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1

The effects of dopamine D1 and D2 receptors agonists, give alone or jontly with a nitric oxide donor, on expression of proteins involved in the nitrergic signaling and on cGMP production in 6-OHDA-lesioned rats

100%
Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The aim of the present study was to examine the effects of selective dopamine (DA) D1 and D2 receptors agonists administered chronically, alone or in combination with the nitric oxide donor molsidomine on expression of proteins involved in the nitric oxide – soluble guanylyl cyclase – cGMP signaling pathway and on the cGMP levels in the striatum (STR) of 6-OHDA-lesioned rats. METHODS:Two weeks after unilateral injection of 6-OHDA(8 µg/4 µl) into the medial forebrain bundle, rats were treated chronically (15 days) with DA D1 (SKF38393; 3 mg/kg sc) or DA D2 (quinpirole 0.2 mg/kg sc) receptor agonists and molsidomine (2 mg/kg ip), alone and in combination. The contents of neuronal nitric oxide synthase (nNOS), sGC and phosphodiesterase 1B (PDE-1B) proteins were determined in the STR by Western blot technique while cGMP level using competitive enzyme immunoassay cGMP kit. RESULTS: In the ipsilateral STR chronic treatment with SKF38393 alone or jointly with molsidomine did not affect nNOS protein level. Quinpirole alone had no effect on nNOS level while given jointly with molsidomine decreased it markedly. Both SKF38393 and quinpirole alone did not change sGC protein level in the ipsilateral STR while their joint administration with molsidomine enhanced it markedly. SKF38393 and quinpirole alone decreased PDE-1B protein expression but only combined administration of quinpirole + molsidomine enhanced the content of this protein. As to cGMP level, chronic treatment with molsidomine alone increased cGMP concentration in the ipsi- and contralateral STR. SKF38393 administered chronically alone or jointly with molsidomine enhanced cGMP content only in the ipsilateral STR while quinpirole alone or in combination with molsidomine did not evoke such effects. CONCLUSION: The obtained results suggest that the treatment with selective DA D1 and D2 agonists differently modulates the NO-sGC-cGMP signaling pathway in 6-OHDA-lesioned rats.
2

Antidepressants enhanced the antipsychotic-like effect of aripiprazole in the tests used for evaluaion of some positive and cognitive symptoms of schizophrenia in mice

63%
Rogoz Z., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Schizophrenia is a devastating psychiatric disorder that impairs mental and social functioning and affects approximately 1% of the world’s population. It is known that in contrast to pharmacotherapy with typical antipsychotics, atypical antipsychotics alleviate not only the positive symptoms of schizophrenia but also the cognitive ones, however those effects are small and the mechanisms of this action are still unknown. A few clinical reports have suggested that antidepressants (ADs) are able to augment the activity of atypical antipsychotics. AIM(S): In the present study, we aimed to evaluate the effect of ADs escitalopram (ESC) or mirtazapine (MIR) and aripiprazole (ARI, an atypical antipsychotic drug) given separately or jointly, on the MK-801-induced positive and cognitive symptoms of schizophrenia in mice. METHOD(S): The experiments were conducted on male Albino Swiss mice (25–27 g). ADs and ARI were given 30 min before MK-801 injection. Locomotor hyperactivity induced by MK-801 (0.3 mg/kg) was measured for 30 min, starting 30 min after MK-801 administration. In the novel object recognition test, MK-801 (0.2 mg/kg) was given 30 min before the first introductory session. Memory retention was evaluated for 5 min, starting 90 min after the introductory session. RESULTS: ARI (0.3 mg/kg) decreased locomotor hyperactivity induced by MK-801 (0.3 mg/kg). Co-treatment with an inactive dose of ARI (0.01 mg/kg) and ESC (5 or 10 mg/kg) or MIR (2.5 and 5 mg/kg) inhibited the effect of MK‑801. Moreover, MK-801 (0.2 mg/kg) decreased the memory retention. ARI (0.3 mg/kg) reversed that effect. Co‑treatment with an inactive dose of ARI (0.03 mg/kg) and ESC (5 and 10 mg/kg) or MIR (2.5 and 5 mg/kg) abolished the deficit of object recognition memory induced by MK-801. CONCLUSIONS: The obtained results suggest that ADs may enhance the antipsychotic‑like effect of ARI in the animal tests used for evaluation of some positive and cognitive symptoms of schizophrenia. FINANCIAL SUPPORT: This study was financially supported by statutory funds of the Institute of Pharmacology Polish Academy of Sciences, Krakow, Poland.
3

Influence of 8-OH-DPAT, a selective 5-HT1A receptor agonist, on the haloperidol- induced muscle rigidity in rats

51%
Lorenc-Koci E., Pietraszek M., Wolfarth S.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
4

The effect of co-treatment with aripiprazole and antidepressants on the MK-801-induced deficits in the social interaction test in rats

51%
Rogoz Z., Kaminska K., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Schizophrenia is a devastating psychiatric disorder that impairs mental and social functioning and affects approximately 1% of the world’s population. Although the atypical antipsychotics have some efficacy in alleviating social dysfunction in schizophrenic patients, this effect is small and mechanisms of this action are still unknown. Moreover, preclinical and clinical studies have suggested that the antidepressant-induced augmentation of atypical antipsychotics activity may efficiently improve the treatment of negative and some cognitive symptoms of schizophrenia. In the present study, we aimed to evaluate the effect of the atypical antipsychotic drug aripiprazole (ARI) and the antidepressant mirtazapine (MIR) or escitalopram (ESC), given separately or jointly, on the MK-801 (a NMDA receptor antagonist)-induced deficits in the social interaction test (an animal test modeling some negative symptoms of schizophrenia). METHODS: The experiments were conducted on male Wistar rats (185–200 g). The social interaction was measured 4 h after the subcutaneously administration of MK-801 (0.1 mg/kg), and 60 or 30 min after injection of the antidepressant and ARI, respectively. RESULTS: The present results showed that MK-801 (0.1 mg/kg) induced deficits in both parameters studied, i.e. the number of episodes and the time of interactions. ARI at a higher dose (0.3 mg/ kg) reversed that effect. Co-treatment with an ineffective dose of ARI (0.03 mg/kg) and MIR or ESC (5 mg/kg) abolished the deficits evoked by MK-801, and this effect was partly blocked by a 5-HT1A receptor antagonist (WAY 100635, 0.1 mg/kg) or a dopamine D1 receptor antagonist (SCH23390, 0.5 mg/kg). CONCLUSIONS: The obtained results suggest that the enhancement of antipsychotic-like effect of ARI by antidepressants on the MK-801-induced deficits in the social interaction test may be associated with serotonin 5-HT1A and dopamine D1 receptors.
5

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

51%
Konieczny J., Lorenc-Koci E., Wardas J.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
6

Influence of intrastriatal injections of 5,7- dichlorokynurenic acid, an antagonist of glycine site of the NMDA receptor, on the haloperidolinduced muscle tone

51%
Lorenc-Koci E., Wolfarth S., Ossowska K.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
7

A relationship between glutathione deficiency during the early postnatal life and schizophrenia-like behavior in adulthood of sprague-dawley rats

51%
Lorenc-Koci E., Gorny M., Kaminska K., Rogoz Z.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: A growing body of evidence implicates glutathione (GSH) deficiency and dysregulation of redox state in the pathophysiology of schizophrenia. AIM(S): The aim of the present study was to examine the effects of buthionine-S,R-sulfoximine (BSO)-mediated inhibition of glutamate cysteine ligase (GCL; an enzyme contributing to the GSH synthesis), during the early postnatal life on the GSH and cysteine (Cys) levels in the liver and kidney of 16-days old Sprague-Dawley rats and on the rat performance in the behavioral tests that were evaluated in the adulthood. METHOD(S): Male Sprague-Dawley pups between the postnatal day p5 and p16 were treated sc with the selective inhibitor of GCL, compound BSO (3.8 mmol/kg) and the dopamine reuptake inhibitor GBR 12909 (5 mg/kg every second day), alone or in combination. Biochemical parameters, i.e. GSH and cysteine (Cys) levels were determined in the rat liver and kidney 4h after the last doses of the drugs. Other groups of rats treated with BSO and GBR 12909 were examined during adulthood in the social interaction test (p42, p60, p90), novel object recognition test (p43, p61, p91) and in the open field test (p44, p63, p93). RESULTS: BSO alone or especially with GBR 12909 significantly decreased GSH level measured 4h after its last doses both in the liver and kidney. However, Cys concentration was distinctly reduced only in the kidney. Treatment with BSO and GBR 12909 induced deficits in both parameters of the social interaction test (number and time of interactions) assessed in the defined time points in adulthood. Such treatment also evoked a decrease in the memory retention in the novel object recognition test and an increase in exploratory activity in the open field test. CONCLUSIONS: Our results suggest that the inhibition of GSH synthesis and the dopamine reuptake during the early postnatal development induces in rats long-term behavioral changes that correspond to negative and positive symptoms of schizophrenia. FINANCIAL SUPPORT: Partially supported by statutory funds of the Institute of Pharmacology Polish Academy of Sciences, Krakow, Poland.
8

Does haloperidol induce parkinsonian rigidity?

51%
Lorenc-Koci E., Wolfarth S., Ossowska K.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
9

Metabotropic glutamate receptors counteract muscle rigidity induced by haloperidol

45%
Wolfarth S., Konieczny J., Lorenc-Koci E., Pilc A., Ossowska K.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
10

Antioxidative properties of A-lipoic acid examined in the striatum and prefronta cortex of the reserpine-treated rats

45%
Bilska A., Dubiel M., Sokolowska-Jezewicz M., Lorenc-Koci E., Wlodek L.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
11

An involvement MAPK/ERK1/2 pathway in mechanism of lactacystin-induced cell damage in primary cortical neurons

45%
Jantas D., Konieczny J., Lenda T., Lason W., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Proteasome dysfunction is involved in pathomechanism of several neurodegenerative diseases where an accumulation of aberrant proteins occurs (e.g. Parkinson’s disease, Alzheimer’s disease). Lactacystin (LC) has been used for induction of proteasome inhibition-dependent neuronal cell death for several years but mechanism of its toxic action on neurons is still poorly understood. In the present study we showed time- and concentration-dependent toxic action of lactacystin (0.25–50 μM) in mouse cortical neurons. Although, lactacystin induced caspase-3 activation, its toxic action was not attenuated by caspase-3 inhibitor AcDEVD-CHO. We demonstrated that inhibitors of MAPK/ERK1/2 cellular signaling (U0126 and PD98052) were protective against LC-evoked cell death as confi rmed by LDH and MTT reduction assays. Moreover, these data were verifi ed by Western Blot analysis, where we observed the increase in ERK1/2 activity after LC treatment and this effect was inhibited by U0126. The obtained data point to engagement of activation of MAPK/ERK1/2 in toxic action of lactacystin and give a rationale for using agents which inhibit this intracellular pathway in treatment of neurodegenerative diseases connected with proteasome dysfunction. Supported by Polish MNSW Scientifi c Network Fund no 26/E-40/BWSN-0023/2008.
12

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

45%
Wardas J., Konieczny J., Lorenc-Koci E., Smialowska M., Dziedzicka-Wasylewska M.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
13

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

45%
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.
14

Plasma levels of total, free and protein bound thiols as well as sulfane sulfur in different age groups of rats

45%
Iciek M., Chwatko G., Lorenc-Koci E., Bald E., Wlodek L.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 3
The redox status of plasma thiols can be a diagnostic indicator of different patho­logical states. The aim of this study was to identify the age dependent changes in the plasma levels of total, free and protein bound glutathione, cysteine and homocysteine. The determination was conducted in plasma of three groups of rats: 1) young (3-month-old), 2) middle aged (19-month-old), and 3) old (31-month-old). To­tal levels of glutathione, cysteine and homocysteine and their respective free and protein-bound fractions decreased with age. The only exception was a rise in free homocysteine concentration in the middle group, which indicates a different pattern of transformations of this thiol in plasma. The drop in the level of protein-bound thiols suggests that the antioxidant capacity of plasma diminishes with age, which, consequently, leads to impaired protection of -SH groups through irreversible oxida­tion. The plasma sulfane sulfur level also declines with age, which means that aging is accompanied by inhibition of anaerobic sulfur metabolism.
15

Parkinsonian-like and senile muscle rigidity

39%
Wolfarth S., Ossowska K., Lorenc-Koci E., Konieczny J., Kaminska A., Schulze G.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
16

The effect of chronic treatment with the selected SSRIs and L-DOPA on rotational behavior and monoamine metabolism in the motor and limbic brain structures of 6-ohdalesioned rats

39%
Kaminska K., Lenda T., Konieczny J., Czernecka A., Rogoz Z., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The objective of the present study was to examine rotational behavior and monoamine metabolism in motor (striatum, STR; substantia nigra, SN) and limbic (prefrontal cortex, PFC; hippocampus, HIP) brain structures of unilaterally 6-OHDA-lesioned rats treated chronically with the chosen selective serotonin reuptake inhibitors (SSRIs): fluoxetine or paroxetine alone or jointly with L-DOPA. METHODS: The experiment was performed on male Wistar rats injected unilaterally with 6-OHDA (16 μg/4 μl) into the medial forebrain bundle. Two weeks later, the animals were tested for the rotational behavior induced by apomorphine. Rats exhibiting more than 100 contralateral turns/1 h were administered fluoxetine (5 mg/kg) or paroxetine (5 mg/kg) and L-dopa (12 mg/kg), alone or in combination, once daily for 21 consecutive days. Rotational behavior was recorded after the first and the penultimate doses of the examined drugs. The levels of dopamine (DA), serotonin (5-HT), and their metabolites were determined in the tissue homogenates of motor and limbic brain structures 1h after the last drug injections using HPLC method. RESULTS: Chronic combined administration of fluoxetine+L-DOPA significantly increased while paroxetine+L-DOPA decreased the number of contralateral rotations compared to the group receiving L-DOPA alone. L-DOPA given alone or jointly with SSRIs increased DA levels on both sides of all the examined structures. Fluoxetine intensified L-DOPA effect in the HIP while paroxetine in the SN. Joint administration of fluoxetine+L-DOPA decreased 5-HT level in the ipsilateral SN more distinctly than each of these drugs alone. Paroxetine+L-DOPA evoked similar decreases in tissue 5-HT content in the ipsilateral STR, HIP and PFC. CONCLUSION: The obtained data are discussed in the context of motor and psychiatric disturbances observed in Parkinson’s disease. The study was supported by the Project “Depression-MechanismsTherapy” – POIG.01.01.02-12-004/09-00.
17

The parkinsonian-like muscle rigidity induced by Tetrahydroisoquinoline (TIQ) in rats

39%
Ossowska K., Lorenc-Koci E., Antkiewicz-Michaluk L., Smialowska M., Bajkowska M., Wolfarth S.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
18

Let genes talk: transcriptomic changes in the PFC induced by L-DOPA in hemiparkinsonian rats

39%
Radlicka A., Kaminska K., Piechota M., Korostynski M., Lorenc-Koci E., Pera J., Parkitna J. R.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: The hallmark symptoms of Parkinson’s disease (PD) are progressive motor impairments. Nevertheless, PD is also associated with altered executive function and other cognitive impairments. While treatments of PD provide at least temporary relief from the motor symptoms, the effects of L-DOPA on the cognitive impairments may provide mixed effects and require further investigation. AIM(S): Here we assess changes in gene expression in the prefrontal cortex (PFC) of rats with unilateral lesion of midbrain dopamine neurons. METHOD(S): Male Wistar Han rats were infused with 6‑hydroxydopamine (6‑OHDA, 8 µg/4 µl) into the left medial forebrain bundle. The experimental animals were treated i.p. with L‑DOPA (12.5 mg/kg) supplemented with benserazide hydrochloride (6.25 mg/kg) daily for 14 days. An hour after the last dose, the rats were killed, and the left and right PFC were isolated separately. Analysis of gene expression was performed by RNA‑seq (Illumina PE 150, 20M pair reads per sample). Reads were aligned to rn6 rat reference genome using hisat2 2.1.0. RESULTS: We identified 12,459 genes with FPKM > 1 after L‑DOPA treatment in both ipsi‑ and contralateral portions of the PFC of rats lesioned with 6‑OHDA. Two‑way ANOVA revealed 48 genes with differential expression profiles. The effect of treatment was the most pronounced, and included transcripts linked to activity-regulated expression in neurons and metabolism in the glia. Ontology analysis of the genes with altered expression indicated over-representation of terms associated with cytokine and glucocorticoid signalling. The involvement of altered glucocorticoid signalling induced by L-DOPA treatment was also confirmed by analysis of the promoter regions of the regulated genes. CONCLUSIONS: Unilateral lesions of dopamine neurons lead to enhanced sensitization of neurons in PFC to L‑DOPA action. We show that, to a large extent, these changes appear to bilaterally affect the molecular profile of PFC.
19

Toxicity of tetrahydroisoquinolines (TIQs) in the HEK293 cell lines expressing dopamine and organic cation transporters

39%
Lenda T., Schulze G., Rommelspacher H., Bonish H., Bojarski A., Lorenc-Koci E.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
20
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Muscle rigidity induced by fluphenazine in rats is antagonized by L-DOPA, an antiparkinsonian drug

39%
Ossowska K., Konieczny J., Lorenc-Koci E., Schulze G., Coper H., Wolfarth S.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 2
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