AMPA receptor subunit GluR2 gates injurious signals in ischemic stroke
Abbreviated Journal Title
hippocampus; CA1 neurons; selective neuronal injury; AMPA receptors; Ca-21/Zn-21-permeable channels; Ca2+/Zn2+ signals; ischemic stroke; TRANSIENT FOREBRAIN ISCHEMIA; HIPPOCAMPAL PYRAMIDAL NEURONS; NITRIC-OXIDE SYNTHASE; D-ASPARTATE RECEPTORS; CELL-DEATH; CEREBRAL-ISCHEMIA; BRAIN-INJURY; AMPA/KAINATE CHANNELS; GLUTAMATE; RECEPTORS; MICE DEFICIENT; Neurosciences
Ischemic stroke, or a brain attack, is the third leading cause of death in developed countries. A critical feature of the disease is a highly selective pattern of neuronal loss; certain identifiable subsets of neurons-particularly CA1 pyramidal neurons in the hippocampus-are severely damaged, whereas others remain intact. A key step in this selective neuronal injury is Ca2+/Zn2+ entry into vulnerable neurons through alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor channels, a principle subtype of glutamate receptors. AMPA receptor channels are assembled from glutamate receptor (GluR)1, -2, -3, and -4 subunits. Circumstance data have indicated that the GluR2 subunits dictate Ca2+/Zn2+ permeability of AMPA receptor channels and gate injurious Ca2+/Zn2+ signals in vulnerable neurons. Therefore, targeting to the AMPA receptor subunit GluR2 can be considered a practical strategy for stroke therapy.
"AMPA receptor subunit GluR2 gates injurious signals in ischemic stroke" (2005). Faculty Bibliography 2000s. 5690.