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1

Genetic basis of autosomal dominant nocturnal frontal lobe epilepsy

100%
Rozycka A., Trzeciak W. H.
Journal of Applied Genetics
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2003
|
tom 44
|
nr 2
2

Association of the CHRNA4 1674plus11C>T polymorphism with juvenile myoclonic epilepsy

81%
Rozycka A., Steinborn B., Dorszewska J., Trzeciak W. H.
Acta Neurobiologiae Experimentalis
|
2011
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tom 71
|
nr 1
The α-4 subunit gene (CHRNA4) of the neuronal nicotinic acetylcholine receptor (nAChR), linked to an idiopathic partial epilepsy, autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), may also play a key role in the development of the idiopathic generalized epilepsy syndrome (IGE), juvenile myoclonic epilepsy (JME). This study was designed to explore an association of four polymorphisms of the CHRNA4 with JME in Polish children and young patients. The study included 92 JME patients and 222 unrelated healthy individuals. In each group the frequencies of the CHRNA4 c.555C>T, c.594C>T, 1674+11C>T, and 1674+14A>G polymorphisms were determined using PCR-RFLP analyses. An association between the 1674+11C>T polymorphism of the CHRNA4 and JME was evidenced. Allele T (the risk factor) appeared with a significantly higher frequency in the JME patients than in the controls (p=0.0299). The patients harboring the 1674+11CT+TT genotypes showed an increased risk of JME (CT+TT versus CC: OR=1.925; 95% CI=1.021-3.629; p=0.0408). No association was found for the other CHRNA4 polymorphisms tested. The CHRNA4 1674+11C>T polymorphism may be a susceptibility factor for epilepsy, and its higher frequency in patients with juvenile myoclonic epilepsy suggests that the CHRNA4 may be one of the candidate genes for this epileptic syndrome.
3

Neuronal acetylcholine receptor alpha-7 subunit gene (CHRNA7) is expressed in lymphocytes of healthy individuals but not in the ADNFLE patients

81%
Rozycka A., Kempisty B., Trzeciak W. H.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
4

Polymorphic variants within the alpha-4 subunit of the neuronal nicotinic acetylcholine receptor gene

81%
Rozycka A., Skorupska E., Kostyrka A., Trzeciak W.
Acta Biochimica Polonica
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2003
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tom 50
|
nr Supplement 1
5

Gabaergic system in aging. Focus on somatostatin containing interneurons

81%
Rozycka A., Zakrzewska R., Liguz-Lecznar M.
Acta Neurobiologiae Experimentalis
|
2017
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tom 77
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nr Suppl.1
INTRODUCTION: Molecular aging, defined as an age‑related transcriptome changes, and biochemical protein-related alterations within synapses weaken the plastic potential of neurons. Previously, we have shown an age-related impairment of learning-related functional plasticity in mouse somatosensory cortex (SI), induced by associative fear learning and visualized with brain mapping using 2-deoxyglucose technique. AIM(S): The aim of the study was to investigate age-related changes in somatostatin-containing GABAergic interneurons, which are involved in learning – related plasticity in mouse SI. METHOD(S): Learning-related plasticity was induced with classical conditioning, where tactile stimulus to large sensory whiskers was coupled to the tail shock. Two groups of mice were used in the experiments: young (3 months old) and aged (1 year old). We have investigated mRNA and protein level of GAD67 (enzyme synthesizing GABA) and SOM (somatostatin) in mouse SI using q-RT-PCR and ELISA, respectively. Using immunofluorescence we compared the number of both types of neurons in SI. RESULTS: Analysis of q-RT-PCR results revealed no change in investigated mRNAs levels between young and aged mice. We also observed an upregulation of GAD67 and GABA levels after training in young but not in aged animals. Immunohistochemistry results showed an increase in the number of GAD67+ cells, however, we did not observe an elevation in the number of SOM+/GAD67+ cells. CONCLUSIONS: Increase in GAD67+ neurons density after sensory training in aged animals without parallel upregulation in GAD67 and GABA levels suggests lower GABA synthesis resulting in reduced effectiveness of aged GABAergic neurons. Lack of increase in SOM+ neurons density after sensory training in aged mice, suggest that upregulation of SOM+ cells is necessary for training induced plasticity. FINANCIAL SUPPORT: Supported by National Science Centre grant 2013/09/B/NZ3/00540.
6

Cognitive control modified on-the-fly in the Eriksen task

81%
Rozycka A., Zurawska vel Grajewska B., Jakubiak M., van der Labbe R.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr Suppl.1
In perceptual-motor tasks, the influence of flankers can be modified. Their influence can increase when they are more often congruent with the target and decrease when they are more often incongruent. The black horizontal string of shapes was presented on a white background. The string contained: two flanker arrows in the middle, the target arrow on the left (or right) and a square on the right (or left). In one half of trials the target was more often congruent (arrow pointing in the same direction as flankers) when it was presented on the left, in the second it was more often congruent when it appeared on the right. Our results showed that the reaction time for incongruent trials was shorter when the target was presented on the side with predominance of incongruent targets than for incongruent trials with target presentation on the side with predominance of congruent targets. Reactions were faster for congruent than for incongruent trials in both cases of predominance. Related results were observed in the modulation of N2PC amplitude. The influence of flankers can be modified by changing the proportion of congruent targets in the selected location.
7

The response of main subclasses of GABAergic interneurons to plasticity induction and aging: changes in mRNA levels

81%
Rozycka A., Zakrzewska R., Liguz-Lecznar M.
Acta Neurobiologiae Experimentalis
|
2019
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tom 79
|
nr Suppl.1
INTRODUCTION: Inhibitory interneurons undergo age-related alterations that may have tremendous consequences on cellular and network computations and account for cognitive and behavioral deficits. Accordingly, we have shown that mechanisms governing fear learning‑induced plasticity were weakened in aged (1 y.o.) mice somatosensory cortex, hampering manifestation of plastic changes, while in old (2 y.o.) mice the plasticity was absent. AIM(S): To investigate age-related mRNA changes of distinct markers that are characteristic of GABAergic interneurons, define their main subtypes, and correlate potential changes with age‑related plasticity impairments. METHOD(S): Plasticity was induced with a classical conditioning paradigm, in which tactile stimulus to one row of whiskers was paired with a tail electric shock. Three groups of mice were used: young (3 months old), aged (1 y.o.) and old (2 y.o.). Using qRT‑PCR, we investigated mRNA levels of GAD67, GAD65, parvalbumin (PV), somatostatin (SST), calretinin (CR), calbindin (CB), vasoactive intestinal polypeptide (VIP), and Neuropeptide Y (NPY). RESULTS: qRT‑PCR analysis showed changes in mRNA levels, resulting from both aging itself and from plasticity induction. mRNA level of CB decreased in aged and old animals, whereas PV increased in the old group. After plasticity induction, we observed a reduction of NPY in the young group, while aged animals presented a decline of VIP mRNA levels. We observed decrease in CB along with an increase in PV mRNA levels, which may result in calcium homeostasis disruption in neurons and may consequently be involved in the plasticity impairments observed in aged and old animals. CONCLUSIONS: Being a part of the VIP-SST disinhibitory circuit that exist in many cortical areas, VIP mRNA changes may contribute to dysregulation of this important mechanism controlling plasticity. FINANCIAL SUPPORT: National Science Centre grant 2013/09/B/NZ3/00540.
8

Potential role of dopamine transporter in behavioral flexibility

71%
Cybulska-Klosowicz A., Dabrowska J., Niedzielec S., Zakrzewska R., Rozycka A.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr 2
Behavioral flexibility is subserved by the prefrontal cortex and the basal ganglia. Orbitofrontal cortex (OFC) and dorsomedial striatum (DMS) form a functional frontocorticostriatal circuit crucial for the mediation of flexibility during reversal learning via dopamine (DA) neurotransmission. The regulatory control in maintaining DA homeostasis and function is provided by the dopamine transporter (DAT), which therefore likely plays a significant role in controlling the influence of DA on cognitive processes. Here we used a gene knockout mouse model to investigate the role of DAT in the performance on the Attentional Set‑Shifting Task (ASST) stages dependent upon the OFC and the DMS. Additionally, behavior of mice after repeated administration of selective DAT inhibitor, GBR 12909, was examined. The animals were treated with the inhibitor to elicit a compensatory DAT up‑regulation following withdrawal. Learning was slower and the number of errors during reversal learning and intra‑dimensional shift stages was higher in DAT+/− mutant mice than in WT mice. GBR 12909‑treated mice had deficits in reversal stages of the ASST. Neuronal activation in the OFC and DMS during the ASST was examined with early growth response proteins 1 and 2 (egr‑1, egr‑2) immunohistochemistry. Density of egr‑2 labeled cells in the OFC was lower in mutant mice than in wild‑types during reversal learning and the expression of the egr‑1 was lower in mutant mice in the OFC and DMS during reversal and intra‑dimensional shift stages. Mice with decreased DAT levels displayed behavioral difficulties that were accompanied by a lower task‑induced activation of neurons in brain regions involved in the reversal learning. Altogether, these data indicate the role of the DAT in the behavioral flexibility.
9

Polymorphism of MTHFR, MTR and MTHFD1 as related to the oxidative DNA damage, and the level of thiols in Alzheimer's and Parkinson’s diseases

51%
Florczak J., Dorszewska J., Rozycka A., Kempisty B., Chojnacka K., Jaroszewska-Kolecka J., Trzeciak W. H., Kozubski W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
10

Elevated expression of alpha7 neuronal nicotinic acetylcholine receptor during the early stages of damage by oxidative stress in the aging rat brain

51%
Dorszewska J., Rozycka A., Helias-Rodzewicz Z., Kempisty B., Grzelak T., Ziemnicka K., Oczkowska A., Steinborn B., Jagodzinski P.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Aging is accompanied by a high level of oxidized form of guanine, 8-oxo-2’deoxyguanosine (8-oxo-2’dG), and decreased level of 8-oxoguanine glycosylase 1 (OGG1) in the brain. The development and progression of neurodegenerative disorders are also characterized by dysfunction or loss of the brain nicotinic acetylcholine receptors (nAChRs). To study whether the differences in nAChRs expression in the rat brain occur due to aging or oxidative stress we analyzed RNA and protein levels of α7, α4 and β2 subunits by RQ-PCR and Western blot validation in three brain structures: cerebral grey matter (CGM), sub-cortical white matter (SCWM) and cerebellum (Ce) of twenty one female Wistar rats. The first group consisted of five 3.0–3.5-month-old females, which was assigned as a young control group. The remaining sixteen females aged of 18–24 month were divided into three following groups: (1) aged control group of 5 rats; (2) a vehicle group of 5 rats which received intraperitoneal injections of deionized water; (3) memantine-treated group of 6 rats. In each group, the selected brain areas have also been analyzed to determinate the levels of oxidative stress. In this study, age- and stress- dependent differential RNA and protein expression levels were approved only in OGG1 and α7 nAChR proteins. In all analyzed brain structures of young and old controls, the levels of oxidized form of guanine were similar. Stress relevant to water injection increased the level of 8-oxo-2’dG in the cerebellum of old control rats (Ce, P<0.05). The old controls demonstrated an important reduction of OGG1 mRNA expression in CGM and Ce regions compared to young individuals (CGM P=0.03; Ce P=0.2). Western blot analysis has also revealed a reduction of OGG1 protein in the sub-cortical white matter of old individuals (SCWM, P=0.03). However, there was no important influence of water administration on OGG1 expression in all brain regions. In all analyzed brain structures, expression of α7 nAChR was down-regulated in old controls compared to young controls. However, this decrease was only significant in SCWM area (SCWM, P<0.05). Treatment with H2O caused a significant increase in RNA and protein levels of α7 nAChR in SCWM as compared to this brain structure of the aged control rats (SCWM, P<0.01). Our results suggest that aging of the rat brain is mostly associated with decreased expression of OGG1 as well as with deficit of α7 nAChR in the sub-cortical white matter. Stress relevant to water injection increases the level of 8-oxo-2’dG in the aging rat brain, but clearly overcomes the α7 nAChR deficit. A significant increase of the α7 nAChR expression in the SCWM of H2O-treated rats suggests that these receptors play an important role in compensatory mechanisms facilitating the impaired cholinergic neurotransmission following oxidative stress in the aging rat brain.
11

SNCA, PARK2 and LRRK-2 mutations in Polish patients with sporadic Parkinson’s disease

51%
Polrolniczak A., Dorszewska J., Florczak J., Owecki M., Rozycka A., Rubis B., Jagodzinski P. P., Kozubski W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Parkinson’s disease (PD) is one of the most common neurodegenerative disorders in Poland. Although the genetic basis of familial PD is now well established, the majority of PD is sporadic and occurs without a clear mode of inheritance. The etiology of sporadic PD remains unknown, but it is currently assumed that genetic susceptibilities may be involved. The observation that mutations in α-synuclein (SNCA), parkin (PARK2)and leucine-rich repeat kinase 2 (LRRK2) genes are common in familial PD and increasing evidence supporting a direct role for PARK2 and LRRK-2 in sporadic both early- and late-onset disease make those genes a particularly compelling candidate for intensified investigation. The aim of the study was analysis and identification of SNCA, PARK2 and LRRK-2 mutation in Polish patients with sporadic PD. Peripheral blood was collected from 34 patients with sporadic PD clinical diagnosis (the average age 58 years), and 22 patients with the other neurological diseases (the average age 55 years) as well as from 25 healthy donors (the average age 60 years). Genomic DNA was isolated using standard protocols. SNCA mutations analysis was performed to exclude one of the familial forms of PD. Restriction-enzyme digestion of polymerase-chain reaction (PCR) amplified genomic DNA fragment of SNCA exon 3 detected no G88C mutation. PCR-amplification of parkin exons 2 and 4 also detected no exon deletion. Moreover exon 41 of LRRK-2 gene as well as exons 4, 7 and 11 of PARK2 gene was screened using realtime PCR/HRM and exon sequencing. None of the patients as well as control subjects tested had mutation of LRRK2 gene. These results are consistent with previous reports in the Polish population Mutation in tested exons of PARK2 gene were identified in 20,6% patients with sporadic PD, 4,5% patients with the other neurological disorders and 4,0% control subjects. All detected mutations were heterozygous. One of the PD patients had two mutations in PARK2 gene (G1281A, G601A). It can be concluded, that both G88C SNCA and G2019S LRRK-2 mutations as well as deletion of 2 and 4 exon of parkin gene are rare causes of PD in Poland. Moreover point mutation in PARK2 seems to be associated with sporadic PD in polish population. Thus, the results of this study suggest that screening for PARK2 mutations may be a component of genetic testing for sporadic PD.
12

Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer's and Parkinson's diseases

51%
Dorszewska J., Florczak J., Rozycka A., Kempisty B., Jaroszewska-Kolecka J., Chojnacka K., Trzeciak W. H., Kozubski W.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 2
Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are accompanied by increased levels of 8-oxo-2'deoxyguanosine (8-oxo2dG) and alterations in levels of homocysteine (Hcy), methionine (Met), and cysteine (Cys). Hcy may undergo remethylation due to involvement of MTHFR, MTR and MTHFD1 proteins. Present studies are aimed at determination of 8-oxo2dG, Hcy, Met, and Cys in AD and PD patients as well as in control groups, using HPLC/EC/UV, as well as estimation, by restriction analysis, frequency of following gene polymorphisms: MTHFR (C677T, A1298C, G1793A), MTHFD1 (G1958A), and MTR (A2756G). In AD there were significant differences of the levels of only Cys (GG, MTHFR, G1793A) and Met/Hcy (AA, MTHFD1, G1958A) whereas in PD there were more significant differences of the levels of thiols: Hcy [MTHFR: CT (C677T) and GG (G1793A); MTR, AG (A2756G)], Met [MTR, AA (A2756G)], Cys [MTR, AG (A2756G)], and Met/Hcy [MTHFR: CC, CT (C677T) and AA (A1298C), and GG (G1793A); MTHFD1 AA (G1958A); MTR AA (A2756G)]. Significant differences in the levels of Cys/Hcy, MTHFD1 GA (G1958) were varied between AD and PD groups. The results indicate that of the enzymes studied only polymorphisms of folate-dependent enzyme MTHFD1 have pointed to significant differences in intensity of turnover of circulating thiols between AD and PD patients.
13

Memantine up-regulates nicotinic acetylcholine receptors expression in the cortex and sub-cortical white matter of aging rat brain

51%
Polrolniczak A., Rozycka A., Helias-Rodzewicz Z., Kempisty B., Grzelak T., Ziemnicka K., Steinborn B., Jagodzinski P. P., Dorszewska J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Memantine (MEM) is a potent open channel blocker of N-methyl-Daspartate receptors (NMDARs), and primary has been developed for treatment of neuropathic pain, symptoms of dementia and AD. On the other hand, MEM is able to act as an open channel blocker on several other ligand gated ion channels, e.g., the α4β2 and α7 nicotinic acetylcholine receptors (nAChRs). The aged-related decline in the nAChRs expression could be associated with other senescence markers, such as increased oxidative stress leading to oxidative DNA changes (high level of 8-oxo-2’dG), accompanied with significant decrease in level of the OGG1 protein involved in DNA repair process. To study whether MEM treatment might influence on the α7 and α4 nAChRs expression in the aging rat brain tissues, we analyzed RNA and protein levels by RQ-PCR and Western blot validation in three brain structures: cerebral grey matter (CGM), sub-cortical white matter (SCWM) and cerebellum (Ce) of twenty one female Wistar rats. The animals were divided into following experimental groups: the first group consisted of five 3.0–3.5-month-old females, which was assigned as a young control group, and the remaining sixteen females aged of 18–24 month were divided into three following sub-groups: (1) aged control group of 5 rats; (2) a vehicle group of 5 rats which received intraperitoneal injections of deionized water (3) memantine-treated group of 6 rats. In each group, the selected brain areas have also been analyzed to determinate the levels of oxidative stress. In CGM and SCWM brain structures the level of 8-oxo-2’dG was significantly reduced in old rats after MEM administration (CGM P=0.05; SCWM P<0.05). Western blot analysis has also revealed a significant up-regulation of OGG1 level in CGM after MEM administration (CGM P=0.05). MEM specifically up-regulated mRNA level of cortical α4 subunit in the CGM region of aging rat brain (CGM, P<0.05). In the sub-cortical white matter an important increase of α7 mRNA level has been observed after MEM administration (SCWM P<0.05). The level of α7 nAChR protein was significantly up-regulated also in CGM and Ce regions of MEM treated rats (SCWM P=0.05; CGM P<0.05; Ce P<0.05). We demonstrated that processes related to aging, such as a decreases in OGG1 and nAChRs expression can be modified after memantine administration: (1) A significant increase in the CGM of α4 and α7 subunits, as well as up-regulated α7 level in the SCWM after MEM administration suggests that nAChRs play an important role in compensatory mechanisms facilitating the impaired cholinergic neurotransmission following treatment with MEM. (2) MEM significantly up-regulates cortical OGG1 protein expression and reduces the level of 8-oxo-2’dG in CGM. (3) A significant increase in both mRNA and protein levels of α7 nAChR along with reduction of 8-oxo-2’dG in SCWM, following treatment with MEM, suggests that the effect of MEM on cholinergic function may be associated with antioxidant mechanisms. Whether these protective effects of MEM are direct or are mechanistically remote from NMDARs antagonism, have to be evaluated in the further studies.
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