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Abstract in english

We have studied in developing and epileptic brain and in neuronal and astroglial cultures the expression and localisation of beta actin, one of the two non-muscle actin isoforme, and L-caldesmon and acidic calponin, two F-actin binding proteins that stabilise actin filaments and inhibit the actomyosin ATPase activity. We show that: 1. beta Actin immunoreactivity is enriched in microglia-macrophages and is associated with morphological changes that occurred to these cells during the postnatal development and after seizures. 2. In vivo, caldesmon and calponin are localised in the postsynaptic area and are concentrated in the dendritic spines and in the postsynaptic densities of mature neurones; these two proteins are rather adjacent than superimposed in the same domain of the cell and both colocalise with actin and myosin. 3. Calponin is present in astroglial cells in vivo and is specially enriched in radial glial cells, while no caldesmon immunoreactivity is detected in glial cells in vivo, nevertheless its presence in cultured astrocytes have been reported. 4. Both proteins are spatially and temporally regulated during the brain development. As caldesmon, calponin is particularly enriched in growth cones lamellipodia but is absent from filopodial extensions. 6. After seizures, both immunoreactivities of caldesmon and calponin increase in degenerating neurones, disappear in the sclerotic fields, and persist in the surviving cells. Furthermore, the expression of acidic calponin is tightly associated with the astroglial reaction in the CA3 area and the hilus of the hippocampus. Expression and localisation of these three proteins in cells and subcellular domains having high capacity of remodelling in developing, adult and epileptic brain suggest that they play an important role in the morphological changes associated with neuronal plasticity.