Chemical induction of mGluR5-and protein synthesis-dependent long-term depression in hippocampal area CA1
Chemical induction of mGluR5-and protein synthesis-dependent long-term depression in hippocampal area CA1
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DOI：
10.1152/jn.2001.86.1.321
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发表时间：
2001-07-01
影响因子：
2.5
通讯作者：
Bear, MF
中科院分区：
文献类型：
--
作者：
Huber, KM;Roder, JC;Bear, MF
最近的研究表明，特定的突触刺激模式可以诱导CA 1区的长期抑制（LTD），这取决于代谢型谷氨酸受体（mGluRs）的激活和快速的蛋白质合成。在这里，我们表明，同样形式的突触修饰可以通过简单地应用选择性mGluR激动剂（RS）-3，5-二羟基苯甘氨酸（DHPG）诱导。DHPG-LTD 1）是突触可塑性的可饱和形式，2）需要mGluR 5，3）在机制上不同于N-甲基-D-天冬氨酸受体（NMDAR）依赖性LTD，以及4）与使用突触刺激诱发的蛋白质合成依赖性LTD共享共同的表达机制。DHPG-LTD应该是有用的mGluR 5和蛋白质合成依赖性突触修饰的生化分析。
Recent work has demonstrated that specific patterns of synaptic stimulation can induce long-term depression (LTD) in area CA1 that depends on activation of metabotropic glutamate receptors (mGluRs) and rapid protein synthesis. Here we show that the same form of synaptic modification can be induced by brief application of the selective mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG). DHPG-LTD 1) is a saturable form of synaptic plasticity, 2) requires mGluR5, 3) is mechanistically distinct from N-methyl-D-aspartate receptor (NMDAR)-dependent LTD, and 4) shares a common expression mechanism with protein synthesis-dependent LTD evoked using synaptic stimulation. DHPG-LTD should be useful for biochemical analysis of mGluR5- and protein synthesis-dependent synaptic modification.