Biomedical subjects

W Kostowski

Publications and source records attributed to W Kostowski.

At least 55 records · Page 3Linked to original sources

PubMed1992

[The effect of naloxone on the activation, inducible by chronic alcoholic intoxication, of the membrane-bound form of enkephalin convertase in the midbrain and hypothalamus of rats].

The activity of membrane-bound and soluble enkephalin convertase was determined with dansyl-Phe-Leu-Arg as substrate in midbrain, including hypothalamus, of Wistar rats, who were given ethanol (20% solution i.g., 9-15 g/kg per day during 4 days) or naloxone (2 mg/kg i.p. twice a day during 4 days) or their combination. It was shown that activation of membrane-bound enzyme, observed after alcohol treatment of rats, didn't develop by combined ethanol-naloxone administration. It's supposed that alcohol-stimulating effect on this enzyme realizes throughout the hyperstimulation of opioid receptors by enkephalins and, possible, by other opioid-active compounds.

Alcoholism↗

PubMed1991

Chronic oral treatment with diltiazem or verapamil decreases isolation-induced activity impairment in elevated plus maze.

Adult male Wistar rats were either socially isolated or group-housed for 6 weeks and then tested in an elevated plus maze. During isolation the rats received either water or two concentrations of the calcium channel inhibitors, diltiazem or verapamil, in drinking solutions (approximately 5 and 10 mg/kg daily). Isolated rats showed a significantly lower total number of arm entries, a lower percentage of open arm entries and negligible time spent therein than did group-housed animals. Verapamil, in the higher dose, prevented that effect of isolation. Treatment with diltiazem brought about a similar tendency, though the effect did not reach statistical significance. Chronic treatment of group-housed rats with either drug failed to influence their behavior in the plus maze. We conclude that certain calcium channel inhibitors may decrease the behavioral deficit in the elevated plus maze that follows chronic social isolation.

Animals↗

PubMed1991

Serotonergic mechanisms in the nucleus accumbens affected by chronic desipramine treatment.

The effects of repeated treatment of rats with desipramine on 5-HT mechanisms within the nucleus accumbens (NAS) have been studied in a functional model. Local microinjections of 5-HT, quipazine as well as 5-HT1A receptor agonist buspirone, 8-OH-DPAT and NDO-008, inhibited rat locomotor activity in the open-field test. The effect of 5-HT and buspirone was blocked by serotonergic receptor antagonists methysergide and cyanopindolol, respectively. Chronic, but not acute treatment of rats with desipramine (10 mg/kg, PO, twice a day for 21 days, tests were performed 24 h after the last dose) significantly attenuated behavioral depression after 5-HT and quipazine microinjections, while the effect of buspirone was left unchanged. On the basis of present data, it may be concluded that whereas both accumbens 5-HT1A and 5-HT2 receptors appear to be important to regulation of animals' motility, only 5-HT2 receptors seem to be the most likely targets of antidepressive treatment. These data, along with previously reported changes in limbic noradrenergic and dopaminergic activity after antidepressive treatment, may explain the energizing influence of drugs and electroconvulsive shocks on psychomotor retardation, a part of endogenous depression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

Myorelaxant effect of baclofen injected to the nucleus accumbens septi.

The GABAergic modulation in the nucleus accumbens septi (NAS) of muscle tone was investigated in rats using behavioral tests. The GABAB receptor agonist baclofen dose-dependently decreased muscle tone in the wire-mesh and bar holding tests both after local injection into the NAS (1.0 and 2.5 micrograms), and after intraperitoneal administration in a dose of 20 mg/kg. In the Wirth's test haloperidol (5 mg/kg i.p.), produced catalepsy, whereas baclofen (20 mg/kg, i.p.) significantly deteriorated rats' performance. Intraaccumbens microinjections of muscimol, midazolam, nicardipine, as well as peripheral injections of haloperidol and midazolam failed to modify muscle tone in the wire-mesh test. These findings argue against the involvement of GABAA receptors, benzodiazepine receptors, as well as dopaminergic- and calcium channel-related mechanisms in the effect of baclofen. Hence, the muscle relaxant effect of baclofen seems to be also mediated through GABAB receptor sites within the NAS.

Animals↗

PubMed1990

GABAergic mechanisms in the nucleus accumbens septi regulating rat motor activity: the effect of chronic treatment with desipramine.

The influence of chronic treatment with desipramine upon GABAergic mechanisms within the nucleus accumbens septi (NAS) affecting rat motor behavior was studied in the automatic open fields. It was shown that intra-accumbens injections of picrotoxin on one hand and muscimol and baclofen on the other, produced dose-dependent increase or decrease in rat motility, respectively. Locomotor stimulation usually observed after picrotoxin did not occur in rats given local injections of a solution containing both picrotoxin and GABA A receptor agonist muscimol. Muscimol (130 ng as a pure compound) blocked also hypermotility produced by intra-accumbens administration of dopamine releasing drug d-amphetamine (10 micrograms). This part of the experiment was summarized as indicating that both GABA A and GABA B receptor-related mechanisms, which are under negative control of dopaminergic neurons in the NAS, play an important role in regulating behavior in the rat. In the second part of the experiment it was observed that chronic treatment of rats with desipramine (DMI) (10 mg/kg, PO, twice daily for 21 days, rats were tested 24 hr after the last dose of the drug) significantly attenuated or blocked the inhibitory effect on locomotion of both baclofen and muscimol. The stimulatory influence of picrotoxin seemed also to be diminished, but it still attained the level of accepted statistical significance. On the basis of these and other data it is concluded that observed changes in the effects of GABAergic agonists in DMI-treated rats are probably due to an enhancement of local dopaminergic mechanisms, thus leading to the potentiation of a negative interaction between dopaminergic and GABAergic mechanisms within the NAS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1990

Effects of intra-accumbens administration of dopamine agonists on stress-induced behavioural deficit.

The effect of post-footshock injections of (+)-amphetamine, the selective D2-receptor agonist quinpirole (LY 171555), and the D2-receptor antagonist metoclopramide, into the nucleus accumbens, on the formation of the open field deficit, has been studied in rats. Microinjections of (+)-amphetamine (10 micrograms) stimulated rat locomotor activity tested 5 min later, while quinpirole (10 micrograms) significantly inhibited animal motility in the test. The open field behaviour was not changed 24 h after injection of either drug. Amphetamine applied immediately after inescapable footshock did not modify stress-induced locomotor depression, when the rats' behaviour was examined 24 h later. On the other hand, post-shock injections of quinpirole significantly attenuated the long-term effects of the stressor, in the open field. Metoclopramide (10 micrograms) inhibited rat locomotor activity 5 min, but not 24 h, after local injection. Administration of a solution containing both quinpirole (10 micrograms) and metoclopramide (1 microgram) decreased motor activity of unstressed rats to a smaller degree than did quinpirole (10 micrograms) alone. Post-footshock injection of metoclopramide did not affect stress-induced hypomotility. It is concluded that the present data support the hypothesis that local depletion of brain dopaminergic stores causes some behavioural effects of stressors.

Animals↗

PubMed1990

Effects of intra-amygdaloid TRH injections on motor activity and dominant-submissive behavior in rats competing for water.

The effect of thyrotropin releasing hormone (TRH) microinjections into the central amygdala (10 g in 0.5 1 into each side) on locomotor activity water intake and dominance behavior in a water competition test was investigated in male Wistar rats. TRH increased the general motility without altering the number of rearings. Intra-amygdaloid TRH injection to submissive rats resulted in a loss of subordinate position in these animals in the water competition test. A tendency to decrease dominance followed the injection of the peptide to the dominant animals. The effect of TRH in the dominance test does not appear to involve influence on the thirst drive as microinjection of the peptide did not change significantly the water consumption in thirsty rats.

Amygdala↗

PubMed1989

Intra-hippocampal buspirone in animal models of anxiety.

The effect of intra-hippocampal injections of the serotonergic 5-HT1A receptor agonist, buspirone, on rat exploratory activity was evaluated in the 'open field' and 'elevated plus maze' tests. The dose of 2.5 micrograms, but not of 1 microgram, of buspirone administered to the dentate gyrus of the hippocampus increased the time spent on exploration of open arms in the elevated plus maze, as well as it increased the number of central entries in the open field. The results indicate an anti-emotional influence of local stimulation of 5-HT1A receptors by buspirone.

Animals↗

PubMed1989

Interaction between accumbens D1 and D2 receptors regulating rat locomotor activity.

The effect of intra-accumbens injections of various dopaminergic agonists and antagonists on the rat locomotor activity has been evaluated in automated open fields. Locomotor stimulation has been observed after local administration of d-amphetamine (10 micrograms), apomorphine (10 micrograms), as well as of solution containing the D1 agonist SKF 38 393 and D2 receptor agonist LY 171 555 (quinpirole) in doses (10 and 4 micrograms, respectively) which were inactive when both drugs were administered separately. On the other hand separate injections of metoclopramide (0.1 microgram) and SCH 23 390 (0.5 microgram) (D2 and D1 receptor antagonists) very potently inhibited animals' locomotor activity. The data indicate that concomitant stimulation of both accumbens D1- and D2-receptor related mechanisms is a necessary condition to increase rat motility. Moreover, it seems that accumbens D1 receptors may be differently involved in the control of facilitatory versus inhibitory motor processes.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1989

The influence of antidepressive treatment on GABA-related mechanisms in the rat hippocampus: behavioral studies.

The effect of antidepressive treatment upon central GABAergic mechanisms has been studied in a behavioral model. Local injections (dentate gyrus of the dorsal hippocampus) of picrotoxin, a chloride channel blocker linked with the function of GABA-A receptor complex, potently stimulated rat motility recorded in the automated open fields. The intra-hippocampal administration of GABA antagonized the behavioral effect of picrotoxin (0.5 microgram). Similar effects were produced by addition to picrotoxin solution (0.25 microgram) of the GABA-A receptor agonist muscimol (0.25 microgram). Chronic (21-day), but not single, treatment of rats with desipramine (10 mg/kg, IP, daily) significantly attenuated picrotoxin-induced locomotor stimulation, when the GABA antagonist was given 24 hr after the last dose of the antidepressant. Repeated electroconvulsive shocks did not significantly change picrotoxin effect, while single shock produced some degree of inhibition of drug-induced motor stimulation. It is hypothesized that chronically applied desipramine, but not electroconvulsive shocks, may enhance the activity of hippocampal GABA-A receptor-related system.

Animals↗

PubMed1989

Restraint stress-induced changes in saccharin preference: the effect of antidepressive treatment and diazepam.

The effect of antidepressive treatment and of diazepam on saccharin preference has been studied in a model of acute restraint stress-induced saccharin preference deficit. It has been shown that 1-hr stressor produces short-term, and significant decrease of saccharin preference in a two-bottle test, measured at 24-hr periods of time. Single doses of desipramine and citalopram (10 mg/kg, IP) given prior to stress session significantly attenuated the deficit in saccharin preference. Less strong, but similar effects appeared after postshock antidepressant administration. On the other hand, electroconvulsive shock treatment rather enhanced the depressive influence of the stressor, while diazepam (1 mg/kg, IP) antagonized the suppression of saccharin preference, especially when the drug was given immediately after restraint stress. It is concluded that the acute immobilization-induced decrease in saccharin preference most probably reflects changes in brain emotional processes. The role of disturbances in central motivational mechanisms and its contribution to the effects of antidepressive drugs remains to be established.

Animals↗

PubMed1989

Serotonin and depression: old problems and new data.

1. Several lines of evidence implicating some dysfunction or alteration to brain serotonergic systems in depressive states are summarized. 2. Some aspects of the interactions between the 5-HT and catecholamine pathways in the action of antidepressant drugs are examined. 3. Finally, the important role of NA modulation of serotonergic activity in the action of antidepressants is suggested.

Animals↗

PubMed1989

On the relative importance of D-1 vs. D-2 dopaminergic receptors in the control of audiogenic seizures in ethanol withdrawn rats.

Bromocriptine, a mixed D-1/D-2 dopaminergic receptor agonist and SKF 38393, a D-1 specific agonist were found to alleviate the incidence and intensity of audiogenic convulsions in ethanol withdrawn rats. (+) and (-)3-PPP, putative D-2 autoreceptor agonists, were without effect in the test. SCH 23390, a D-1 specific antagonist did not influence seizure intensity in ethanol withdrawn or ethanol naive animals. It is suggested that D-1 receptors may play a role in convulsive response during ethanol withdrawal.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1989

The role of brain serotonin in the electroconvulsive shock-induced changes in behavioural effects of intra-hippocampally injected clonidine.

The influence of central serotonin depletion upon behavioural effects of intra-hippocampally injected clonidine in the electroconvulsive shock-treated rats (ECS), was studied. Repeated ECS significantly attenuated the depressive influence of clonidine upon the locomotor activity of the rats in the open field test. Chemical lesions to the median raphe nucleus (MR) did not significantly affect ECS-induced changes in clonidine activity in this test. In the forced swimming the MR lesions revealed the stimulatory potency of clonidine microinjections upon rat active behaviour. In animals pretreated with repeated ECS, clonidine also significantly potentiated swimming activity, but no evident synergism of ECS and MR lesion could be observed. Taking into account these and other data it is concluded that central serotonin depletion might differentially affect the adaptive processes occurring in the alpha 2-adrenoceptors in the course of treatment with tricyclic antidepressants and ECS, but it does not seem to be a strong phenomenon. Moreover, it is suggested that clonidine effects in the open field and forced swimming tests may be mediated by different neuronal substrates within the rat hippocampus.

Animals↗

PubMed1988

Diltiazem suppresses apomorphine-induced fighting and pro-aggressive effect of withdrawal from chronic ethanol or haloperidol in rats.

Dopaminergic receptor stimulation with apomorphine (5 mg/kg, i.p.) induced irritable aggression consisting of defensive upright postures, vocalization and biting attacks in pairs of responsive rats. Aggression was considerably decreased when the animals were pretreated with diltiazem, a Ca2+ channel inhibitor (5 or 10 mg/kg, i.p.). Originally non-responsive rats exhibited apomorphine-induced fighting upon withdrawal from prolonged ethanol (21 days, 3 g/kg, twice daily, intragastrically, i.g.) or haloperidol (14 days, 0.5 mg/kg, twice daily i.g.). If the animals were co-administered diltiazem i.g. 30 min prior to each dose of ethanol or haloperidol the aggressive response to apomorphine was significantly decreased; reduction in attack score being the most prominent. Chronic (14 or 21 days) diltiazem by itself did not facilitate the appearance of apomorphine-induced fighting in non-responsive rats. These results suggest that diltiazem can inhibit apomorphine-induced fighting and prevent the development of ethanol and haloperidol-induced behavioural supersensitivity to apomorphine.

Aggression↗

PubMed1988

Brain neurotransmitter systems mediating behavioral deficits produced by inescapable shock treatment in rats.

The effect of inescapable footshock (IS) upon rats' motor activity (the open field and forced swim tests) was studied in rats subjected to drugs, and neurotoxin treatments, affecting their central neurotransmitter systems. The agonists of GABA-receptor complex, dopamine, noradrenaline and serotonin neuronal systems, as well as the cholinergic antagonist, partially reversed motor suppression induced by IS, while the dopamine agonist, chlorpromazine, and the cholinergic antagonist, physostigmine, potentiated it. The effects of chemical lesions of the brain monoaminergic neurons with p-chlorophenylalanine (pCPA), N-chloro-ethyl-2,2-bromo-benzylamine (DSP-4), 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (5,7-DHT) were more complex, depending upon the extent of monoamine depletion, and the kind of test applied. It is concluded that a decrease in the brain noradrenergic, serotonergic, dopaminergic and GABAergic neuronal activity, as well as the central cholinergic hyperactivity, might contribute to the behavioral suppression after IS. Thus the central mechanisms of behavioral deficits produced by IS involve multiple neurotransmitter systems, and the analysis of their role in more complicated behavioral patterns must also take into account changes in animals' baseline and stimulated motor activity.

Alanine↗

PubMed1988

Inhibition of p-chlorophenylalanine-induced muricide behavior following TRH microinjection into the limbic structures in the rat.

The effect of central microinjections of thyrotropin releasing hormone (TRH) on muricide behavior was investigated in rats with chronically implanted cannulas into one of the limbic structures: the amygdala, the hippocampus or the nucleus accumbens. The rats were made aggressive by p-chlorophenylalanine administration. Saline injection did not inhibit muricide, whereas TRH (10 micrograms in 0.5 microliter per side) significantly suppressed mouse-killing reaction upon injection into each of three regions. It is suggested that the observed antiaggressive effect of TRH may involve stimulation of the central noradrenergic and/or serotonergic transmission.

Amygdala↗

PubMed1988

Some aspects of stress and depression.

1. The role of stress in depressive illness is discussed together with utility of the "learned helplessness" model and some neuropharmacological correlates of uncontrollable shock. 2. Similarities and differences between chronic antidepressant treatment and chronic stress treatment regimes are reviewed. 3. Finally the role of adaptive process in stress on antidepressant treatments is discussed.

Animals↗