| First Author | Pereira de Vasconcelos A | Year | 2006 |
| Journal | Neurobiol Dis | Volume | 23 |
| Issue | 1 | Pages | 219-27 |
| PubMed ID | 16690320 | Mgi Jnum | J:111221 |
| Mgi Id | MGI:3653304 | Doi | 10.1016/j.nbd.2006.03.002 |
| Citation | Pereira de Vasconcelos A, et al. (2006) Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: a genetic approach using knockout mice. Neurobiol Dis 23(1):219-27 |
| abstractText | The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS-/-) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, quantitative [14C]iodoantipyrine method) was measured 3-6 h after unilateral kainate (KA) injection in the dorsal hippocampus; controls received saline. In WT mice, KA seizures induced a 22 to 50% LCBF increase restricted to the ipsilateral hippocampus, while significant LCBF decreases (15-33%) were noticed in 22% of the contralateral areas, i.e., the parietal cortex, amygdala and three basal ganglia areas, compared to saline-injected WT mice. In eNOS-/- mice, no LCBF increases were recorded within the epileptic focus and generalized contralateral LCBF decreases (22-46%) were noticed in 2/3 of the brain areas, compared to saline-injected eNOS-/- mice. Thus, endothelial NO is the mediator of the cerebrovascular response within the epileptic focus and participates in the maintenance of LCBF in distant areas. |
