title: Increased perivascular laminin predicts damage to astrocytes in CA3 and piriform cortex following chemoconvulsive treatments.
abstract: Status epilepticus (SE) induced by pilocarpine or kainate is associated with yet not systemically investigated astrocytic and vascular injuries. To investigate their possible association with neuronal damage, the changes in glial fibrillary acidic protein (GFAP), laminin and neuron-specific nuclear protein (NeuN) immunoreactivities were analyzed in rats treated with pilocarpine (380 mg/kg) or kainate (15 mg/kg), and receiving diazepam (20mg/kg) after 10 min of SE. A different group of rats was injected with endothelin-1 (ET-1) in the caudate putamen to reproduce the changes in GFAP and laminin immunoreactivities associated with ischemia. Focal loss of GFAP immunostaining was accompanied by increased laminin immunoreactivity in blood vessels, in all the examined groups. Regression analysis revealed a significant (P<0.01) relationship between astrocytic lesion and increased laminin immunoreactivity in the piriform cortex (Pir) of both pilocarpine (R(2)=0.88) and kainate (R(2)=0.94) groups of treatment. A significant relationship (P<0.01; R(2)=0.81) was also present in the cornu Ammonis 3 (CA3) hippocampal region of pilocarpine-treated rats. At variance, neuronal and glial lesions were significantly related (P<0.05, R(2)=0.74) only in the substantia nigra of pilocarpine-treated rats. The ratio between areas of GFAP and laminin changes of immunoreactivity in the ET-1 group was similar to those found in pilocarpine- and kainate-treated rats in specific brain regions, such as the hippocampal CA3 subfield, Pir and the anterior olfactory nucleus. The amygdala and submedius thalamic nucleus in the pilocarpine group, and the perirhinal and entorhinal cortices in the kainate group, also presented ischemic-like changes. These results indicate that laminin immunoreactivity is upregulated in the basal lamina of blood vessels after SE induced by pilocarpine or kainate. This phenomenon is significantly associated with lesions involving more glial than neuronal cells, in specific cerebral regions.
authors.affiliation: Department of Biomedical Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Gualtieri
authors.forename: G
authors.initials: G
authors.lastname: Curia
authors.forename: C
authors.initials: C
authors.lastname: Marinelli
authors.forename: G
authors.initials: G
authors.lastname: Biagini
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology*; D001485:Basement Membrane / Q000378:metabolism / Q000473:pathology; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000378:metabolism / Q000473:pathology; D056654:CA3 Region, Hippocampal / Q000378:metabolism* / Q000473:pathology*; D003292:Convulsants / Q000633:toxicity; D007150:Immunohistochemistry; D007608:Kainic Acid / Q000633:toxicity; D007797:Laminin / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000473:pathology; D010862:Pilocarpine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*
chemical_list: D003292:Convulsants; D007797:Laminin; D010862:Pilocarpine; D007608:Kainic Acid