期刊
PHARMACOLOGICAL REVIEWS
卷 61, 期 4, 页码 395-412出版社
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
DOI: 10.1124/pr.109.001735
关键词
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资金
- Medical Research Council UK [80049, 57294]
- Biological Sciences Research Council UK [BB/F011326/1]
- Medical Research Council
- BBSRC [BB/F011326/1] Funding Source: UKRI
- MRC [G0601509] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F011326/1] Funding Source: researchfish
- Medical Research Council [G0601509] Funding Source: researchfish
The ability to modify synaptic transmission between neurons is a fundamental process of the nervous system that is involved in development, learning, and disease. Thus, synaptic plasticity is the ability to bidirectionally modify transmission, where long-term potentiation and long-term depression (LTD) represent the best characterized forms of plasticity. In the hippocampus, two main forms of LTD coexist that are mediated by activation of either N-methyl-D-aspartic acid receptors (NMDARs) or metabotropic glutamate receptors (mGluRs). Compared with NMDAR-LTD, mGluR-LTD is less well understood, but recent advances have started to delineate the underlying mechanisms. mGluR-LTD at CA3:CA1 synapses in the hippocampus can be induced either by synaptic stimulation or by bath application of the group I selective agonist (R, S)-3,5-dihydroxyphenylglycine. Multiple signaling mechanisms have been implicated in mGluR-LTD, illustrating the complexity of this form of plasticity. This review provides an overview of recent studies investigating the molecular mechanisms underlying hippocampal mGluR-LTD. It highlights the role of key molecular components and signaling pathways that are involved in the induction and expression of mGluR-LTD and considers how the different signaling pathways may work together to elicit a persistent reduction in synaptic transmission.
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