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1
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Opposite influence of MPEP, an mGluR5 antagonist, on the locomotor hyperactivity induced by PCP and amphetamine

100%
Pietraszek M., Rogoz Z., Wolfarth S., Ossowska K.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 3
Potential antipsychotic effects of a selective non-competitive antagonist of metabotropic glutamate receptor 5 (mGluR5), 2-methyl-6-phenylethynylpyridine (MPEP), was examined in two commonly used screening tests: (1) the hyperactivity induced by an NMDA receptor antagonist phencyclidine (PCP), and (2) the hyperactivity induced by an indirect dopamine agonist, D-amphetamine. PCP was administered at a dose of 2.5 mg/kg s.c. and D-amphetamine was given at a dose of 1 mg/kg s.c. MPEP (5 mg/kg i.p.) significantly enhanced the locomotor activity increased by PCP, but inhibited amphetamine-induced hyperactivity. The opposite effect of MPEP in the two above-mentioned models questions significance of the blockade of mGluR5 receptors to antipsychotic effects.
2
Content available remote

New facts and the concept of physiological regulation of the dopaminergic system function and its disorders

84%
Krzymowski T., Stefanczyk-Krzymowska S.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 3
3

Characterization of mice with genetically evoked selective degeneration of noradrenergic system and its possible influence on dopaminergic system

84%
Jurga A., Kreiner G., Rafa-Zablocka K., Baginska M., Parlato R., Schuetz G., Nalepa I.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Parkinson’s Disease (PD) is characterized by an increased production of oxygen free radicals leading to alteration of the cellular constituents and subsequent dopaminergic cell loss within the region of substantia nigra (SN) and ventral tegmental area (VTA). However, it is well known that PD is not only associated with dopaminergic transmission. Involvement of extranigral structures in PD includes the noradrenergic system as well. Post-mortem studies of human brains revealed that neuronal loss associated with PD may proceed and is even greater in the region of locus ceruleus (LC) than SN/ VTA. In PD animal models, the loss of noradrenaline made worse the dopamine nigrostriatal damage and, in opposite, an enhanced noradrenaline level may have a neuroprotective role. The aim of this study was to determine whether genetically evoked, selective loss of noradrenergic neurons may have any long-term, negative impact on the dopaminergic system. We applied the conditional inactivation of the gene encoding transcription factor TIF-IA (essential for the regulation of rRNA synthesis) by the Cre-loxP system to induce the progressive and selective loss of noradrenergic neurons which was achieved by expressing Cre recombinase under dopamine beta-hydroxylase (DBH) promoter. Resulting TIFIADBHCre mice were born at expected rates, viable but showed clear signs of noradrenergic innervations failure e.g. ptosis, reduced locomotor activity, growth retardance and shorten life span. The animals were analyzed at 8 and 12 weeks of age. The selective loss of noradrenergic neurons was confirmed by immunofluorescent staining with the anti-tyrosine hydroxylase (TH) antibody. We observed approx. 90% reduction of TH positive cells in the LC of 8 weeks TIF-IADBHCre mice. The number of TH+ cells was not changed in the region of SN/VTA, neither in 8 nor 12 week old mutants. However, our preliminary data indicate that lack of the noradrenergic transmission may lead to enhanced expression of selected markers associated with neurodegeneration within the region of SN/VTA. Namely, we have found 1.4 fold up-regulation of mRNA encoding for glial fibrillary acidic protein (GFAP) as revealed by quantitative real-time PCR and increased level of oxidative stress shown by immunoblot detection of carbonyl groups by Western Blot in the SN/VTA of 12 weeks TIF-IADBHCre mice compared to control animals. If we provide additional evidences that selective noradrenergic degeneration affects functioning of dopaminergic neurons, TIF-IADBHCre mice may became a valuable, new model for study possible anti-PD treatment at early stages of the disease as dopaminergic neurons in these mice are not directly affected by the mutation. As for today, there are no experimental studies on a possible long-term negative impact of progressive noradrenergic degeneration on other neurotransmitter systems despite of clinically observed concomitant loss of SN/VTA and LC neurons in PD. This study was supported by the grant no 2011/03/B/NZ7/05949 financed by National Science Centre and statutory funds of the Institute of Pharmacology, Polish Academy of Sciences.
4
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Chronic stress changes prepulse inhibition after amphetamine challenge: the role of the dopaminergic system

84%
Lehner M. H., Karas-Ruszczyk K., Zakrzewska A., Gryz M., Wislowska-Stanek A., Kolosowska K., Chmielewska N., Skorzewska A., Turzynska D., Sobolewska A., Mierzejewski P., Plaznik A.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 3
5

Nitric oxide [NO] and central dopamine [DA] D3 receptor reactivity to quinpirole in rats

84%
Brus R., Szkilnik R., Kostrzewa R. M.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
6

CGP 42112A abolishes facilitation of recognition caused by angiotensin II and angiotensin II[3-7] in rats

84%
Braszko J. J., Kulakowska A., Winnicka M. M., Karwowska-Polecka W.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 3
7

Effect of unilateral injection of MK-801 into the area of A10 cells on feeding evoked by stimulation of homologous area in the contralateral hemisphere

84%
Maliszewska-Scislo M., Trojniar W.
Acta Neurobiologiae Experimentalis
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2000
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tom 60
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nr 4
It was found previously that unilateral electrolytic and 6-OHDA lesions of the ventral tegmental area (VTA) and unilateral intra-VTA injection of bicuculline resulted in facilitation of behavioral responses evoked by electrical stimulation of the symmetrical VTA area in the contralateral hemisphere. We postulated that „the contralateral facilitation effect", which may reflect the yet unexplored mechanism of immediate compensation after acute unilateral brain injury, is attributable to the A10 DA neurons and their regulatory inputs. The present study was aimed at examining the possible involvement of NMDA-mediated glutamatergic transmission in VTA in the „contralateral facilitation effect". The behavioral model of the VTA stimulation-induced feeding in rats was used. Latency to eat was measured as a function of stimulation frequency before and after unilateral intra-VTA injection of non-competitive NMDA receptors antagonist, MK-801, (doses 0.0, 1.25 and 2.5 p,g). MK-801 caused a dose-dependent augmentation of feeding evoked by stimulation of the contralateral VTA, which manifested as a decrease in the reaction frequency threshold and a leftward shift of the latency/frequency curve. Dose 2.5 replicated the facilitatory effect of electrolytic and 6-OHDA lesions. The results are interpreted in terms of MK-801-evoked depression of excitatory glutamatergic tone over A10 DA cells and compensatory increase in DA release in the contralateral hemisphere.
8

The effect of prolonged administration of lithium on the level of dopamine D2 receptor mRNA in the rat striatum and nucleus accumbens

84%
Dziedzicka-Wasylewska M., Wedzony K.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
9
Content available remote

Countercurrent transfer of dopamine from venous blood in the cavernous sinus to the arterial blood supplying the brain - the perfused rabbit head as an experimental model

67%
Muszak J., Krzymowski T., Gilun P., Stefanczyk-Krzymowska S.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 5
10

Cholecystokinin facilitation of cognitive processes is mediated by mesolimbic dopaminergic system

67%
Winnicka M. M., Hryniewicz A., Mikoda J., Krasicka E., Wisniewski K.
Journal of Physiology and Pharmacology. Supplement
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2001
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tom 52
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nr 2
11

Pharmacological and physicochemical properties of collagen breakdown-products

67%
Telejko E., Wrobel K., Wisniewski K., Bankowski E.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 4
12

Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus

59%
Borkowska H. D., Oja S. S., Hilgier W., Saransaari P., Albrecht J.
Acta Neurobiologiae Experimentalis
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2000
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tom 60
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nr 1
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
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