PubMed Health⌕ Search

Biomedical subjects

A Bidzinski

Publications and source records attributed to A Bidzinski.

At least 19 recordsLinked to original sources
PubMed2002

Pentylenetetrazol-kindling of seizures selectively decreases [3H]-citalopram binding in the CA-3 area of rat hippocampus.

The present study was aimed at determining the changes in the 5-HT transporter activity, in different brain structures after pentylenetetrazol induced kindling of seizures. We examined [3H]-citalopram binding in the rat brain structures, and the neurodegenerative effects in the hippocampal formation using autoradiographic and immunohistochemical methods. A statistically significant and selective reduction in the binding of [3H]-citalopram was found in the CA3 field of the hippocampus (P=0.009), and a similar tendency, close to the significance level, in the dentate gyrus (P=0.05). This effect was accompanied by a loss of neurons and activation of microglia in the hippocampal formation. The present data suggest the important role for CA3- serotonergic innervation in pentylenetetrazol induced kindling of seizures.

Animals↗
PubMed1996

The effects of repeated administration of diazepam, MK-801 and CGP 37849 on rat behavior in two models of anxiety.

The effects of repeated administration of diazepam, MK-801 and CGP 37849 on rat behavior in the Vogel conflict test, and in the open field test of neophobia, were studied in rats. The drugs were given at doses active acutely, for 5 days, the last dose was administered 30 or 60 min prior to testing. It appeared that diazepam and MK-801 treated animals showed clear-cut signs of behavioral tolerance and motor sensitization, respectively. CGP 37849 was characterized by the best pharmacological profile, in that on repeated administration the drug not only retained its anxiolytic-like potency in the Vogel test, but even enhanced rat exploratory behavior in a new environment, independently of changes in animal motor activity. Repeated injections of the examined agents did not cause any significant modifications in monoamine levels and their turnover rates, in the striatum and limbic forebrain. It is concluded that the new class of competitive NMDA receptor antagonists, exemplified by CGP 37849, is the most promising candidate for clinical trials in anxiety disorders.

2-Amino-5-phosphonovalerate↗
PubMed1994

The effect of serotonin depletion and intra-hippocampal midazolam on rat behavior in the Vogel conflict test.

The effect of intra-hippocampal (dentate gyrus) microinjections of the benzodiazepine, midazolam (10 micrograms per site, bilaterally), was examined in the Vogel conflict test in serotonin depleted rats (pretreated with p-chlorophenylalanine). p-Chlorophenylalanine and midazolam, when given separately, significantly disinhibited rat conflict behavior. Midazolam retained its anticonflict potency in the p-chlorophenylalanine pretreated animals. These and other data indicate: (i) the specific involvement of limbic serotonin in emotional control, (ii) a dissociation of the effects of serotonin depletion and intra-hippocampal benzodiazepine on conflict behavior, and (iii) the important role of the hippocampus in processing emotional input.

Animals↗
PubMed1994

Antidepressant treatment and limbic serotonergic mechanisms regulating rat locomotor activity.

The effects of chronic administration of desipramine, citalopram, and electroconvulsive shocks (ECS) on changes in rat motility after intraaccumbens (NAS) injections of selective serotonergic drugs were studied in intact and 5.7-DHT lesioned animals. It was shown that local injections of 8-OHDPAT and DOI-HCl depressed rat locomotor activity. Their effects appeared to be mediated postsynaptically, and could be antagonized by NAN-190 and ritanserin, respectively. Chronic but not acute pretreatment of rats with antidepressants (21 days long; the experiment was performed 24 h after the last dose) as well as repeated ECS (shocks were applied five times every second day), antagonized behavioral depression after 8-OHDPAT and DOI-HCl. The influence of antidepressant treatment was prevented by serotonergic lesions. Chronic administration of antidepressants and ECS did not equivocally affect the levels or metabolism of 5-HT, dopamine, and noradrenaline in the rat limbic forebrain. It is concluded that the present data indicate diminished activity of 5-HT systems related to the 5-HT1A and 5-HT2 receptors in the limbic nucleus, after chronic antidepressant treatment. This effect of drugs and ECS concerns nervous processes linked with the function of postsynaptically localized 5-HT receptor subtypes, and it probably depends on intact presynaptic 5-HT innervation.

5,7-Dihydroxytryptamine↗
PubMed1990

Antidepressant-like action of nicardipine, verapamil and hemicholinium-3 injected into the anterior hypothalamus in the rat forced swim test.

Male Wistar rats, chronically implanted with cannulas into the anterior hypothalamus, were acutely injected with the calcium channel inhibitors, diltiazem, nicardipine and verapamil, or the choline uptake blocker hemicholinium-3 and tested in the forced swim test. Hemicholinium-3, nicardipine and verapamil markedly increased the duration of active swimming. This antidepressant-like effect did not appear to reflect merely a hyperactive state as the drug-treated rats did not differ from vehicle-injected controls in their open field motility scores. Diltiazem failed to influence rats' performance in either test. Since nicardipine and verapamil, but not diltiazem, share choline uptake property with hemicholinium-3, it seems that this action plays a role in the antidepressant-like effect of all three drugs in the forced swim test.

Animals↗
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↗
PubMed1987

Striatal cholinergic function reflects differences in D-2 dopaminergic receptor activation.

The ergot derivatives, bromocriptine, lisuride and quinpirole (Ly-171555), activators of D-2 receptors, increased striatal acetylcholine (ACh) content by about 40% and induced a 30% inhibition of ACh evoked release from striatal slices, similar to the effects of the dopaminergic agonist apomorphine. These actions were a consequence of dopaminergic activation since they were antagonized by pretreatment with the neuroleptic agent, pimozide. In contrast, pretreatment with L-sulpiride (100 mg/kg), a specific antagonist for the D-2 dopaminergic receptor only, prevented the rise of ACh levels induced by apomorphine or quinpirole but did not interfere with the lisuride- or bromocriptine- induced ACh increases. Similarly, inhibition of the ACh evoked release produced by lisuride (3 microM) was prevented by pimozide (1 mg/kg) but not by pretreatment with L-sulpiride. Addition of L-sulpiride (5 microM) to the Krebs solution had no effect on the inhibition of ACh-evoked release induced by lisuride, but a lower concentration (1 microM) antagonized the inhibition induced by quinpirole. Lisuride and bromocriptine responses were both insensitive to sulpiride. These results are discussed in terms of different interaction with the dopaminergic D-2 receptors by the drugs studied.

Acetylcholine↗
PubMed1984

Brain serotonergic neurons: their role in a form of dominance-subordination behavior in rats.

The present study evaluated the possible role of brain serotonergic neurons in dominant-subordinate (D-S) behavior in Wistar male rats competing for water. Treatment of D rat with drugs that stimulate serotonergic neurons of receptors (tryptophan, 5-hydroxytryptophan, quipazine, femoxetine) resulted in D-S reversal. A similar effect was observed when the S animal was treated with drugs that blocked serotonin synthesis (p-chlorophenylalanine) or receptors (metergoline). The D-S relationship was unchanged when serotonergic drugs were given to the S subject (tryptophan or quipazine) or when D animal received p-chlorophenylalanine. None of the drugs tested influence the water intake and the general activity of rats. Rats with lesioned midbrain raphe nuclei were always dominant when paired with sham lesioned counterparts. Our results indicate that one form of dominance behavior can be inversely related to the activity of brain 5-HT system.

Animals↗
PubMed1984

Failure to correlate urinary MHPG with clinical response to amitriptyline.

On the basis of studies carried out in a group of 44 patients with endogenous depressive illness, the authors conclude that MHPG in urine is not a good predictor of response to amitriptyline treatment. There are no correlations between MHPG level and clinical improvement after 2 weeks' treatment and with final results of the therapy.

Amitriptyline↗
PubMed1983

Differential clonidine effects on EEG following lesions of the dorsal and median raphe nuclei in rats.

The effects of clonidine on EEG activity and gross behavior were studied in rats with electrolytic lesions of the median (MR) and dorsal (DR) raphe nuclei. Lesioned animals showed significant depletion in forebrain serotonin concentrations. Clonidine (0.1 mg/kg and 0.2 mg/kg IP) produced synchronization in cortical EEG pattern and markedly increased alpha and theta activities in unlesioned animals. Clonidine treatment resulted also in a sedative response. In MR lesioned rats clonidine effect upon EEG was significantly reduced and, additionally, sedative response was not seen. On the other hand clonidine effect on EEG was markedly increased in rats with lesioned DR. These results are discussed on the basis of possible interaction between serotonergic and noradrenergic neurons in the brain.

Animals↗
PubMed1983

Studies on biogenic amine metabolizing enzymes (DBH, COMT, MAO) and pathogenesis of affective illness. II. Erythrocyte catechol-O-methyltransferase activity in endogenous depression.

Erythrocyte COMT activity was determined in 31 healthy persons (16 men, 15 women) and in 34 persons with endogenous depressive syndrome (12 men, 22 women). It was found that enzyme activity is significantly higher in healthy men than in healthy women. In the group of women with endogenous depressive syndrome COMT activity is elevated as compared with the group of healthy women (P less than 0.05). This is true of all forms of affective disease: bipolar, unipolar, and undifferentiated. High COMT activity in women with depression is apparent mainly in patients whose first and second degree relatives revealed psychiatric disturbances, particularly affective disorders. This supports the significance of the sex factor in the genetic transmission of affective disorders, and a possible involvement of COMT activity changes in the pathogenesis of such disorders in women. No correlation was found between the changes in COMT activity and the psychopathological picture of depression or the severity of endogenous depressive syndrome.

Adult↗
PubMed1981

Lesion of serotonergic neurons antagonizes clonidine induced suppression of avoidance behavior and locomotor activity in rats.

The effects of clonidine on avoidance acquisition and locomotor activity were studied in male Wistar rats with 5,6-dihydroxytryptamine (5,6-DHT) lesions of the median raphe nucleus. Lesioned animals showed marked depletion in forebrain serotonin and 5-hydroxyindole acetic acid concentrations. clonidine (0.2 mg/kg IP in a single daily dose for 6 consecutive days) inhibited avoidance acquisition and reduced locomotor activity in unlesioned rats. In 5,6-DHT rats clonidine failed to produce depressive effect. The resistance of raphe-lesioned rats to clonidine is discussed on the basis of possible interaction between noradrenergic and serotonergic brain systems.

5,6-Dihydroxytryptamine↗
PubMed1978

Studies on the effect of lesions of the ventral noradrenergic tract on the antinociceptive action of morphine.

In rats, lesions were placed in the ventral tegmental noradrenergic tract (VT). In some animals lesions also involved the dorsal tegmental noradrenergic tract (DT). Morphine (Mf) analgesia was examined by the tail compression method 8-9 days after lesions. VT lesions produced no changes in Mf activity, while lesions involving VT + DT produced a partial attenuation of the antinoceptive action of Mf. These results suggest that the ascending NA fibres forming the VT are not essential for the antinoceptive effect of Mf.

Analgesics↗
PubMed1978

Effects of lesions in the ventral noradrenergic bundle on behavior and response to psychotropic drugs in rats.

Bilateral lesions of the ventral noradrenergic bundle (VB) decreased concentration of noradrenaline within the mesendiencephalon but not in the cortex. Lesioned rats showed increased activity measured in the open field test. Cataloptogenic effects of chlorpromazine and haloperidol were almost completely abolished in VB-lesioned animals. The stereotypy induced by both--amphetamine and apomorphine was, however, unchanged. It is supposed that lesions of the VB lead to increased activity in dopaminergic neurons in the brain.

Amphetamine↗
PubMed1977

Behavioral effects of neuroleptics, apomorphine and amphetamine after bilateral lesion of the locus coeruleus in rats.

Bilateral lesions of the locus coeruleus (LC) markedly increased susceptibility to the cateleptogenic effects of neuroleptics. The apomorphine-induced stereotypy was enhanced in rats with lesioned LC whilst amphetamine stereotypy was only slightly increased. No changes in locomotor activity have been observed in LC-lesioned rats treated with apomorphine and amphetamine. This data indicates that lesions of the LC produce decreased activity of dopaminergic brain neurons as well as supersensitivity of dopaminergic receptors.

Animals↗