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Dive into the research topics where M. Kusmider is active.

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Featured researches published by M. Kusmider.


Journal of Neurochemistry | 2010

Effect of chronic mild stress and imipramine on the proteome of the rat dentate gyrus

Sylwia Kedracka-Krok; Ewelina Fic; Urszula Jankowska; Marcin Jaciuk; Piotr Gruca; Mariusz Papp; M. Kusmider; Joanna Solich; Janusz Dębski; Michal Dadlez; Marta Dziedzicka-Wasylewska

J. Neurochem. (2010) 113, 848–859.


Neurochemistry International | 2011

Norepinephrine transporter (NET) knock-out upregulates dopamine and serotonin transporters in the mouse brain.

Joanna Solich; Agata Faron-Górecka; M. Kusmider; P. Palach; Magdalena Gaska; Marta Dziedzicka-Wasylewska

The noradrenaline, serotonin and dopamine transporters are three main transporters, which are the target of the antidepressant drugs. In the present study we demonstrate that the life-long deletion of the noradrenaline transporter (NET) induced up-regulation of two other monoamine transporters, dopamine and serotonin (DAT and SERT, respectively). An increase in the binding of [(3)H]paroxetine to the SERT and [(3)H]GBR12935 to the DAT was observed in various brain regions of NET-KO mice, without alterations of mRNA encoding these transporters, as measured by in situ hybridization. This important finding impacts the interpretation of previous data indicating the supersensitizity of NET-KO mice for psychostimulants or stronger effect of citalopram in behavioral tests. While using the NET-KO mice in various psychopharmacological studies is very important, one has to be aware that these mice lack NET from the earliest period of their existence, thus compensatory alterations do take place and have to be considered when it comes to interpretation of the obtained results.


Molecular Neurobiology | 2017

Reciprocal MicroRNA Expression in Mesocortical Circuit and Its Interplay with Serotonin Transporter Define Resilient Rats in the Chronic Mild Stress

Dariusz Zurawek; M. Kusmider; Agata Faron-Górecka; Piotr Gruca; Paulina Pabian; Joanna Solich; Magdalena Kolasa; Mariusz Papp; Marta Dziedzicka-Wasylewska

Prolonged stress perturbs physiological balance of a subject and thus can lead to depression. Nevertheless, some individuals are more resilient to stress than the others. Defining molecular factors underlying resilience to stress may contribute to the development of a new antidepressant strategy based on the restoration of resilient phenotype in depressed subjects. We used chronic mild stress (CMS) paradigm—well-characterized animal model of depression which caused in rats behavioral deficits (anhedonia) manifested by decreased consumption of sucrose solution. CMS also generated a proportion of resilient rats which did not alter sucrose consumption despite being stressed. Recently, regulation of a gene expression associated with microRNA (miRNA) is considered as an important factor modulating biochemical response to stress. Based on our previous work and literature survey, we investigated changes in the expression level of seven miRNAs (i.e., miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, miR-872-5p) in mesocortical circuit—crucially involved in stress response in order to find differences between susceptible and resilient phenotype. Bioinformatic analysis showed that all miRNAs of interest potentially target serotonin transporter (SERT). Chronic stress caused global increase in the expression of the abovementioned miRNAs in ventral tegmental area (VTA) of stressed rats followed by parallel decrease in miRNA expression in prefrontal cortex (PCx). This effect was more profound in resilient than anhedonic animals. Moreover, we observed decreased level of SERT in VTA of resilient rats. Our findings show that mesocortical circuit is involved in the response to stress and this phenomenon is more efficient in resilient animals.


Brain Research | 2015

Norepinephrine transporter knock-out alters expression of the genes connected with antidepressant drugs action.

Joanna Solich; Magdalena Kolasa; M. Kusmider; Agata Faron-Górecka; Paulina Pabian; Dariusz Zurawek; Kinga Szafran-Pilch; Marta Dziedzicka-Wasylewska

Norepinephrine transporter knock-out mice (NET-KO) exhibit depression-resistant phenotypes. They manifest significantly shorter immobility times in both the forced swim test and the tail suspension test. Moreover, biochemical studies have revealed the up-regulation of other monoamine transporters (dopamine and serotonin) in the brains of NET-KO mice, similar to the phenomenon observed after the chronic pharmacological blockade of norepinephrine transporter by desipramine in wild-type (WT) animals. NET-KO mice are also resistant to stress, as we demonstrated previously by measuring plasma corticosterone concentration. In the present study, we used a microdissection technique to separate target brain regions and the TaqMan Low Density Array approach to test the expression of a group of genes in the NET-KO mice compared with WT animals. A group of genes with altered expression were identified in four brain structures (frontal and cingulate cortices, dentate gyrus of hippocampus and basal-lateral amygdala) of NET-KO mice compared with WT mice. These genes are known to be altered by antidepressant drugs administration. The most interesting gene is Crh-bp, which modulates the activity of corticotrophin--releasing hormone (CRH) and several CRH-family members. Generally, genetic disturbances within noradrenergic neurons result in biological changes, such as in signal transduction and intercellular communication, and may be linked to changes in noradrenaline levels in the brains of NET-KO mice.


European Neuropsychopharmacology | 2015

Life-long norepinephrine transporter (NET) knock-out leads to the increase in the NET mRNA in brain regions rich in norepinephrine terminals

Joanna Solich; Magdalena Kolasa; M. Kusmider; Paulina Pabian; Agata Faron-Górecka; Dariusz Zurawek; Kinga Szafran-Pilch; Sylwia Kedracka-Krok; Urszula Jankowska; Marta Dziedzicka-Wasylewska

These studies aimed to identify the genes differentially expressed in the frontal cortex of mice bearing a life-long norepinephrine transporter knock-out (NET-KO) and wild-type animals (WT). Differences in gene expression in the mouse frontal cortex were studied using a whole-genome microarray approach. Using an alternative approach, i.e. RT-PCR (reverse transcription polymerase chain reaction) with primers complementary to various exons of the NET gene, as well as TaqMan arrays, the level of mRNA encoding the NET in other brain regions of the NET-KO mice was also examined. The analyses revealed a group of 92 transcripts (27 genes) that differentiated the NET-KO mice from the WT mice. Surprisingly, the studies have shown that the mRNA encoding NET accumulated in the brain regions rich in norepinephrine nerve endings in the NET-KO mice. Because there is no other source of NET mRNA besides the noradrenergic terminals in the brain regions studied, these results might speak in favor of the presence of mRNA in axon terminals. RNA-Binding Protein Immunoprecipitation approach indicated that mRNA encoding NET was detected in the Ago2 protein/mRNA complex. In addition, the amount of Ago2 protein in the frontal cortex was significantly higher in NET-KO mice as compared with that of the WT animals. These results are important for further characterization of the NET-KO mice, which - besides other merits - might serve as a good model to study the fate of truncated mRNA in neurons.


European Neuropsychopharmacology | 2013

P.1.015 Time-dependent adaptations at the level of dopamine D2 receptor in stress-resilient rats

Dariusz Zurawek; Agata Faron-Górecka; M. Kusmider; Magdalena Kolasa; Piotr Gruca; Mariusz Papp; Marta Dziedzicka-Wasylewska

p< 0.05). I.c.v. administration of IL-1b significantly disrupted PPI at the lowest dose only (0.5 ng). Conclusion: Present results support the hypothesis that IL-1b and KYNA are important players in the pathophysiology of psychotic diseases, such as schizophrenia and bipolar disorder. Notably, only administration of the lowest dose IL-1b had a PPI disruptive effect, indicating that this effect may be mediated by the increased brain KYNA concentrations observed at this dose. Present data are also in line with recent in-vitro data from our laboratory showing that IL-1b, by induction of tryptophan 2,3-dioxygenase, increase KYNA production in human cortical astrocytes.


European Neuropsychopharmacology | 2012

S.04.05 Effect of antidepressant drugs on the heterodimerization of dopamine D2 and somatostatin Sst5 receptors

K. Szafran; S. Lukasiewicz; Agata Faron-Górecka; M. Gaska; M. Kusmider; Joanna Solich; Marta Dziedzicka-Wasylewska

manic-like behavior. In addition, we evidenced that SD decreased cell proliferation in the dentate gyrus. Interestingly, this effect was acutely rescued by both PKC inhibitors. Taken together, our results support the hypothesis that an overactivation of the PKC signaling system may be crucial for the deficits of neuroplasticity associated with bipolar disorder. Overall, these findings may provide new insights on the pathophysiology of mania and the use of PKC inhibitors as possible novel treatments for mood disorders.


Animal Reproduction Science | 2007

Expression of proopiomelanocortin, proenkephalin and prodynorphin genes in porcine theca and granulosa cells

Jaroslaw Staszkiewicz; Mariusz T. Skowronski; Tadeusz Kaminski; Gabriela Siawrys; Bartlomiej E. Krazinski; M. Kusmider; Jadwiga Przala; S. Okrasa


European Neuropsychopharmacology | 2016

Time-dependent miR-16 serum fluctuations together with reciprocal changes in the expression level of miR-16 in mesocortical circuit contribute to stress resilient phenotype in chronic mild stress – An animal model of depression

Dariusz Zurawek; M. Kusmider; Agata Faron-Górecka; Piotr Gruca; Paulina Pabian; Magdalena Kolasa; Joanna Solich; Kinga Szafran-Pilch; Mariusz Papp; Marta Dziedzicka-Wasylewska


European Neuropsychopharmacology | 2011

P.1.028 Serum levels of somatostatin-28 and its binding sites in medial habenular nucleus differentiate rats responding and non responding to chronic mild stress

Agata Faron-Górecka; M. Kusmider; Dariusz Zurawek; M. Gaska; Piotr Gruca; Mariusz Papp; Marta Dziedzicka-Wasylewska

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Joanna Solich

Polish Academy of Sciences

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M. Gaska

Polish Academy of Sciences

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Mariusz Papp

Polish Academy of Sciences

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Piotr Gruca

Polish Academy of Sciences

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Dariusz Zurawek

Polish Academy of Sciences

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P. Palach

Polish Academy of Sciences

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Magdalena Kolasa

Polish Academy of Sciences

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Paulina Pabian

Polish Academy of Sciences

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