Status epilepticus (SE) induced by pilocarpine or kainate is associated with yet notsystemically investigated astrocytic and vascular injuries. To investigate their possibleassociation with neuronal damage, the changes in glial fibrillary acidic protein (GFAP),laminin and neuron-specific nuclear protein (NeuN) immunoreactivities were analyzed in ratstreated 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) inthe caudate putamen to reproduce the changes in GFAP and laminin immunoreactivitiesassociated with ischemia. Focal loss of GFAP immunostaining was accompanied byincreased laminin immunoreactivity in blood vessels, in all the examined groups. Regressionanalysis revealed a significant (P < 0.01) relationship between astrocytic lesion andincreased laminin immunoreactivity in the piriform cortex (Pir) of both pilocarpine (R2 = 0.88)and kainate (R2 = 0.94) groups of treatment. A significant relationship (P < 0.01; R2 = 0.81)was also present in the CA3 hippocampal region of pilocarpine-treated rats. At variance,neuronal and glial lesions were significantly related (P < 0.05, R2 = 0.74) only in thesubstantia nigra of pilocarpine-treated rats. The ratio between areas of GFAP and lamininchanges of immunoreactivity in the ET-1 group was similar to those found in pilocarpineandkainate-treated rats in specific brain regions, such as the hippocampal CA3 subfield, Pirand the anterior olfactory nucleus. The amygdala and submedius thalamic nucleus in thepilocarpine group, and the perirhinal and entorhinal cortices in the kainate group, alsopresented ischemic-like changes. These results indicate that laminin immunoreactivity isupregulated 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 neuronalcells, in specific cerebral regions.
Increased perivascular laminin predicts damage to astrocytes in CA3 and piriform cortex following chemoconvulsive treatments / Gualtieri, Fabio; Curia, Giulia; C., Marinelli; Biagini, Giuseppe. - In: NEUROSCIENCE. - ISSN 0306-4522. - STAMPA. - 218(2012), pp. 278-294.
|Data di pubblicazione:||2012|
|Titolo:||Increased perivascular laminin predicts damage to astrocytes in CA3 and piriform cortex following chemoconvulsive treatments.|
|Autore/i:||Gualtieri, Fabio; Curia, Giulia; C., Marinelli; Biagini, Giuseppe|
|Digital Object Identifier (DOI):||http://dx.doi.org/10.1016/j.neuroscience.2012.05.018|
|Codice identificativo ISI:||WOS:000312612900027|
|Codice identificativo Scopus:||2-s2.0-84863775797|
|Codice identificativo Pubmed:||22609936|
|Citazione:||Increased perivascular laminin predicts damage to astrocytes in CA3 and piriform cortex following chemoconvulsive treatments / Gualtieri, Fabio; Curia, Giulia; C., Marinelli; Biagini, Giuseppe. - In: NEUROSCIENCE. - ISSN 0306-4522. - STAMPA. - 218(2012), pp. 278-294.|
|Tipologia||Articolo su rivista|
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