期刊
NATURE COMMUNICATIONS
卷 5, 期 -, 页码 -出版社
NATURE RESEARCH
DOI: 10.1038/ncomms5501
关键词
-
资金
- RIKEN BSI funds
- Strategic Research Program in RIKEN
- MEXT [21240031, 25110736]
- POSCO TJ PARK Foundation
- National Research Foundation [2011-0028337]
- Basic Science Research Program through National Foundation of Korea (NRF) - Ministry of Education, Science and Technology [NRF-2013R1A6A3A04061338]
- National Research Foundation of Korea [2011-0028337] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- Grants-in-Aid for Scientific Research [25640026, 25110736, 21240031, 24621012, 26430003, 23500461, 25670481] Funding Source: KAKEN
GABAergic interneurons are highly heterogeneous, and much is unknown about the specification and functional roles of their neural circuits. Here we show that a transinteraction of Elfn1 and mGluR7 controls targeted interneuron synapse development and that loss of Elfn1 results in hyperactivity and sensory-triggered epileptic seizures in mice. Elfn1 protein increases during postnatal development and localizes to postsynaptic sites of somatostatin-containing interneurons (SOM-INs) in the hippocampal CA1 stratum oriens and dentate gyrus (DG) hilus. Elfn1 knockout (KO) mice have deficits in mGluR7 recruitment to synaptic sites on SOM-INs, and presynaptic plasticity is impaired at these synapses. In patients with epilepsy and attention deficit hyperactivity disorder (ADHD), we find damaging missense mutations of ELFN1 that are clustered in the carboxy-terminal region required for mGluR7 recruitment. These results reveal a novel mechanism for interneuron subtype-specific neural circuit establishment and define a common basis bridging neurological disorders.
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