Altered taurine release following hypotonic stress in astrocytes from mice deficient for GFAP and vimentin.

Astrocytes maintain their volume in response to changes in osmotic pressure in their environment by an afflux/influx of ions and organic osmoequivalents. The initial swelling of an astrocyte transferred to a hypoosmotic medium is thus reversed within minutes. The mechanisms which trigger this process as well as the sensors for cell volume are largely unknown, however, the cytoskeleton appears to be involved. We have addressed the role of one component of the cytoskeleton, the intermediate filaments, in the maintenance of astrocytic cell volume. Astrocytes from wild type mice were compared with cells from mice deficient for either glial fibrillary acidic protein (GFAP-/-) or vimentin (vimentin-/-) and with astrocytes from mice deficient for both proteins (GFAP-/-vim-/-). Whereas GFAP-/- and vimentin-/- cultured or reactive astrocytes retain intermediate filaments, the GFAP-/-vim-/- astrocytes are completely devoid of these structures. The rate of efflux of the preloaded osmoequivalent 3H-taurine from primary and passaged cultures of astrocytes was monitored. A reduction of NaCl (25 mM) in the perfusion medium led to a 400-900% increase of 3H-taurine afflux in astrocytes from wild type mice. The stimulated efflux was not significantly affected in astrocytes from GFAP-/- or vimentin-/- mice. However, the efflux from astrocytes from GFAP-/-vim-/- mice was 25-46% lower than the wild type levels. The results strengthen the role of the cytoskeleton in astrocyte volume regulation and suggest an involvement of intermediate filaments in the process.