Alteration in NMDA Receptor Mediated Glutamatergic Neurotransmission in the Hippocampus During Senescence

被引:54
作者
Kumar, Ashok [1 ]
Foster, Thomas C. [1 ,2 ]
机构
[1] Univ Florida, Dept Neurosci, McKnight Brain Inst, POB 100244, Gainesville, FL 32610 USA
[2] Univ Florida, Genet & Genom Program, Gainesville, FL 32611 USA
关键词
Aging; Calcium homeostasis; Hippocampus; Glutamatergic neurotransmission; N-Methyl-d-aspartate receptor; Synaptic function; LTP; LTD; LONG-TERM POTENTIATION; CA1 PYRAMIDAL NEURONS; D-ASPARTATE RECEPTORS; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; SYNAPTIC PLASTICITY DEFICITS; MESSENGER-RNA EXPRESSION; NEUROMODULATOR D-SERINE; AGE-RELATED DEFICITS; PROTEIN-KINASE; RYANODINE RECEPTOR;
D O I
10.1007/s11064-018-2634-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Glutamate is the primary excitatory neurotransmitter in neurons and glia. N-methyl-d-aspartate (NMDA), -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainate receptors are major ionotropic glutamate receptors. Glutamatergic neurotransmission is strongly linked with Ca2+ homeostasis. Research has provided ample evidence that brain aging is associated with altered glutamatergic neurotransmission and Ca2+ dysregulation. Much of the work has focused on the hippocampus, a brain region critically involved in learning and memory, which is particularly susceptible to dysfunction during senescence. The current review examines Ca2+ regulation with a focus on the NMDA receptors in the hippocampus. Integrating the knowledge of the complexity of age-related alterations in Ca2+ homeostasis and NMDA receptor-mediated glutamatergic neurotransmission will positively shape the development of highly effective therapeutics to treat brain disorders including cognitive impairment.
引用
收藏
页码:38 / 48
页数:11
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