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海马 CA1 锥体神经元的突触外 NMDA 受体依赖性长时程增强。

Extrasynaptic NMDA receptor dependent long-term potentiation of hippocampal CA1 pyramidal neurons.

机构信息

Key laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Key Laboratory of Psychotic Disorders, Institute of Social Cognitive and Behavioral Sciences, and Brain Science and Technology Research Center, Shanghai Jiao Tong University, Shanghai, China.

Department of Neurobiology, Key Laboratory of Medical, Neurobiology (Ministry of Health of China), Collaborative Innovation Center for Brain Science, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310058, China.

出版信息

Sci Rep. 2017 Jun 8;7(1):3045. doi: 10.1038/s41598-017-03287-7.

DOI:10.1038/s41598-017-03287-7
PMID:28596523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5465207/
Abstract

In the adult mouse hippocampus, NMDA receptors (NMDARs) of CA1 neurons play an important role in the synaptic plasticity. The location of NMDARs can determine their roles in the induction of long-term potentiation (LTP). However, the extrasynaptic NMDARs (ES-NMDARs) dependent LTP haven't been reported. Here, through the use of a 5-Hz stimulation and MK-801 (an irreversible antagonist of NMDARs) in the CA1 neurons of adult mice hippocampal slices, synaptic NMDARs were selectively inhibited and NMDAR-mediated excitatory postsynaptic currents were not recovered. We found that a robust LTP was induced by 3-train 100-Hz stimulation when the synaptic NMDARs and extrasynaptic NR2B containing NMDARs were blocked, but not in the any of the following conditions: blocking of all NMDARs (synaptic and extrasynaptic), blocking of the synaptic NMDARs, and blocking of the synaptic NMDARs and extrasynaptic NR2A-containing NMDARs. The results indicate that this LTP is ES-NMDARs dependent, and NR2B-containing ES-NMDARs modulates the threshold of LTP induction.

摘要

在成年小鼠海马体中，CA1 神经元的 NMDA 受体（NMDARs）在突触可塑性中发挥重要作用。NMDAR 的位置可以决定它们在长时程增强（LTP）诱导中的作用。然而，尚未报道依赖于突触外 NMDA 受体（ES-NMDARs）的 LTP。在这里，通过在成年小鼠海马脑片 CA1 神经元中使用 5-Hz 刺激和 MK-801（NMDARs 的不可逆拮抗剂），选择性抑制突触 NMDARs，并且 NMDAR 介导的兴奋性突触后电流未恢复。我们发现，当阻断突触 NMDAR 和包含 NR2B 的突触外 NMDAR 时，通过 3 次 100-Hz 刺激可以诱导强烈的 LTP，但在以下任何一种情况下均不会诱导：阻断所有 NMDAR（突触内和突触外）、阻断突触 NMDARs 和阻断突触 NMDARs 和包含 NR2A 的突触外 NMDARs。结果表明，这种 LTP 依赖于 ES-NMDARs，并且包含 NR2B 的 ES-NMDARs 调节 LTP 诱导的阈值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/4189b816386a/41598_2017_3287_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/1dc84070aa71/41598_2017_3287_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/986e8c40dbd1/41598_2017_3287_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/e3a9583198b9/41598_2017_3287_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/49bc25207b88/41598_2017_3287_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/17a4b7505b99/41598_2017_3287_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/4189b816386a/41598_2017_3287_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/1dc84070aa71/41598_2017_3287_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/986e8c40dbd1/41598_2017_3287_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/e3a9583198b9/41598_2017_3287_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/49bc25207b88/41598_2017_3287_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/17a4b7505b99/41598_2017_3287_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d829/5465207/4189b816386a/41598_2017_3287_Fig6_HTML.jpg

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