The Regulation Of PTEN On Neuron NMDA Receptor And Relative Molecular Mechanisms

Cerebrovascular disease, with both high morbidity and mortality, is a serious hazard to human health and ranks as the third disease leading to death. The pathogenesis mechanisms about cerebrovascular disease, cerebral anoxia injury and secondary brain damage are unclear at present. Recent studies suggest that some channel blocking drugs and inhibitors in cerebral ischemia give good therapy results, but usually accompanying side effects in different degrees . Thus, to explore special drugs blocking ion channel is of necessity. The excitatory toxicity of glutamic acid is one of the important reasons of secondary injury after cerebral trauma or ischemic injury, in which the Ca2+ intracellular overload is the main pathogenesis.The N-methyl-D-aspartate receptor (NR), a subtype of ion-tropic glutamate receptor, provides sites for phosphorylation and for channel blocking. NRs are composed of NR1 and NR2A-D subunits. Activity of NMDA receptor after ischemic injury will mediate Ca2+ inward influx and Ca2+ overload, which leads to neuronal injury and apoptosis and induce pathological changes. NR2B, which is the primary modulating subunits of NMDARs, distributes extensively. NR2B subunit plays a crucial role in excitatory synaptic transmission and neuronal excitotoxicity of the CNS, especially synaptic plasticity, long-term potentiation (LTP) as well as learning and memory ability. Tyrosine phosphorylation of NR2B plays an important role in Ca2+ inward influx, which leads to neuronal injury.