期刊
NEURON
卷 75, 期 3, 页码 451-466出版社
CELL PRESS
DOI: 10.1016/j.neuron.2012.06.017
关键词
-
资金
- MRC [G0700188]
- BBSRC Industrial CASE [BB/H016600/1]
- UCL Neuroscience BSc program
- Fondation pour la Recherche Medicale [SPE20100518403]
- Royal Society Industry [IF080019/AM]
- UCL Impact Studentship
- UCL Neuroscience MSc program
- Fundacao para a Ciencia e a Tecnologia
- Fundacao para a Ciencia e a Tecnologia and the EPSRC
- Royal Society Research Grant [2008/R1]
- University of London Central Research Fund
- EU [243914]
- CFI Leaders Opportunity Fund [28331]
- McGill University Health Centre
- Medical Research Council [G0700188] Funding Source: researchfish
- Royal Society [IF080019] Funding Source: Royal Society
- BBSRC [BB/H016600/1] Funding Source: UKRI
- MRC [G0700188] Funding Source: UKRI
Traditionally, NMDA receptors are located postsynaptically; yet, putatively presynaptic NMDA receptors (preNMDARs) have been reported. Although implicated in controlling synaptic plasticity, their function is not well understood and their expression patterns are debated. We demonstrate that, in layer 5 of developing mouse visual cortex, preNMDARs specifically control synaptic transmission at pyramidal cell inputs to other pyramidal cells and to Martinotti cells, while leaving those to basket cells unaffected. We also reveal a type of interneuron that mediates ascending inhibition. In agreement with synapse-specific expression, we find preNMDAR-mediated calcium signals in a subset of pyramidal cell terminals. A tuned network model predicts that preNMDARs specifically reroute information flow in local circuits during high-frequency firing, in particular by impacting frequency-dependent disynaptic inhibition mediated by Martinotti cells, a finding that we experimentally verify. We conclude that postsynaptic cell type determines presynaptic terminal molecular identity and that preNMDARs govern information processing in neocortical columns.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据