of the drug was relatively weak. Unlike desipramine, alprazolam failed to reduce the immobility of rats in the forced swim test and was unable to prevent clonidine-induced hypothermia. Alprazolam, unlike desipramine, failed also to potentiate behavioral effect of noradrenaline injected into the hippocampus. Alprazolam after acute but not chronic administration antagonized the synchronizing effect of clonidine on EEG pattern. On the other hand, alprazolam similarly to tricyclic antidepressants, prevented the suppression of dominance behavior by clonidine in rats competing for food. The results indicate that alprazolam acts only weakly upon noradrenergic mechanisms related to depression and to antidepressant action of drugs.

Alprazolam↗
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Basomedial amygdaloid lesions and p-CPA induced muricidal aggression.

Bilateral lesions of basomedial amygdaloid nuclei are capable of significantly inhibiting muricidal aggression induced by oral p-chlorophenylalanine (p-CPA) in male rats. Rats lesioned in extra-amygdaloid structures or sham-lesioned show the usual p-CPA-induced muricidal activity, which ranges from 70 to 80% of treated animals. The results obtained indicate that basomedial amygdaloid nuclei play an important role in regulating p-CPA-induced muricidal aggression, even though the effect lasts for a relatively limited period of time. This fact is probably due to the intervention of still unidentified compensatory mechanisms.

Amygdala↗
PubMedDate not supplied

Possible relationship of the locus coeruleus--hippocampal noradrenergic neurons to depression and mode of action of antidepressant drugs.

Recent studies performed in our laboratory suggest involvement of locus coeruleus (LC) and hippocampal noradrenergic (NE) neurons in the mechanism of depression and mode of action of antidepressants. Both electrolytic and 6-OHDA lesions to the LC abolished desipramine action in forced swim test in rats. The action of desipramine was also reduced in rats pretreated with alpha 1 adrenolytic drugs -- phenoxybenzamine and prazosin. Electrical stimulation of the LC produced, like desipramine, activating effect in forced swim test, the phenomenon never observed in phenoxybenzamine-pretreated animals. Chronic (but not acute) administration of desipramine potentiated activatory effects of intrahippocampal injections of NE and phenylephrine but not isoprenaline in both open field and forced swim test. Depressant effect of intrahippocampal clonidine was reversed by chronic desipramine (in the open field test). The effect of desipramine was partially shared by citalopram.

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On the role of noradrenergic neurotransmission in the action of desipramine and amitriptyline in animal models of depression.

Three weeks of treatment with desipramine (DMI) and amitriptyline (AMI) reduced the hypothermic action of clonidine in rats. Both electrolytic and 6-hydroxydopamine lesions of the locus coeruleus (LC) and administration of DSP-4 counteracted the reduction of clonidine hypothermia produced by antidepressants. Lesions of the LC and DSP-4 administration also antagonized the anti-immobility action of single doses of DMI but failed to modulate the action of AMI in the forced swim test. Chronic DMI action on the rat immobility was reduced by 6-hydroxydopamine lesions of the LC: other lesions (electrolytic, DSP-4) were ineffective. Electrical stimulation of the LC increased the rat activity in the forced swim paradigm, producing an effect similar to that of antidepressants. The anti-immobility effect of DMI as well as LC stimulation were antagonized by drugs blocking alpha-adrenoceptors (phenoxybenzamine, prazosin) but not by propranolol, a non-selective antagonist of beta-adrenoceptors. On the other hand, the anti-immobility action of AMI was unchanged by all adrenolytics used in that study. The results indicate that the LC system and alpha 1-adrenoceptors play an important role in the antidepressive action of DMI, but not AMI, in the forced swim test.

Amitriptyline↗
PubMedDate not supplied

Desipramine antagonizes clonidine-induced suppression of dominance in rats: possible involvement of amygdaloid nuclei.

Bilateral microinjections of clonidine into the medial or basal amygdaloid nuclei suppressed the dominance behavior in rats competing for food. Desipramine given in five repeated daily doses antagonized clonidine effect. On the other hand suppression of dominance induced by clonidine given bilaterally into the cortical amygdaloid nucleus was resistant to desipramine treatment. The result suggests that the former nuclei are important target areas for clonidine-desipramine interaction at social interaction behavioral level.

Amygdala↗