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1

The role of creb in neurodegenerative diseases

100%
Rodriguez-Parkitna J.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
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nr S
The cAMP response element binding protein (CREB) is an essential regulator of stimulus-driven gene expression, best described for its role in immediate-early gene transcription and neuronal plasticity. Together with the closely related cAMP response element modulator (CREM), it has been shown to be necessary for survival of specific types of forebrain neurons, most notably in the striatum or hippocampus, but dispensable in other neuron types, like the monoamine cells. This selective role of CREB in neuronal survival prompted investigation into its involvement in neurodegenerative disorders, particularly Huntington’s and Niemann-Pick type C diseases. In order to assess the role of CREB-dependent transcription in triggering neuronal death, using the Cre/loxP system we have generated mice with a selective ablation of CREB in the forebrain and deletion of CREM. Gene expression profiling in the striatum and hippocampus of double-mutant mice revealed that neurodegeneration was accompanied with strong increase in abundance of transcripts associated with activation of the glia, but also changed expression of genes participating in sterol metabolism. Moreover, comparison of expression profiles with those reported in other models of striatal neurodegeneration reveals a common pattern of changes, involving several genes associated with the medium spiny neurons of the striatum. Interestingly, in a mutant mouse with a single CREM allele, no neurodegeneration was observed, and their expression profile allows to identify key CREB/CREM-dependent transcripts essential for cell survival. These observations help to understand the roles of CREB and CREM in neuronal homeostasis and their involvement in neurodegenerative disorders affecting forebrain neurons.
2
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Neuronalne mechanizmy motywacji

51%
Rodriguez-Parkitna J., Cieslak P., Lopata K., Zygmunt M.
Wszechświat
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2014
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tom 115
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nr 01-03
3

Anxiety, depressive, cognitive and motivational phenotype in mice with selective ablation of NMDA receptors in noradrenegic neurons

45%
Solecki W., Rodriguez-Parkitna J., Kubik J., Schutz G., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
The noradrenergic system of the brain has been postulated to mediate arousal, selective attention, as well as anxiety, depression and learning and memory. Here we report the behavioral phenotype of transgenic mouse (NR1DbhCre) with selective ablation of the NMDA receptor subunit NR1 in noradrenergic cells. We focused on behaviors modulated by the noradrenergic system, in particular anxiety-like behaviors in the light/dark box, and open fi eld as well as depressive-like behaviors in forced swim test. Furthermore, memory performance was measured using elevated plus maze spatial learning (EPMSL), Y maze, right/left discrimination, habituation to open fi led and novel object recognition and motivation-dependent behaviors was studied using food pellet self-administration paradigm. While no alterations were found in anxiety- and depressive-like behaviors in NR1DbhCre mice, the transgenic animals displayed impaired object recognition memory, but increased performance in right/left discrimination test. In addition, the NR1DbhCre mice displayed higher food reward sensitivity as evidenced by faster acquisition of food self-administration and higher breaking point in progressive ratio schedule of reinforcement. In conclusion, the ablation of NMDA receptors in noradrenergic neurons in mice produce impairment of recognition memory and alteration of motivational systems.
4

Regulation of alternative gene expression in the mouse striatum in response to cocaine

39%
Zygmunt M., Rodriguez-Parkitna J., Golda S., Piechota M., Ficek J., Korostynski M.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: Cocaine is a potent psychostimulant that increases levels of striatal dopamine and activates neuronal circuits controlling motivation and reward-based learning. Transcriptional response to cocaine includes expression of alternative gene isoforms and splicing variants. Unraveling the regulatory mechanisms that are involved in selection of active transcription start and termination sites provides novel insight into molecular basis of drug-induced brain plasticity. METHODS: We used next-generation sequencing (RNA-seq) to comprehensively map expression of genesin the mouse striatum. Total RNA and small RNA resequencing was performed in samples collected 1 h after acute treatment with 25 mg/kg cocaine. To identify transcripts responsive to drug treatment we used Tophat read-mapper and Cufflinks algorithm for FPKM quantification. The seqinterpreter online tool was used to search for key regulatory factors that control alternative gene transcription in the brain (http://seqinterpreter.cremag.org). RESULTS: In addition to increased expression of activity-regulated genes, different types of cocaine-inducible splicing variants and transcript biotypes were identified. Examples of different modalities of gene expression include alternative first exon (e.g. Stxbp1), alternative last exon (Hsph1), intron retention (Dnajb5), long noncoding RNA (Gm13889) and small RNA (Mir92b and Mir130a). In order to investigate neuron-type specificity of gene expression we have used fluorescence-activated cell sorting to isolate genetically labeled dopamine receptor 1 expressing neurons. CONCLUSIONS: Our results provide a comprehensive assessment of neuronal activity-induced gene expression at the level of individual transcriptional units rather than whole genes. Further experiments will explore differences in activity-regulated gene expression in discrete neuron types, i.e. the D1 or D2 expressing medium spiny neurons of the striatum. This work was supported by NCN grant SONATA 2011/03/D/ NZ3/01686.
5

Inactivation of the GluN1 subunit of the NMDA receptor modifies functions of dopaminoceptive neurons in the rat nucleus accumbens

39%
Sowa J., Bobula B., Tokarski K., Rodriguez-Parkitna J., Przewlocki R., Hess G.
Acta Neurobiologiae Experimentalis
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2014
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tom 74
|
nr 3
Adaptive behavior, such as regulation of appetitive motivation or reward processing, is associated with plasticity of the brain’s dopamine system. We examined different types of adaptive behavior in the transgenic mouse line (NR1D1CreERT2) where the GluN1 subunit is selectively inactivated in dopaminoceptive neurons. We used electrophysiological recordings to investigate if functions of D1-expressing neurons are modified. In transgenic animals the amplitude of field potentials in the NAcc was not different form controls, however, LTP was reduced from 138% in control to 118% in D1ERT2 [Tg-N/0-N] animals. Recordings of spontaneous EPSCs from medium spiny neurons of the NAcc demonstrated that approximately 50% of the cells lacked the NMDAR-dependent component of sEPSCs. These results suggest that the mutation significantly alters functions of dopaminoceptive neurons.
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