脑源性神经营养因子通过增加N-甲基-D-天冬氨酸受体活性来调节海马突触传递。
Brain-derived neurotrophic factor modulates hippocampal synaptic transmission by increasing N-methyl-D-aspartic acid receptor activity.
作者信息
Levine E S, Crozier R A, Black I B, Plummer M R
机构信息
Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School/University of Medicine and Dentistry of New Jersey, 675 Hoes Lane, Piscataway, NJ 08854, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10235-9. doi: 10.1073/pnas.95.17.10235.
Abstract
Neurotrophins (NTs) have recently been found to regulate synaptic transmission in the hippocampus. Whole-cell and single-channel recordings from cultured hippocampal neurons revealed a mechanism responsible for enhanced synaptic strength. Specifically, brain-derived neurotrophic factor augmented glutamate-evoked, but not acetylcholine-evoked, currents 3-fold and increased N-methyl-D-aspartic acid (NMDA) receptor open probability. Activation of trkB NT receptors was critical, as glutamate currents were not affected by nerve growth factor or NT-3, and increased open probability was prevented by the tyrosine kinase inhibitor K-252a. In addition, the NMDA receptor antagonist MK-801 blocked brain-derived neurotrophic factor enhancement of synaptic transmission, further suggesting that NTs modulate synaptic efficacy via changes in NMDA receptor function.
摘要
神经营养因子（NTs）最近被发现可调节海马体中的突触传递。对培养的海马神经元进行的全细胞和单通道记录揭示了一种增强突触强度的机制。具体而言，脑源性神经营养因子使谷氨酸诱发的电流（而非乙酰胆碱诱发的电流）增强了3倍，并增加了N-甲基-D-天冬氨酸（NMDA）受体的开放概率。trkB NT受体的激活至关重要，因为谷氨酸电流不受神经生长因子或NT-3的影响，且酪氨酸激酶抑制剂K-252a可阻止开放概率的增加。此外，NMDA受体拮抗剂MK-801可阻断脑源性神经营养因子对突触传递的增强作用，进一步表明NTs通过改变NMDA受体功能来调节突触效能。
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