S. Dabhi, K. Duberly, J. Alnasir, N. Wijesiriwardana, B. Austen
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引用次数: 0
Abstract
Excitatory glutamatergic neurotransmission via N-methyl-D-aspartate receptor (NMDAR) is critical for synaptic plasticity and survival of neurons. Excessive NMDAR activity, however can cause excitotoxicity and promote cell death, underlying a potential mechanism of neurodegeneration occurring in Alzheimer’s disease (AD). The regulation of calcium levels at synapses is important for pre- and post-synaptic activation in the hippocampus, where glutamate is the primary neurotransmitter, acting via metabotropic and ionotropic receptors.
n -甲基- d -天冬氨酸受体(NMDAR)介导的兴奋性谷氨酸能神经传递对神经元突触可塑性和存活至关重要。然而,过度的NMDAR活性可引起兴奋性毒性并促进细胞死亡,这是阿尔茨海默病(AD)发生神经变性的潜在机制。突触钙水平的调节对于海马突触前和突触后的激活是重要的,在海马中,谷氨酸是主要的神经递质,通过代谢和嗜离子受体起作用。