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1

Co dzieje się na peryferiach synapsy?

100%
Ziemlinska E., Czarkowska-Bauch J., Skup M.
Postępy Biologii Komórki
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2014
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tom 41
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nr 2
2

Obłaskawione wirusy w służbie nauki i medycyny

100%
Ziemlinska E., Platek R., Skup M.
Kosmos
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2011
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tom 60
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nr 3-4
3

Enhancing proprioceptive input to motoneurons differentialy affects expression of neurotrophin 3, BDNF and TrkB/TrkC receptors in rat Hofman-reflex circuitry

88%
Gajewska-Wozniak O., Ziemlinska E., Piotrowska K., Skup M., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr Suppl.1
The importance of neurotrophin 3 (NT-3) for motor control prompted us to ask whether direct low-threshold electrical stimulation of the tibial nerve aimed at activation of Ia fibers, could increase the pool of NT-3 and its receptor TrkC in the Hoffmannreflex circuitry of the soleus (Sol) muscle. The effects were compared with those on BDNF and its TrkB receptor. Cuff-electrode over the tibial nerve was used to deliver continuous bursts of stimuli in awake rats. Functional mapping of neuronal activation with c-Fos showed that a number of spinal neurons was activated by Ia stimuli. Stimulation produced a strong increase of NT-3 protein (ELISA), in L3- 6 spinal segments and in Sol with minor effect on BDNF level in L3-6. Protein level of NT-3 and BDNF corresponded to the changes of NT-3 mRNA and BDNF mRNA expression in L3-6 segments but not in Sol muscle. TrkC and TrkB mRNA tended to decrease in L3-6 but in the Sol muscle TrkB mRNA decreased and TrkC mRNA strongly increased showing sensitization of the Sol muscle to NT-3 signaling. The possibility of increasing NT-3/TrkC signaling in the neuromuscular system, with minor effects on BDNF/TrkB signaling, by selective stimulation of peripheral nerve, which in humans might be applied in non-invasive way, offers an attractive therapeutic tool. Supported by N N 401 0480 33, BIOIMAGINE grants.
4

Lack of prodomain abolishes BDNF constitutive secretion by HEK 293 cells

88%
Ziemlinska E., Skup M., Czarkowska-Bauch J., Bahr M., Kugler S.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
|
nr 3
Brain-derived neurotrophic factor (BDNF) and its proBDNF precursor are released both in constitutive and activity-dependent manner. Prodomain itself proved to be necessary for BDNF targeting to regulated secretory pathway [Egan et al. (2003) Cell, Chen et al. (2005) J Neurosci] but its role in constitutive secretion is elusive. As mature BDNF (mBDNF) conveys trophic and prosurvival signals whereas proBDNF may convey growth inhibiting and death signals, an important issue arises: can we control the type of signal being triggered by BDNF? To verify this we cut off the prodomain and generated plasmid coding only for rat mBDNF. To test the constitutive mBDNF construct secretion we have chosen HEK 293 cell line. Two other plasmids coding either for proBDNF (template for both BDNF forms) or proBDNF protected from prodomain cleavage (source of proBDNF only), served as controls. BDNF secretion was evaluated with WB technique using antibodies detecting (1) both BDNF forms, (2) HA tag (mBDNF construct) and (3) MYC tag (proBDNF constructs). We found all three constructs being stably expressed in HEK cells. However, in contrast to both proBDNF constructs, which were secreted and detected in media fraction, mBDNF construct was revealed only in the cell lysate fraction, not being released to the media. This is the fi rst observation showing that mBDNF can be constitutively released only when accompanied by prodomain. Support: ASTF 211-00-2007 for EZ, Polish-German grant to MS and SK.
5

What locomotor training brings to intact and injured spinal cord?

76%
Skup M., Macias M., Dwornik A., Ziemlinska E., Strzalkowski R., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
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2007
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tom 67
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nr 3
6

The impact of training and neurotrophins on functional recovery after complete spinal cord transection: cellular and molecular mechanisms contributing to motor improvement

76%
Skup M., Ziemlinska E., Gajewska-Wozniak O., Platek R., Maciejewska A., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
2014
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tom 74
|
nr 2
Beneficial effects of locomotor training on the functional recovery after complete transection of the spinal cord indicate that in chronic spinal animals spontaneous recovery processes are enhanced and shaped by the training. The mechanisms of that use-dependent improvement are still not fully understood. This review tackles three aspects of this issue: (1) neurochemical attributes of functional improvement showing that concentrations of excitatory and inhibitory amino acids in the lumbar spinal segments, which were changed after transection, normalize after the training, or even raise beyond normal. As it does not translate to functional equilibrium between excitatory and inhibitory neurotransmission and may lead to hyperexcitability, the postsynaptic mechanisms which might be responsible for the hyperexcitability are discussed, including (i) dysfunction of K+-Cl- cotransporter KCC2, which controls the strength and robustness of inhibition, and (ii) altered function of 5-HT2 receptors, which may be targeted to restore KCC2 activity and intrinsic inhibition; (2) morphological changes of lumbar motoneurons and their inputs related to functional improvement of spinal animals, pointing to use-dependent diminution/ reversal of the atrophy of the dendritic tree of the hindlimb motoneurons and of their synaptic impoverishment, which in paraplegic animals differs depending on the degree of disuse of the muscles; (3) the role of neurotrophins in motor improvement of spinal animals showing, that increases in neurotrophins due to training or due to efficient viral vector-based transgene expression, that might be responsible for the enrichment of the dendritic tree, elongation of processes and influence neurotransmitter systems in the areas subjected to plastic modifications after injury, correlate with improvement of locomotor functions.
7

The effect of AAV1/2-mediated BDFN transgene overexpression on trkbFL and trkbTK receptor transcripts and on TrkBFL cellular lokalization in the transected spinal cord of the rat

76%
Ziemlinska E., Wiewior I., Grygielewicz P., Czarkowska-Bauch J., Kugler S., Skup M.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
|
nr S
Brain-derived neurotrophic factor (BDNF) regulates its fulllength TrkB (TrkBFL) receptor. BDNF administration to the brain or spinal cord after injury stimulates neuronal plasticity and brings some improvement of impaired functions, but a prolonged exposure of neurons to BDNF in vitro and BDNF infusions to the brain downregulate TrkBFL protein and reduce its downstream signaling, thus limiting BDNF effectiveness. In our recent study we used AAV-mediated transfer of BDNF transgene to cause long-term delivery of BDNF to isolated spinal cord transected at Th11 – Th12 segments. Three groups of rats were used: intact, spinal PBS (spPBS), and spinal AAV-BDNF (spBDNF) injected. The treatment resulted in substantial improvement of treadmill locomotion at two weeks after spinalization, but its effect weakened in time (7 weeks). The mechanism underlying this effect may arise from decreased abundance and availability of TrkBFL and its truncated forms. To verify it, we compared levels of trkbFL/trkbTK transcripts (qPCR) and evaluated TrkBFL segmental distribution (immunohistochemistry). Both transcripts decreased in the scar and in L1 – L2 segments in spPBS rats, but tended to increase in L1 – L2 in spBDNF rats (p<0.07). In L3 – L6 segments no group differences in transcripts were found. Comparison of TrkBFL and c-Myc labeling of transgene-derived BDNF revealed that: (1) caudally to the transection, TrkBFL was abundant in neurons and white matter oligodendroglia (2) c-Myc (+) or (-) neurons showed comparable intensity of TrkBFL labeling (3) neuronal TrkBFL labeling was higher in segments with BDNF excess. In summary, BDNF overproduction in isolated spinal network does not downregulate TrkB transcripts, either it alters cellular abundance and pattern of TrkBFL segmental expression. Data suggest that other aspects of TrkB-mediated signaling are responsible for weakening of functional effect of BDNF. Supported by S007/PolishGerman/2007/01 grant and EMBO fellowship (for EZ).
8

In vivo transduction of spinal cord cells in adult, spinalized rats, with adeno-associated viral vectors:long-term efficiency and specificity of AAV1/2-hSYN and AAV5-mCMV, encoding eGFP

76%
Platek R., Ziemlinska E., Czarkowska-Bauch J., Kugler S., Schachner M., Skup M.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
|
nr 1
We compared the efficiency and specificity of in vivo transduction of spinal cord cells in adult, spinalized rats, with adeno-associated viral vectors: AAV1/2 and AAV5, with human synapsin (hSYN) and murine cytomegalovirus (mCMV) promoters, respectively. Both AAV vectors carried eGFP transgen, and were injected bilaterally to the lumbar L1 segment immediately after spinal transection at the Th10/11. At 5-6 weeks postlesion (1) the distribution and extent of eGFP expressing cells and fibers and (2) their phenotype (immunohistochemical identification; IHC) were determined. To evaluate virus expansion we compared distribution of eGFP signal at the microscopical reconstructions (parasagittal sections). A comparison between serotypes showed, that caudorostral range of cells expressing eGFP was comparable (AAV1/2 – 6.8 mm; AAV5 – 8 mm), with a core of transduced cells (AAV1/2 – 4.2/4.6 mm; AAV5 – 3.4/3.8 mm), surrounding the injection site. Fibers emerging from AAV1/2 -transduced cells reached the lesion border, many of them entered the lesion and occasionally went across the scar, whereas fibers of AAV5-transduced cells faded in a proximity of 300 µm to it. Dorsoventrally, cellular eGFP signal was detected in a gray matter of the subjects transduced with both serotypes, whereas only AAV5 - mCMV transduced cells also in a white matter. Morphology of eGFP expressing cells indicated that both serotypes transduced interneurons and large neurons of Lamina IX. IHC documented that AAV5 and, to a lesser extent, AAV1/2, transduced cholinergic cells (VAChT), whereas none of the transduced neurons were GABAergic (GAD67) or glutamatergic (VGLUT2). AAV5 transduced also glial cells, some identified as astrocytes (GFAP). In conclusion, both vectors efficiently transduce neurons in spinal animals; mCMV promoter drives eGFP expression also in glia. Support: Polish-German Project PBZ-MIN-001/P05/13, S007/PN/2007/01and statutory grant to Nencki Institute.
9

Spinal cord transection leads to attenuation of determinants of GABAergic and glycinergic transmission not accompanied by changes in inhibitory inputs to motoneurons

76%
Ziemlinska E., Maciejewska A., Platek R., Gajewska-Wozniak O., Czarkowska-Banach J., Skup M.
Acta Neurobiologiae Experimentalis
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2013
|
tom 73
|
nr Suppl.1
The data on the responses of inhibitory circuits to the spinal cord transection are conflicting. We examined the segmental distribution of determinants of GABAergic and glycinergic transmission in adult rats five weeks after complete spinal cord transection at Th9-10. Concentrations of the GABA and glycine (Gly) in segments below the lesion were evaluated in rats that did not receive any treatment. Decreases in GABA (24%) and Gly (26%) were found only in the lumbar L1-2 segments. Two other groups of spinal rats received microinjections of PBS (SP-PBS) or AAV- EGFP transgene (SPEGFP) to L1-2. Both led to GABA decrease (43% in L1-2 and 23% in L3-6 segments) and a decrease in mRNA for GAD67 (43% in L1-2 in both groups and 10% in L3-6 segment of SP-PBS vs 49% in L3-6 of SP-EGFP rats). The respective decreases in mRNA for Gly transporter GlyT2 were 68 vs. 72% in L1-2 and 29 vs. 76% in L3-6 segments. These changes were not accompanied by changes in the density of GABAergic/glycinergic network and inputs to motoneurons identified with GAD67/GlyT2 immunostaining. We conclude that albeit spinalization does not reduce inhibitory inputs to lumbar motoneurons it leads to long-term impairment in presynaptic determinants of inhibitory neurotransmission which may attenuate inhibitory signaling. Support: NN401 324739 grant.
10

Spinal cord sortilin distribution and levels change in region-specific mode after spinalization: p75 complexing in motoneurons?

76%
Gajewska O., Mankovskaya T., Ziemlinska E., Korczynski J., Czarkowska-Bauch J., Skup M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Membrane receptor sortilin is involved in sorting and processing of proteins. In complex with p75 receptor binds proneurotrophins what can lead to apoptosis and remodeling of neuronal network. To study sortilin involvement in spinal cord (SC) remodeling after injury, we characterized its distribution patterns, levels and relation to p75 expression in L3/L4 segments, 6 weeks after SC transection at low thoracic level. In intact rats sortilin immunoreactivity (IR) was widely distributed in white and grey matter. The strongest IR was observed in glial cells of lateral and ventral funiculi. In the grey matter sortilin IR appeared in number of neurons and glial cells, except for the lamina 2, where it rarely occurred. In contrast, p75 was limited to the bundle of strongly IR fi bers in dorso-lateral lamina 2. Sortilin and p75 did not colocalise there and overlapped in isolated large neurons of lamina 9. Spinalization caused a 5% decrease of sortilin IR in the white matter not accompanied by p75 IR changes. In the grey matter sortilin IR level was not changed but frequency of p75/sortilin IR overlapping increased in lamina 9 neurons. This result indicates postlesion increase of p75/sortilin complexing in motoneurons which may refl ect activation of proneurotrophin-mediated dysfunction. Our data show lack of such interaction in primary sensory afferents. Sortilin IR in numerous cells devoid of p75 labeling confi rms that it plays also other roles. Supported by MSE P-N/029/2006 grant.
11

Locomotor exercise of spinal rats causes an increase in size of cholinergic terminals in extensor motor nuclei

64%
Czarkowska-Bauch J., Mankovskaya T., Zaremba M., Gajewska O., Ziemlinska E., Platek R., Mlodkowski M., Korczynski J., Skup M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Spinal cord transection causes dramatic, sustained decrease of vesicular acetylcholine transporter VAChT in terminals contacting motoneurons, as reported by Kitzman (2006, Exp Neurol 197). Cholinergic projection is known to regulate excitability of motoneurons during locomotion. The question arises if locomotor exercise of spinal, paraplegic animals might restore the role of this projection. Three groups of adult rats were tested: intact control (n=6), spinal (n=7) and spinal trained subjected to 5 weeks of treadmill locomotor training (n=8). Animals were spinalized at low thoracic segments. Gastrocnemius/soleus and anterior tibial motoneurons were prelabeled with fl uorescent dyes (FG, DY), injected to the muscles. VAChT immunoreactivity (IR) was detected using polyclonal Sigma antibody. We have found that the spinal cord transection caused a decrease of VAChT IR in boutons synapsing on cell bodies and proximal dendrites of motoneurons in L3 and L4 segments compared with that of intact rats. Surprisingly, training caused its further decay. Mean number of VAChT IR boutons did not differ consistently between groups. However, in the extensor motoneuron pools of trained animals the number of bigger VAChT IR boutons was clearly higher than in spinal non-trained and intact animals. The latter effect is in line with functional improvement of spinal trained animals, which is the most prominent in the support phase of locomotion. Supported by MSE P-N/029/2006 and N N401 0480 33 grants.
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