Head: Małgorzata Skup



2014 Professor of Biological Sciences, nomination by the President of the Republic of Poland, Nencki Institute of Experimental Biology, PAS

2004 DSc Habil, Nencki Institute of Experimental Biology, PAS

1988 PhD in Biology, Nencki Institute of Experimental Biology, PAS


Research trainings:

1998 Visiting professor, National Institute of Physiological Sciences (S. Mori), Okazaki, Japan

1991-1993 Postdoctoral trainee, McGill University, Department of Pharmacology and Therapeutics (A.C. Cuello, A. Ribeiro-da-Silva), Montreal, Canada


Short visits:

2007 Universität Goettingen, Germany

2003 Zentrum für Molekulare Neurobiologie, Universität, Hamburg, Germany

1991 Neurologische Instytut, Max Pfchlesig Universität, Leipzig, Germany

1984 Fidia Research Laboratories, Department of Biochemistry (G. Toffano), Abano Terme, Italy

1982 Universita degli Studi di Firenze, Department of Pharmacology (G. Pepeu), Italy

1981 Freie Universitat Berlin, Institute of Pharmacology (F. Cooper/H. Rommelspacher), Germany


Professional employments:

2016-present Head of the Group of Restorative Neurobiology, Nencki Institute of Experimental Biology, PAS

2014-present Head of the Department of Neurophysiology, Nencki Institute of Experimental Biology, PAS


Honors and fellowships:

2015-2017 President of the Polish Neuroscience Society

2015-2017 Member of the Governing Council of Federation of European Neuroscience Societies

2011-2015 Vice-President of the Committee of Neurobiology, Polish Academy of Sciences

2009-2011 Vice-President of the Polish Neuroscience Society

1991 Medical Research Council of Canada Fellowship, Canadian Network of Excellence for Neuronal Regeneration and Functional Recovery

Staff:  Julita Czarkowska (Professor emeritus), Olga Gajewska-Woźniak, Anna Głowacka (PhD student), Kamil Grycz (PhD student), Benjun Ji (PhD student)


Research profile:

Injury of the CNS alters transcriptional programs that determine neuronal fate: survival and recovery, or death. A powerful pro-survival/recovery program in neurons and glial cells may be triggered by neurotrophic factors. We focus on neurotrophins, their receptors, and related molecules; assuming that their selective regulation may limit signaling through pro-apoptotic pathways and promote recovery processes. To modulate their expression after spinal cord injury; locomotor exercise, electrical stimulation of the peripheral nerves and tissue transduction with AAV-carried transgenes are in use. These treatments cause remodeling of the spinal network and lead to functional improvement. We search for the mechanisms of neurotrophic regulation of neurotransmission in motoneurons and at the neuro-muscular junction. Contribution of extracellular matrix proteoglycans and postsynaptic excitatory and inhibitory receptors are in focus.

Advanced immunohistochemistry combined with wide field and confocal microscopy are used to study architecture and activation of neuronal networks. Neuronal, dendritic and axonal tracing supported by immunolabeling, DNA/RNA staining and histological identification of myelin and glia are used to examine morphological changes and localization of specific proteins in single cells and synapses. Tissue sampling and Laser Capture Microdissection of single cells are used to identify local changes in gene and protein expression with the use of RT PCR, ELISA, and Western blotting. Behavioral and electrophysiological setups provide data on animal kinematics during locomotion.

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Current research activities:

  • potential of AAV-mediated BDNF transgene overexpression in early responses of excitatory and inhibitory neurotransmitter systems in the transected spinal cord: assessment of contribution of pre-and postsynaptic molecules to altered signaling to motoneurons and at neuro-muscular junctions
  • the reorganization of synaptic input to the ankle flexor and extensor motoneurons induced by chronic electrical stimulation of proprioceptive fibers in rats after complete transection of the spinal cord
  • the role of extracellular matrix and perineuronal nets surrounding motoneurons in the spontaneous recovery processes in the transected spinal cord: modulation by locomotor exercise and electrical stimulation of proprioceptive fibers


Selected publications:

Gajewska-Woźniak O., Grycz K., Czarkowska-Bauch J., Skup M. (2016) Electrical Stimulation of Low-Threshold Proprioceptive Fibers in the Adult Rat Increases Density of Glutamatergic and Cholinergic Terminals on Ankle Extensor α-Motoneurons. PLoS One, 11(8): e0161614.


Wójcik-Gryciuk A., Skup M., Waleszczyk W.J. (2015) Glaucoma - state of the art and perspectives on treatment. Restor Neurol Neurosci, 34: 107-123.


Ziemlińska E., Kügler S., Schachner M., Wewiór I., Czarkowska-Bauch J., Skup M. (2014) Overexpression of BDNF Increases Excitability of the Lumbar Spinal Network and Leads to Robust Early Locomotor Recovery in Completely Spinalized Rats. PLoS One, 9(2): e88833.


Gajewska-Woźniak O., Skup M., Kasicki S., Ziemlińska E., Czarkowska-Bauch J. (2013) Enhancing proprioceptive input to motoneurons differentially affects expression of neurotrophin 3 and brain-derived neurotrophic factor in rat hoffmann-reflex circuitry. PLoS One, 8(6):e65937.


Skup M., Gajewska-Wozniak O., Grygielewicz P., Mankovskaya T., Czarkowska-Bauch J. (2012) Different effects of spinalization and locomotor training of spinal animals on cholinergic innervation of the soleus and tibialis anterior motoneurons. Eur J Neurosci, 36(5): 2679-2688.


  • List of Figures: Effects of complete spinal cord injury and treatment on the neuromuscular system in the rat. Changes in the organization and neurochemical response are evaluated by immunohistochemical techniques at the level of the spinal network, peripheral nerve and neuromuscular junction. Bottom left: α-motoneuron identified with neurotracer True Blue. Its synaptic inputs are immunolabeled for synaptophysin (marker of all synaptic terminals; red); VGluT1 (turquise) and VAChT (green), identifying Ia glutamatergic and cholinergic terminals, respectively. Bottom centre: spinal neuron in inhibitory synaptic network. Receptors for neurotransmitters Glycine (red) and GABA (green) are accompanied by Gephyrin (blue) anchoring them in the plasma membrane. Bottom right: Neuromuscular junctions (NMJ) in the tibialis anterior muscle. Cholinergic presynaptic terminal (VAChT, green) abuts on postsynaptic membrane rich in acetylocholine receptors (BTX, red). Nerve with terminal Schwann cells (S-100, turquise) is shown. 3D reconstruction of NMJs, created in Imaris software, allows for detailed morphology analysis. Top right: Semi-thin cross section of tibial nerve stained with Toluidine Blue. In two small nerve bundles, the dark rings of the the myelin sheath formed by Schwann cells surrounding axons are visible. In the main nerve bundle the myelinated nerve fibers are colored according to their thickness by means of ImagePro Premier software.