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INTRODUCTION: Perineuronal nets (PNNs), which restrict axonal regeneration in the glial scar and limit synaptic plasticity, are composed of chondroitin sulfate proteoglycans (CSPGs) and Crtl1/Hapln1 link protein essential for PNN formation. Spinal cord transection (SCT) leads to changes of various CSPG proteins differently distributed between 2nd– 8th postlesion weeks. This raises the question if...
INTRODUCTION: Complete spinal cord transection (SCT) leads to loss of motor control due to disruption of supraspinal tracts and altered functioning of both central and peripheral synapses. We showed that SCT at low thoracic segments causes deficiency in cholinergic input to ankle extensor (soleus) motoneurons, whereas brain-derived neurotrophic factor (BDNF) overexpression below the lesion site increases...
INTRODUCTION: Complete spinal cord transection (SCT) disturbs the balance between inhibitory and excitatory inputs to motoneurons increasing their excitability. However SCT causes deficiency in excitatory cholinergic input to ankle extensor motoneurons, whereas brain-derived neurotrophic factor (BDNF) overexpression below the lesion site increases markers of spinal neurotransmission and improves locomotor...
BACKGROUND AND AIMS: The effects of low-threshold stimulation of muscle afferents (Ia) on glutamatergic and cholinergic innervation of α-motoneurons (Mns) were tested. Two types of synaptic terminals were analyzed: (1) glutamatergic Ia carrying VGLUT1, contacting monosynaptically Mns; (2) cholinergic C-terminals, carrying VAChT, originating from V0c-interneurons of lamina X, which might receive indirect...
BACKGROUND AND AIMS: Complete spinal cord transection (SCT) causes reorganization of spinal networks involving changes ofsynaptic terminals abutting on α-motoneurons(MNs).We showed that SCT impoverishes excitatory cholinergic input to ankle extensor but not to flexor MNs and locomotor training leads to its enrichment on both MNs groups (Skup et al. 2012). The opposite effect of training after SCT...
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...
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...
Recovery after spinal cord injury requires neuronal remodeling which is regulated by cell adhesion molecules (CAMs) and chondroitin sulfate proteoglycans (CSPGs). CSPG may be potentially both inhibitory and supportive of regenerative plasticity. To verify whether chronic (5 weeks) L1 CAM overexpression in transected spinal cord of the rat, proven to promote recovery in mice, affects CSPG phosphacan...
Locomotor exercise, sufficient to increase expression of brainderived neurotrophic factor and neurotrophin 4 in the lumbar spinal cord, does not affect protein level of neurotrophin 3 (NT-3), as we have shown previously. The effect of 7 days of direct, lowfrequency electrical stimulation of the tibial nerve on expression of NT-3 was also negligible although this stimulation was addressed to low-threshold...
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...
Among approaches targeting restoration of function after spinal cord injury a promising one is to use L1 cell adhesion molecule, known to promote axon outgrowth, fasciculation, guidance and myelination in regeneration. L1 is upregulated after injury, manifesting requirements of the impaired networks for successful repair. Previously, our strategy to overexpress L1 gene in the lesion site was found...
Availability of brain-derived neurotrophic factor (BDNF) and neurotrophin 4 (NT-4) in the nervous system depends on the neuronal activity. We have previously shown that moderate locomotor exercise causes an increase of BDNF and NT-4 proteins but not neurotrophin 3 (NT-3) in the lumbar spinal cord. The questions arise whether NT-3 is regulated in a different way than BDNF and NT-4 or, that proprioceptive...
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...
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...
Jerzy Choróbski, a distinguished neurosurgeon, who established Polish modern neurosurgery, graduated in medicine from the Jagiellonian University in 1926 and developed his career in European and American clinics. In 1920s he studied in Paris and mastered his talent among the elite European neurologists, neurosurgeons and psychiatrists of those days (Bidziński 2008). In 1930s, as a grantee of M. Ottman...
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...
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...
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