title: Down-regulation of astroglial proteins in the rat cerebellum after portacaval anastomosis.
abstract: The effect of short-term portacaval anastomosis (PCA) on the expression of specific astroglial markers [glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS)] in the rat cerebellum was examined to determine the influences of PCA on astroglial cells. The results suggest that PCA directly interferes with astroglial cytoskeleton, as indicated by the irregular distribution and reduced expression of GFAP observed after 1 month. PCA also decreased GS immunoreactivity in the Bergmann glial processes of the molecular layer, as well as in astrocytes of the granule cell layer. It might also modulate glutamatergic nervous activity as GS expression was reduced in 1 month post-PCA brains. Moreover, the GFAP and GS levels in PCA-exposed rats were lower than in control rats. This might contribute to the appearance of encephalopathy by increasing extracellular glutamate and/or ammonia concentrations. These results show that short-term PCA interferes with astroglial protein expression, with both GFAP and GS levels falling in astroglial cells.
authors.affiliation: Departamento de Biología Celular y Genética, Universidad de Alcalá, Madrid, Spain. isabel.suarez@uah.es
authors.forename: I
authors.initials: I
authors.lastname: Suárez
authors.forename: G
authors.initials: G
authors.lastname: Bodega
authors.forename: M
authors.initials: M
authors.lastname: Rubio
authors.forename: B
authors.initials: B
authors.lastname: Fernández
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology*; D002531:Cerebellum / Q000378:metabolism* / Q000473:pathology*; D015536:Down-Regulation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D015151:Immunoblotting; D007150:Immunohistochemistry; D008297:Male; D011167:Portacaval Shunt, Surgical; D051381:Rats
chemical_list: D005904:Glial Fibrillary Acidic Protein; D005974:Glutamate-Ammonia Ligase