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Locomotor exercise increases neurotrophin BDNF and its receptor TrkBFL expression in the lumbar spinal cord. Involvement of BDNF/TrkBFL in synaptic transmission raises the questions which intracellular compartments are involved in this upregulation and whether exercise leads to redistribution of these proteins related to the duration of exercise. We have investigated the influence of short-term (7 days) locomotor exercise (ST) on intracellular distribution of BDNF and TrkBFL in the rat lumbar spinal cord comparing it with the effects of long-term (28 days) exercise (LT) described earlier. Immunofluorescence (IF) of proteins was analyzed with confocal microscopy. ST exercise caused a redistribution of perikaryonal BDNF IF toward periphery resulting in an increase of dendritic signal. In contrast to an enhancement of perikaryonal BDNF staining following LT, no increase of BDNF IF in cell bodies was observed after ST. An increase of TrkBFL IF in oligodendrocytes was consistent with that caused by LT. The fibers of TrkBFL IF oligodendrocytes surrounding the largest neurons were in close apposition to neuronal membrane. We propose that ST exercise causes (1) BDNF translocation to dendrites and/or local dendritic synthesis to serve increased synaptic activity (2) sensitization of oligodendroglia to BDNF mediated responses.
EN
Injury to the mature central nervous system (CNS) induces a series of transient changes leading not only to death of neurons, but also to spontaneous rearrangement of the affected network. One of such pro plastic events, detected following injury, is an increased level of neurotrophins. Neurotrophins are a family of proteins involved in survival and outgrowth processes. The other one, more difficult to observe, is a change in the complexity of the dendritic tree, causing arborization or pruning, depending on many circumstances: i.e. lesion etiology. Subsequent therapies like enriched environment or locomotor exercise bring about a functional improvement, which was found to further increase the neurotrophin level and induced additional arborization of dendrites. Another important consequence of damage to CNS connections is deafferentation, shown to induce a down regulation of outgrowth inhibitors. Their suppression in turn may facilitate dendritic plasticity. Taken together, these factors may contribute to enhanced plasticity in the injured mature CNS. Thus the proper use of endogenously increased plastic potential seems to be important for design and optimizing therapeutic strategies. Further investigation of mechanisms involved in switching on plasticity may help to improve on existing therapies and find new ways to obtain better recovery following injury.
EN
Furin, PC1, PC2 and PC5 represent mammalian convertases (PCs) found in endocrine, central and peripheral nervous tissues, which cleave a number of precursors at basic residues normally processed in vivo. Typical bonds cleaved by PCs include the pairs Lys-Arg, Arg-Arg and Arg-X-Lys/Arg-Arg. These cleavage sites have been detected following coexpression of each convertase in cell lines together with different precursors as models, including proopiomelanocortin (POMC), proinsulin and proNGF and proBDNF. The presence of PCs and different precursors was revealed by in situ hybridization or immunocytochemistry in cultured AtT-20 cells, in the developing CNS, pituitary, and pancreatic islets. In an experimental model of epilepsy in which epileptiform activities were provoked by kainic acid administration, we observed a similar transient expression of furin and PC1 as compared to that of NGF and BDNF. In conclusion, it is proposed that under different stimuli various precursors are activated by a unique cocktail of convertases, each of which either alone or in combination with others acts to process inactive precursors, and thereby playing an important role in development and in the plasticity of neuronal system.
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