Neuroprotective Actions of Excitatory Amino Acid Receptor Antagonists
作者： V.L. Woodburn , G.N. Woodruff
DOI: 10.1016/S1054-3589(08)60170-2
关键词: Calcium in biology 、 Receptor 、 Postsynaptic potential 、 Neuroscience 、 Biology 、 Pharmacology 、 Amino acid 、 Glutamate receptor 、 Neuroprotection 、 Calcium metabolism 、 Excitatory postsynaptic potential
摘要: Publisher Summary Postischemic neuronal degeneration is caused in part by overactivity of excitatory amino acid (EAA) neurotransmitter systems. Increases extracellular glutamate levels result receptor-mediated increases postsynaptic intracellular calcium levels. This disturbed homeostasis leads to a cascade events including generation free radicals, activation NO synthase, and eventual cell death. Interruption at any stage this affords some degree neuroprotection. Agents are now available that act presynaptically inhibit release. EAA antagonists block the effects postsynaptically radical scavengers, other drugs may contribute survival preserving integrity. Neuroprotective mechanisms within appear be triggered upset homeostasis. A greater understanding these lead pharmacological agents provide protection brain areas vulnerable ischemia.
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