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Journal Article
Cell, ISSN 0092-8674, 2004, Volume 118, Issue 6, pp. 687 - 698
Ca toxicity remains the central focus of ischemic brain injury. The mechanism by which toxic Ca loading of cells occurs in the ischemic brain has become less... 
GATED CATION CHANNELS | GLUTAMATE NEUROTOXICITY | NA+ CHANNEL | NEURONAL DEATH | BIOCHEMISTRY & MOLECULAR BIOLOGY | D-ASPARTATE RECEPTORS | NMDA RECEPTOR ACTIVATION | CENTRAL-NERVOUS-SYSTEM | CEREBRAL-ISCHEMIA | SENSORY NEURONS | EXTRACELLULAR ACIDITY | CELL BIOLOGY | Receptors, Glutamate - metabolism | Calcium - metabolism | Brain Ischemia - metabolism | Male | Acidosis - metabolism | Receptors, Glutamate - drug effects | Calcium - toxicity | Nerve Degeneration - metabolism | Acidosis - complications | Neuroprotective Agents - pharmacology | Drug Design | Sodium Channels - metabolism | Membrane Proteins - metabolism | Disease Models, Animal | Nerve Tissue Proteins - antagonists & inhibitors | Acid Sensing Ion Channels | Acidosis - drug therapy | Membrane Proteins - genetics | Mice, Inbred C57BL | Cells, Cultured | Rats | Sodium Channel Blockers - pharmacology | Excitatory Amino Acid Antagonists - pharmacology | Calcium Channel Blockers - pharmacology | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Animals | Membrane Proteins - antagonists & inhibitors | Calcium Signaling - drug effects | Brain Ischemia - drug therapy | Glutamic Acid - metabolism | Mice | Sodium Channels - genetics | Calcium Signaling - genetics | Glutamic Acid - toxicity | Nerve Degeneration - etiology | COS Cells | Nerve Degeneration - drug therapy | Calcium compounds | Research | Ischemia | Acidosis
Journal Article