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脑源性神经营养因子可通过N-甲基-D-天冬氨酸(NMDA)快速增强突触传递,但在大鼠海马神经元中,它通过非NMDA受体抑制突触传递。

Brain-derived neurotrophic factor rapidly potentiates synaptic transmission through NMDA, but suppresses it through non-NMDA receptors in rat hippocampal neuron.

作者信息

Song D K, Choe B, Bae J H, Park W K, Han I S, Ho W K, Earm Y E

机构信息

Department of Physiology and Institute for Medical Science, Keimyung University School of Medicine, 194, Dongsan-Dong, Choong-Ku, Taegu 700-712, South Korea.

出版信息

Brain Res. 1998 Jul 13;799(1):176-9. doi: 10.1016/s0006-8993(98)00474-0.

Abstract

Brain-derived neurotrophic factor (BDNF) rapidly enhances synaptic transmission among the hippocampal neurons. In order to examine which component of glutamate receptors participates in synaptic potentiation by BDNF, we have studied the effect of glutamate antagonists on excitatory postsynaptic currents (EPSCs) enhanced by BDNF, using cultured embryonic hippocampal neurons. In the presence of AP5, a N-methyl-D-aspartate (NMDA) antagonist, BDNF depressed the EPSCs. In contrast, BDNF enhanced the EPSCs in the presence of a non-NMDA antagonist CNQX. Our results suggest that BDNF acutely activates synaptic transmission via NMDA, but suppresses it via non-NMDA receptors in the hippocampus.

摘要

脑源性神经营养因子(BDNF)能迅速增强海马神经元之间的突触传递。为了研究谷氨酸受体的哪个成分参与BDNF介导的突触增强作用,我们利用培养的胚胎海马神经元,研究了谷氨酸拮抗剂对BDNF增强的兴奋性突触后电流(EPSCs)的影响。在N-甲基-D-天冬氨酸(NMDA)拮抗剂AP5存在的情况下,BDNF会抑制EPSCs。相反,在非NMDA拮抗剂CNQX存在的情况下,BDNF会增强EPSCs。我们的结果表明,BDNF在海马体中通过NMDA急性激活突触传递,但通过非NMDA受体抑制突触传递。

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