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1

Age-related changes in glutamate receptors: an autoradiographic analysis

100%
Wardas J., Pietraszek M.
Acta Neurobiologiae Experimentalis
|
1995
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tom 55
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nr 5
2

Globus pallidus and substantia nigra pars reticulata convey striatal impulses pertinent to neuroleptic catalepsy to the lateral hypothalamus-zona incerta

81%
Wardas J., Karcz-Kubicha M., Ossowska K., Wolfarth S.
Acta Neurobiologiae Experimentalis
|
1992
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tom 52
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nr 3
3

Chronic treatment with neuroleptics alters the level of NMDA receptor subunits in the rat brain: an in situ hybrydization study

81%
Pietraszek M., Wardas J., Dziedzicka-Wasylewska M., Ossowska K.
Acta Neurobiologiae Experimentalis
|
1997
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tom 57
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nr 5
4

The subsensitivity of striatal AMPA receptors, induced by chronic haloperidol in rats: an autoradiographic analysis

81%
Pietraszek M., Wardas J., Ossowska K.
Acta Neurobiologiae Experimentalis
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1995
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tom 55
|
nr 5
5

SCH 58261, an adenosine A2A antagonist, counteracts the reserpine-induced muscle rigidity in rats

81%
Konieczny J., Lorenc-Koci E., Wardas J.
Acta Neurobiologiae Experimentalis
|
1999
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tom 59
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nr 3
6

Pramipexole at a low dose induces beneficial effects in the harmaline-induced model of essential tremor in rats

81%
Kosmowska B., Wardas J., Glowacka U., Ananthan S.
Acta Neurobiologiae Experimentalis
|
2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: Harmaline-induced tremor is a model of essential tremor (ET). Tremor induced by harmaline has been suggested to result from activation of the olivo-cerebellar projection. Recent studies have indicated that cerebellum functions may be modulated by dopamine. METHODS: We examined the effects of preferential agonists of dopamine D3 receptors: pramipexole and 7-OH-DPAT on the harmaline-induced tremor in rats. In order to study receptor mechanisms of these drugs rats were pretreated with dopamine D3 receptor antagonists [SB-277011-A (10 mg/kg ip) and SR-21502 (15 mg/ kg ip)], an antagonist of presynaptic D2/D3 receptors [amisulpride (1 mg/kg ip)], or a non-selective antagonist of postsynaptic dopamine receptors [haloperidol (0.5 mg/kg ip)]. RESULTS: The tremor was measured using fully automated Force Plate Actimeters. The following parameters were calculated: power within 0–8 Hz band (AP1) and 9–15 Hz band (AP2), and tremor index (a difference in power between AP2 and AP1). Harmalinetriggered (15 mg/kg ip) tremor was manifested by an increase in AP2 and tremor index. Pramipexole at a low (0.1 mg/kg sc), but not higher doses (0.3 and 1 mg/kg sc) lowered the harmaline-increased AP2. 7-OH-DPAT (0.1 mg/kg sc) reduced AP2 in the harmalinetreated rats. None of the examined dopamine antagonists influenced the above effect of dopamine agonists. In contrast, SB-277011-A administered alone lowered the harmaline-increased AP2. CONCLUSIONS: The present study indicates that pramipexole reduces the harmaline-induced tremor. However, mechanisms underlying its action are still unclear and require further examination. Financial support: Statutory Funds of the Department of NeuroPsychopharmacology, Institute of Pharmacology, PAS; National Science Center (grant OPUS 6, 2013/11/B/NZ4/04565); Southern Research Institute, Birmingham, AL, USA (S. Ananthan) - SR21502 donation. Barbara Kosmowska is a holder of scholarship from the KNOW sponsored by Ministry of Science and Higher Education, Poland.
7

Influence of adenosine A2A receptor stimulation on proenkephalin (PENK) and prodynorphin (PDYN) mRNAs expression in rat brain

81%
Wardas J., Lenda T., Kuter K.
Acta Neurobiologiae Experimentalis
|
2005
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tom 65
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nr 3
8

Blockade of adenosine A2A receptors decreases haloperidol-induced muscle rigidity in rats

71%
Wardas J., Konieczny J., Lorenc-Koci E., Smialowska M., Dziedzicka-Wasylewska M.
Acta Neurobiologiae Experimentalis
|
1999
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tom 59
|
nr 3
9

Dopamine, serotonin and norepinephrine transporters binding in motor brain structures of 6-OHDA-lesioned rats treated chronically with amitriptyline and L-DOPA

71%
Kaminska K., Wardas J., Konieczny J., Lenda T., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Depression frequently accompanied to Parkinson’s disease (PD). AIM(S): The aim of the study was to examine the effects of chronic treatment with amitriptyline(AMI) and L-DOPA on binding to dopamine (DAT), serotonin (SERT) and norepinephrine (NET) transporters in the substantia nigra (SN) and striatum (STR) of the unilaterally 6-OHDA-lesioned rats. METHOD(S): Experiments were performed on Wistar Han rats receiving unilaterally 16 µg/4 µl of 6-OHDA into the medial forebrain bundle (MFB). Two weeks later, rats exhibiting at least 100 contralateral turns/1 h in the apomorphine test were treated with AMI (10 mg/kg) and L-DOPA (12 mg/kg), alone or in combination, once daily for 21 consecutive days. The rats were sacrificed 1h after the last injection, their brains were dissected and frozen. The binding of [3H] GBR 12,935 to DAT, [3H] citalopram to SERT and [3H] nisoxetine to NET was assayed on nigral and striatal tissue sections. RESULTS: Injection of 6-OHDA into MFB caused a decline in [3H] GBR 12,935 binding to DAT in the ipsilateral SN and STR. On the contralateral side comes to up-regulation of DAT expression both in the STR and SN. AMI but not L-DOPA alone, lowered DAT expression in the contralateral STR. In the contralateral SN, DAT expression in drug treated groups was maintained at a control level. In the SN, the unilateral lesion of dopaminergic innervation caused a significant up-regulation of [3H] citalopram binding to SERT on both sides while in the STR only on the contralateral side. In both structures, L-DOPA did not change [3H] citalopram binding to SERT while AMI, alone or in combination, decreased it markedly on both sides. L-DOPA also decreased NET expression in the STR on both sides while AMI, alone or in combination maintained at the control level. CONCLUSIONS: Our data indicates that AMI can modulate the release of L-DOPA derived dopamine from serotonergic terminals on ipsilateral side and serotonin on contralateral one. The obtained data is discussed within the context of motor functions in PD.
10

An influence of compounds acting on glutamatergic and noradrenergic receptors on the tremor induced by harmaline; automatic measurements by force plate actimeters

61%
Glowacka U., Wardas J., Kuter K., Berghauzen K., Pilc A., Ossowska K., Acher F.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Harmaline, a derivative of beta-carboline is a well-known tremorgenic compound which induces the action and postural tremor in animals. Oscillation frequency of this symptom is equal to 10–12 Hz in rats. A synchronous activation of the olivo-cerebellar pathway and release of glutamate in the cerebellum has been suggested to be a primary cause of the harmaline-induced tremor. Subtype 4 of metabotropic glutamate receptors (mGluR4) is mainly an autoreceptor and its stimulation decreases glutamate release. MGluR4 receptors are abundant in the cerebellum and therefore their influence on the harmaline-induced tremor might be expected. However, mechanisms underlying this symptom are more complex and seem to involve also other neurotransmitter systems, especially the noradrenergic neurotransmission in the cerebellum. The aim of the present study was to examine an influence of an orthosteric agonist of mGluR4 – AF22898:8 on the tremor induced by harmaline in rats. An antagonist of beta-adrenoceptors – propranolol was used as a reference compound. Tremor of animals was measured automatically by actimeters where four force tranducers measured the force exerted by an animal on the floor. The Power Spectra analysis which uses a Fourier transform generated power spectra for examination of the tremor. The average power over three specific frequency bands AP1 (0–8 Hz), AP2 (9–15 Hz), AP3 (16–25 Hz), and tremor indices, which quantified the differences in power between the AP2 and AP1 (T1) and AP3 and AP1 (T2) were used to quantify the tremor intensity. Harmaline in doses of 7.5–25 mg/kg i.p. induced the generalized tremor which was dose-dependent and lasted longer than 2 h. Propranolol in a dose of 20 mg/kg i.p. diminished the tremor (decreased T1 and AP2) induced by harmaline (15 mg/ kg i.p.). In contrast, AF22898:8 administered in doses of 2.5–20 mg/kg i.p. was ineffective. The present results indicate that the harmaline-induced tremor measured in the force plate actimeters consititute a good model for screening antitremorgenic compounds. However, in contrast to earlier expectations the agonist of mGluR4 had no influence on this symptom.The study was supported by the grant of the National Science Centre nr N N401 570638, and partly by Statutory Funds of the Department of Neuro-Psychopharmacology, Institute of Pharmacology, Polish Academy of Sciences, Cracow, Poland.
11

The influence of imipramine and pramipexole on depressivelike behaviour in an animal model of a pre-clinical stage of Parkinson’s disease

61%
Berghauzen K., Wardas J., Kuter K., Kolasiewicz W., Glowacka U., Ossowska K.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Motor disturbances in Parkinson’s disease (PD) results from the massive degeneration of dopaminergic neurons and terminals of the nigrostriatal pathway and a decrease in the dopamine (DA) level in the caudate nucleus and putamen. The clinical phase of PD is preceded by a preclinical period where depression is a frequent comorbid disturbance.Dysfunctions of monoaminergic systems could underlie depression in PD. Clinical trials suggest that a treatment with tricyclic antidepressant drugs can be effective in ameliorating depression in PD. Moreover, recent studies have suggested that the administration of pramipexole (the mixed dopamine D2/D3 receptor agonist) may reduce not only motor symptoms (akinesia, rigidity and tremor at rest) but also depression in PD. The aim of the study was to examine the influence of classic tricyclic antidepressant -imipramine and pramipexole on the ‘depressivelike’ behaviour of rats with moderate lesion of the nigrostriatal system. Male Wistar rats were injected bilaterally with 6-OHDA (3.75–15 µg/2.5 µl) into the ventral striatum (vSTR). Imipramine was injected i.p. at a dose of 10 mg/kg once a day and pramipexole s.c. at a dose of 1 mg/kg twice a day for 14 days. The locomotor activity in actometers and behaviour of rats in the forced swimming test (FS) were measured on the 15th day after the surgery. The lesion extent was analysed by HPLC and immunohistochemically. The lesion increased immobility and swimming and decreased climbing in FS, however, it did not influence the locomotor activity of rats. All the lesion-induced disturbances observed in FS were decreased by pramipexole. Imipramine increased only climbing, but had no influence on immobility in lesioned rats. Moreover, imipramine but not pramipexole reduced the locomotor activity in lesioned animals. After the administration of 6-OHDA levels of DA decreased (ca. 45%) in the dorsal striatum (dSTR), vSTR and frontal cortex (FCX). Pramipexole and imipramine injections had no influence on DA levels in lesioned rats. Levels of DA metabolites (DOPAC, HVA) were markedly increased in dSTR and vSTR after injections of pramipexole. Moreover, pramipexole significantly increased the turnover of DOPAC/DA and HVA/DA in dSTR and vSTR in sham-operated and lesioned rats. These results indicate that a relatively moderate dopaminergic lesion which does not produce any motor disturbances, may induce “depressive-like” symptoms which are reversed by dopamine agonist but not by a classic antidepressant. Acknowledgments Study supported by the Project “Depression-Mechanisms-Therapy” (POIG.01.01.02-12-004/09-00), co-financed by EU from the European Regional Development Fund as a part of the Operational Programme “Innovative Economy 2007-2013”
12

Chronic intraventricular infusion of MPP+ with alzet osmotic minipumps in rats as a model of parkinson's disease

61%
Kuter K., Kolasiewicz W., Zapala M., Kowalska M., Golembiowska K., Morelli M., Wardas J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
An underlying mechanism of degeneration in Parkinson’s disease (PD) is unknown. The animal models of PD, developed so far have certain disadvantages; hence a search for a new model of PD seems necessary. Chronic, unilateral, intraventricular delivery of MPP+ (0.284 and 0.428 mg/kg/day for 28 days) using an ALZET osmotic minipump, implanted s.c., produced a marked, dose-dependent loss of DA and its metabolites DOPAC and HVA (50–90%) in the striatum, ipsilateral to the infusion site. DA concentration was normal in the non-infused, right striatum. Also no changes in the 5-HT level were observed. The stereological counting of the number of dopaminergic neurons in the substantia nigra pars compacta (SNc), stained with the antibody against tyrosine hydroxylase, showed their 30–50% loss on the lesioned side. Those changes were accompanied with a diminished expression of mRNA for the dopamine transporter in the SNc (by ca. 30%). Additionally, in situ hybridization studies indicated an enhanced expression of mRNA for both adenosine A2A and dopamine D2 receptors in the striatum and diminished expression of mRNA for BDNF in the hippocampus. The obtained results showed that this chronic model of continuous, intracerebral infusion of MPP+ , produced a selective nigrostriatal DA cell loss and number of other neurochemical changes resembling PD. Study supported by the grant No. NN401 1137 33 (MS&HE) and by a statutory fund from the Institute of Pharmacology, PAS, Poland.
13

Changes in glutamatergic transmission in the fronto-parietal cortex after chronic treatment with neuroleptics in rats

61%
Pietraszek M., Bijak M., Golembiowska K., Wardas J., Wolfarth S., Ossowska K.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
14

6-OHDA-induced lesion of a8-a9 dopaminergic neurons increases the harmaline-induced tremor in rats

51%
Kuter K., Berghauzen K., Wardas J., Kolasiewicz W., Nowak P., Zapala M., Mikolajun U., Ossowska K.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Degeneration of dopaminergic nigrostriatal pathway is generally accepted to be a cause of Parkinson’s disease (PD) motor symptoms such as akinesia, bradykinesia and tremor. Unfortunately the extent of the degeneration does not correlate with tremor occurrence and intensity, therefore cannot explain sufficiently its appearance. Mechanisms leading to induction of tremor are still not explained. Interestingly, image analysis studies have suggested contribution of an increased activity of the cerebellum to the PD tremor. The aim of the present study was to examine whether a selective, partial lesion of dopaminergic structures – the substantia nigra pars compacta (SNc, A9) and retrorubral field (RRF, A8) would influence the tremor behaviour induced by harmaline. Harmaline model of tremor induces an abnormal synchronous activation of the climbing glutamatergic olivo-cerebellar pathway and cerebellar Purkinje cells. 6-OHDA (8 mg /2 ml) was injected unilaterally into the region of the posterior part of the SNc and RRF to induce moderate size of degeneration, similar to early PD. Harmaline was administered in a dose of 7.5 mg/kg i.p. on the 8th day after the operation and tremor of forelimbs, head and trunk was measured. In precise behavioural studies we have found that the lesion of dopaminergic system increased intensity of the tremor induced by harmaline but did not influence its character. Stereological examination of the lesion extent revealed losses of dopaminergic (tyrosine hydroxylase-immunoreactive) neurons in the anterior (30%) and posterior (72%) SNc, as well as in RRF (72% on the average). Levels of dopamine and all its metabolites, as well as noradrenaline concentrations on ipsilateral to lesioned side were moderately decreased in the caudate-putamen, while, dopamine and DOPAC in the anterior cerebellum were increased. In the caudate-putamen, the ipsi/contra ratio of dopamine level correlated negatively, while that of dopamine turnover positively with the tremor intensity. However, in the anterior cerebellum an inverse relationship was found. Moreover, this symptom correlated positively with serotonin level and negatively with the 5-HIAA/serotonin ratio on the contralateral side of the posterior cerebellum. The presented results indicate that modulation of dopaminergic and serotonergic transmissions by the dopaminergic system lesion, modelling early stages of PD, may influence cerebellar mechanisms triggering tremor. The study was supported by the grant of the Ministry of Science and Higher Education No N_N401_570638 and by Statutory Funds of the Department of Neuropsychopharmacology, Institute of Pharmacology, Polish Academy of Sciences, Cracow, Poland
15

An influence of lesions of the catecholaminergic cerebellar innervation on the harmaline-induced tremor in rats

51%
Wardas J., Kolasiewicz W., Kuter K., Berghauzen K., Nowak P., Mikolajun U., Zapala M., Ossowska K.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Recent studies have suggested a crucial role of the cerebellum in different forms of tremor. Abnormal synchronous activation of the glutamatergic olivo-cerebellar pathway and Purkinje cells results in the essential tremor in humans and the harmaline-induced tremor in animals. Moreover, an increased neuronal activity of the cerebellum has been found to contribute to the tremor in Parkinson’s disease (PD). Since the cerebellum receives dopaminergic and noradrenergic pathways arising from regions affected in PD, the aim of the present study was to examine a contribution of the cerebellar catecholaminergic innervation to the harmaline-induced tremor in rats. Rats were bilaterally injected into the cerebellar vermis (lobules 8–10) with 6-hydroxydopamine (6-OHDA) (8 μg/0.5 μl) either alone or this treatment was preceded by desipramine (15 mg/kg i.p.). Harmaline was administered at a dose of 7.5 mg/kg i.p. on the 9th post-operative day. Tremor of forelimbs was measured as a number of episodes. After completion of behavioural experiments rats were killed by decapitation and the levels of monoamines and their metabolites were measured by HPLC in lobules 1–3, 4–7 and 8–10 of the cerebellum. 6-OHDA injected alone decreased the noradrenaline level by ca. 40–80% in the cerebellum and enhanced the harmaline-induced tremor. When 6-OHDA administration was preceded by desipramine, it decreased dopaminergic transmission in some regions of the cerebellum but induced its compensatory activation in others. Finally no influence of the latter treatment on the tremor induced by harmaline was observed. The present study indicates that the noradrenergic innervation of the cerebellum plays an inhibitory role in the harmaline-induced tremor. The study was supported by the grant of the Ministry of Science and Higher Education No N N401 570638, and partly by Statutory Funds of the Department of Neuro-Psychopharmacology, Institute of Pharmacology, Polish Academy of Sciences, Cracow, Poland.
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