期刊
JOURNAL OF NEUROSCIENCE
卷 33, 期 22, 页码 9536-+出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0034-13.2013
关键词
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资金
- BBSRC
- Wellcome Trust
- MRC
- BBSRC/Eli Lilly
- Biotechnology and Biological Sciences Research Council [1133150] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [1280505] Funding Source: researchfish
- Medical Research Council [984420] Funding Source: researchfish
Kainate receptors (KARs) are ionotropic glutamate receptors that also activate noncanonical G-protein-coupled signaling pathways to depress the slow afterhyperpolarization (sAHP). Here we show that long-term depression of KAR-mediated synaptic transmission (KAR LTD) at rat hippocampal mossy fiber synapses relieves inhibition of the sAHP by synaptic transmission. KAR LTD is induced by high-frequency mossy fiber stimulation and natural spike patterns and requires activation of adenosine A(2A) receptors. Natural spike patterns also cause long-term potentiation of NMDA receptor-mediated synaptic transmission that overrides the effects of KAR LTD on the cellular response to low-frequency synaptic input. However, KAR LTD is dominant at higher frequency synaptic stimulation where it decreases the cellular response by relieving inhibition of the sAHP. Thus we describe a form of glutamate receptor plasticity induced by natural spike patterns whose primary physiological function is to regulate cellular excitability.
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