Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies

被引:103
作者
Carvajal, Francisco J. [1 ]
Mattison, Hayley A. [2 ]
Cerpa, Waldo [1 ]
机构
[1] Pontificia Univ Catolica Chile, Fac Ciencias Biol, Dept Biol Celular & Mol, Lab Func & Patol Neuronal, Santiago 8331150, Chile
[2] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
关键词
TRAUMATIC BRAIN-INJURY; D-ASPARTATE RECEPTORS; PROTEIN-KINASE-II; MAJOR DEPRESSIVE DISORDER; MOTOR-NEURON DEGENERATION; EXCITATORY AMINO-ACIDS; HEAD-INJURY; HUNTINGTONS-DISEASE; SYNAPTIC PLASTICITY; SUBUNIT COMPOSITION;
D O I
10.1155/2016/2701526
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
N-Methyl-D-aspartate receptors (NMDARs) have two opposing roles in the brain. On the one hand, NMDARs control critical events in the formation and development of synaptic organization and synaptic plasticity. On the other hand, the overactivation of NMDARs can promote neuronal death in neuropathological conditions. Ca2+ influx acts as a primary modulator after NMDAR channel activation. An imbalance in Ca2+ homeostasis is associated with several neurological diseases including schizophrenia, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These chronic conditions have a lengthy progression depending on internal and external factors. External factors such as acute episodes of brain damage are associated with an earlier onset of several of these chronic mental conditions. Here, we will review some of the current evidence of how traumatic brain injury can hasten the onset of several neurological conditions, focusing on the role of NMDAR distribution and the functional consequences in calcium homeostasis associated with synaptic dysfunction and neuronal death present in this group of chronic diseases.
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页数:20
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