Brain-derived neurotrophic factor modulates hippocampal synaptic transmission by increasing N-methyl-D-aspartic acid receptor activity
Brain-derived neurotrophic factor modulates hippocampal synaptic transmission by increasing N-methyl-D-aspartic acid receptor activity
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DOI：
10.1073/pnas.95.17.10235
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发表时间：
1998-08-18
影响因子：
11.1
通讯作者：
Plummer, MR
中科院分区：
文献类型：
--
作者：
Levine, ES;Crozier, RA;Plummer, MR
神经营养因子(NTS)最近被发现调节海马区的突触传递。培养的海马神经元的全细胞和单通道记录揭示了导致突触强度增强的机制。具体地说，脑源性神经营养因子使谷氨酸诱发的电流增加3倍，N-甲基-D-天冬氨酸(NMDA)受体开放概率增加，但不增加乙酰胆碱诱发的电流。TrkB NT受体的激活是关键，因为谷氨酸电流不受神经生长因子或NT-3的影响，增加的开放概率可被酪氨酸激酶抑制剂K-252a阻止。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，进一步提示NTS通过改变NMDA受体功能来调节突触效应。
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.