Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis

Voltage-gated sodium channel Nav1.5 contributes to astrogliosis in anin vitromodel of glial injury via reverse Na+/Ca2+exchange

(2014) Laura W. Pappalardo et al.   GLIA

Safinamide and flecainide protect axons and reduce microglial activation in models of multiple sclerosis

(2013) Damineh Morsali et al.   BRAIN

Traumatic scratch injury in astrocytes triggers calcium influx to activate the JNK/c-Jun/AP-1 pathway and switch on GFAP expression

(2013) Kai Gao et al.   GLIA

Astrocytes play a key role in EAE pathophysiology by orchestrating in the CNS the inflammatory response of resident and peripheral immune cells and by suppressing remyelination

(2013) Roberta Brambilla et al.   GLIA

Noncanonical Roles of Voltage-Gated Sodium Channels

(2013) Joel A. Black et al.   NEURON

Astrocytes within multiple sclerosis lesions upregulate sodium channel Nav1.5

(2010) J. A. Black et al.   BRAIN

Brain tissue sodium concentration in multiple sclerosis: a sodium imaging study at 3 tesla

(2010) M. Inglese et al.   BRAIN

Molecular dissection of reactive astrogliosis and glial scar formation

(2009) Michael V. Sofroniew   TRENDS IN NEUROSCIENCES