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nencki.gov.pl » Working Groups » Department of Neurophysiology »
Laboratory of Reinnervation Processes

Head
Julita CZARKOWSKA-BAUCH

Staff
Małgorzata SKUP, Ewelina ZIEMLIŃSKA, Olga GAJEWSKA, Sabina JELEŃ, Tatsiana MANKOYSKAYA, Rafał PŁATEK, Anna WARSZAWSKA, Małgorzata ZAREMBA

Research profile

Injury of the central nervous system (CNS) causes alterations in the transcriptional programs that determine neuronal fate: survival and recovery or death. One of the most powerful pro-survival/recovery programs of neuronal and glial populations in the CNS may be triggered by neurotrophins. We focus on neurotrophins, their receptors as well as on related molecules assuming that their selective upregulation may limit signaling through pro-apoptotic pathways and promote recovery processes. Several approaches to modulate an expression of these molecules after spinal cord injury have been employed: locomotor exercise, electrical stimulation of peripheral nerves and adeno-associated virus transduction mediating neurotrophins or adhesion molecules expression. Histochemical (immunocytochemical, DNA/RNA staining, cell labeling and fiber tracing), neurochemical (HPLC) and molecular biology techniques (electrophoresis and Western blotting, RT PCR, in situ hybridization) are in use. In addition behavioral and electrophysiological methods have been employed to monitor functional aspects of recovery following injury of the nervous system and/or to enhance recovery processes. 

Current research activities

  • changes of neurotrophic activity following spinal cord injury and cortical ischemic lesions in adult rats;

  • modulation of  endogenous level of neurotrophic factors and their receptors in the spinal cord owing to locomotor exercise or electrical stimulation of peripheral nerves;

  •  AAV vector transduction mediating neurotrophins or adhesion molecules expression and their effects on recovery processes following spinal cord injury;

  • exercise- induced reorganization of the spinal neuronal network after injury;

  • the effect of exercise on neurotransmitter content in the spinal animals;

  • recovery processes in genetically modified mice;

  • apoptosis and patterns of expression of transcription factors and prosurvival/proapoptotic proteins following cortical and spinal cord injuries.

Selected publications

Macias M., Dwornik A., Ziemlinska E., Fehr S., Schachner M., Czarkowska-Bauch J., Skup M. (2007) Locomotor exercise alters expression of pro-BDNF, BDNF and its receptor TrkB in the spinal cord of adult rats. European Journal of Neuroscience 25: 2425-2444.

Skup M., Wiater M., Górnicka E., Walentynowicz M., Czarkowska-Bauch J. (2007) Different effect of locomotor exercise on the concentration of amino acids and monoamines in the rostral and caudal lumbar segments of the spinal cord in the rat. Spinal Cord, 45: 140-148.

Chen J., Wu J., Irintchev A., Apostolova I., Skup M., Kuegler S., Schachner M. (2007) Adeno-associated virus-mediated L1 expression ameliorates inhibitory glial scar, promotes axonal regeneration and functional recovery after spinal cord injury in adult mice. Brain 130, 954-969.

Sulejczak D., Ziemlińska E., Czarkowska-Bauch J., Nosecka E., Strzałkowski R., Skup M. (2007) Focal photothrombotic lesion of the motor cortex causes an increase of BDNF level in the motor-sensory cortical areas not accompanied by forelimb motor skills recovery. J. Neurotrauma 24:1362–1377.

Sulejczak D., Czarkowska-Bauch J., Macias M., Skup M. 2004. Bcl-2 and Bax proteins are increased in neocortical but not in thalamic apoptosis following devascularizing lesions of the cerebral cortex in the rat: an immunohistochemical study. Brain Res. 1006/2, 133-149

Skup M., Dwornik A., Macias M., Sulejczak D., Wiater M., Czarkowska-Bauch J. (2002).; Long-term locomotor training up-regulates TrkB FL receptor-like proteins, brain-derived neurotrophic factor, and neurotrophin 4 with different topographies of expression in oligodendroglia and neurons in the spinal cord. Exp. Neurol. 176: 289-307.



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Published at: 2008-05-27 09:49
 

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