The Molecular Mechanisms of Magnesium Neuroprotection in Patients with Eclampsia: A Short Review
Amir Mor *
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel. and Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, NY 11219, USA.
Itai Gat
Department of Obstetrics and Gynecology, Sheba Medical Center, Tel HaShomer, Ramat Gan, 52621, Israel.
Reshef Tal
Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, NY 11219, USA.
Mohamad Irani
Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, NY 11219, USA.
Jigal Haas
Department of Obstetrics and Gynecology, Sheba Medical Center, Tel HaShomer, Ramat Gan, 52621, Israel.
Rotem Inbar
Department of Obstetrics and Gynecology, Sheba Medical Center, Tel HaShomer, Ramat Gan, 52621, Israel.
Hava Golan
Department of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
*Author to whom correspondence should be addressed.
Abstract
Eclampsia has been studied extensively over the last decades. Several pathophysiological mechanisms and animal models have been proposed for the disease. However, to date, none of them can fully explain the neuronal pathophysiology of eclamptic convulsions and the associated deleterious complications. Magnesium is the drug of choice for the prophylaxis and treatment of eclampsia in addition to prompt delivery. There is evidence to suggest that the beneficial effect of magnesium is exerted via modulation of the N-Methyl-D-Aspartate Receptor (NMDAR). The aim of this review is to explore the molecular mechanism by which magnesium exerts its neuroprotective effect and prevents eclamptic convulsions through the NMDAR activation pathway. Future investigations and alternative treatments are discussed.
Keywords: NMDA receptor, convulsion, seizure, animal models