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Content available remote Dendrites as separate compartment ? local protein synthesis
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EN
The article summarizes the most meaningful studies which have provided evidence that protein synthesis in neurons can occur not only in cell perikarya but also locally in dendrites. The presence of the complete machinery required to synthesize cytoplasmic and integral membrane proteins in dendrites, identification of binding proteins known to mediate mRNA trafficking in dendrites and the ability to trigger 'on-site' translation make it possible for the synthesis of particular proteins to be regulated by synaptic signals. Until now over 100 different mRNAs coding the proteins involved in neurotransmission and modulation of synaptic activity have been identified in dendrites. Local protein synthesis is postulated to provide the basic mechanism of fast changes in the strength of neuronal connections and to be an important factor in the molecular background of synaptic plasticity, giving rise to enduring changes in synaptic function, which in turn play a role in local homeostatic responses. Local protein synthesis points to some autonomy of dendrites which makes them 'the brains of the neurons' (Jim Eberwine; from the interview with J. Eberwine ? Barinaga 2000).
EN
Partial deafferentation of the hippocampus due to trymethyltin (TMT) intoxication has been reported to induce plastic rearrangements of neuronal elements but the factors that direct these responses are unknown. To assess the possible involvement of nerve growth factor (NGF) in the phenomenon we evaluated the presumable changes in the expression pattern of NGF immunoreactivity (NGF-IR) in rat hippocampus 21 days after administration of TMT (8 mg/kg, i.p.) when reactive changes are fully developed. Immunolabelling for TrkA known to mediate biological effects of NGF and for GFAP to identify astroglial cells as a one of presumed source of postinjury produced factors was carried out on adjacent sections to establish the relation between expression of these proteins. In control hippocampus NGF-IR and TrkA-IR were localized in neurons and/or nueropil. After exposure to TMT remarkable non-neuronal expression of both proteins was observed. The distribution pattern of NGF, TrkA and GFAP overlapped suggesting that reactive asrtocytes may not only produce NGF but also may become responsive to this neurotrophin. Zones of extensive NGF and TrkA astroglial expression corresponded to areas of axonal-dendritic rearrangements reported earlier. That data suggest that astroglia-derived trophic activity may be involved in neuronal plastic events associated with treatment with TMT.
EN
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
The effect of difluoromethylornithine (DFMO), an irrevesible inhibitor of ornithine decarboxylase (ODC), the rate limiting enzyme of polyamine biosynthesis, and its combined action with GM1 ganglioside, was studied on the GFAP content in a model of remote astrogliosis evoked in the hippocampus by latral fimbria transection.DFMO markedly suppressed hipocampal gliosis as measured by GFAP immunoblotting seven days postsurgery.Combined treatment with DFMO and GM1 ganglioside produced a stronger suppressive effect than DFMO.The results support the hypothesis of a causal link between lesion induced events:polyamine biosynthesis and astroglial reaction.Potentation of the inhibitory effect of DFMO by GM1 ganglioside suggest that the latter does not act through the mechanism involving ODC suppression.
EN
Septal cholinergic neurones depend on trophic support by nerve growth factor (NGF) which can rescue them from injury-induced degeneration.Since NGF exerts its effects via p75NTR and TrkA receptors coexpressed in vast majority of these neurones and down-regulated without NGF treatment after injury.In this study we aimed to examine how does the lesion to the cholonergic tracts affect distribution of both type of receptor proteins in damaged fibres.Early changes (two and seven days) were examined immunocytochemically within the septum and supracallosal stria after unilateral lesion to the supracollosal area and cingulum transecting some septal cholinergic efferents.
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Trk B immunoreactivity (IR) was detected in number of spinal cells at the lumbar level in non-trained animals (Fig. 1A). The strongest IR appeared in the perikarya and processes of small diameter cells rarely scattered in the grey and white matter. The average area of these cells was 50 mm2 (? 10). Exercise increased by over 50% the number of TrkB immunostained small cells (Fig.1B). An enhancement of perikaryonal immunostaining of these cells was also observed (Fig.1B, inset). Testing the identity of Trk B IR small diameter cells did not prove their astroglial (GFAP IR) and gabaergic (GAD IR) phenotype in the grey matter. Some of TrkB IR cells in the white matter were astrocytes. Our data point to physical exercise as a potent method to make spinal cells more receptive to neurotrophic stimuli.
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