The interest of the laboratory is focused on stroke. Cerebral ischemia induces a significant early and sustained increase of the intracellular calcium concentration. It also has been observed that an increase of intracellular calcium lasting long enough could trigger delayed neuronal death. Preventing the intracellular calcium increase during an ischemic insult by reducing the extracellular calcium concentration prevents delayed neuronal death. The research in the laboratory is therefore focused on understanding the alteration of intracellular calcium signaling during an ischemic insult. The effort is currently concentrated on understanding the implication of a specific type of voltage-activated calcium channel present on the plasma membrane during ischemia. Neuronal ischemia is studied on three different models. Electrophysiology and calcium imaging is performed on dissociated neuronal cultures during ischemic insults. Pharamacology and neuroprotection studies are performed first in an in vitro model with organotypic hippocampal slice cultures and then in an in vivo model of global ischemia in rats.
Correction to: Ruptured PICA aneurysms: presentation and treatment outcomes compared to other posterior circulation aneurysms. A Swiss SOS study.
Common Data Elements for Subarachnoid Hemorrhage and Unruptured Intracranial Aneurysms: Recommendations from the Working Group on Subject Characteristics.
Ruptured PICA aneurysms: presentation and treatment outcomes compared to other posterior circulation aneurysms. A Swiss SOS study.
Disturbed flow induces a sustained, stochastic NF-κB activation which may support intracranial aneurysm growth in vivo.
Departement des neurosciences cliniques