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1

Effect of antisense oligodeoxynucleotides (ODNs) complementary to mRNA encoding dopaminergic D2 receptor, and the random sequence, administered bilaterally into the nucleus accumbens of the rat

100%
Margas W., Kolasiewicz W., Dziedzicka-Wasylewska M., Maj J.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
2
Content available remote

Glutamatergic neurons of rat medial prefrontal cortex innervating the ventral tegmental area are positive for serotonin 5-HT1A receptor protein

100%
Wedzony K., Chocyk A., Kolasiewicz W., Mackowiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
The present study was designed to investigate whether serotonin 5-HT1A receptor protein (5-HT1A receptor-immunoreactivity), is present on cortical pyramidal neurons of the rat medial prefrontal cortex (MPC) innervating the ventral tegmental area (VTA). Recent data stress the role of serotonin 5-HT1A receptors in the pathology of schizophrenia, and in the mechanism of action of novel antipsychotic drugs. It was found that approximately 52% of cells in layers II/III of the MPC whose axons initial segments were immunoreactive for serotonin 5HT1A receptor were also labeled with Fluoro-Gold (FG), a retrograde tracer injected into the VTA, indicating that certain portion of neurons forming glutamatergic innervations of the VTA may be controlled by serotonin 5-HT1A receptors. In deep cortical layers (V/VI) retrogradely labeled neurons never colocalized with serotonin 5-HT1A receptor-mmunoreactivity. These anatomical data indicate that serotonin 5-HT1A receptors might potentially control the excitability and propagation of information transmitted by the pyramidal cells to the VTA. Moreover, our results indicate that the drugs operating via serotonin 5-HT1A receptors in the MPC, might control from this level the release of glutamate in the VTA and restore function of glutamate neurotransmission, whose dysfunction is observed for example in schizophrenia.
3

The role of dopamine D2, receptor in the behavioral effects of imipramine - study with the use of antisense oligonucleotides

88%
Maj J., Dziedzicka-Wasylewska M., Kolasiewicz W., Margas W., Rogoz Z.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 5
4
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Content available

The role of dopamine D2 receptor in the behavioral effects of imipramine - study with the use of antisense oligonucleotides

88%
Dziedzicka-Wasylewska M., Kolasiewicz W., Rogoz Z., Margas W., Maj J.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 3
5

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

76%
Berghauzen K., Wardas J., Kuter K., Kolasiewicz W., Glowacka U., Ossowska K.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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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”
6

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

76%
Kuter K., Kolasiewicz W., Zapala M., Kowalska M., Golembiowska K., Morelli M., Wardas J.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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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.
7

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

64%
Kuter K., Berghauzen K., Wardas J., Kolasiewicz W., Nowak P., Zapala M., Mikolajun U., Ossowska K.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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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
8

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

64%
Wardas J., Kolasiewicz W., Kuter K., Berghauzen K., Nowak P., Mikolajun U., Zapala M., Ossowska K.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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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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