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Glutamate Receptors: Not Just for Excitation

机译：谷氨酸受体：不仅仅是为了激励

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摘要

In this issue of Neuron, Fossati et al. (2019) report a new constellation of players regulating inhibitory synapto-genesis. They show that GluD1, through a non-canonical ionotropic-independent mechanism, controls GABAergic synapse formation via trans-synaptic interactions mediated by extracellular cerebellin-4. They identify ARHGEF12 and PPP1R12A as GluD1 intracellular interactors and downstream effectors. While there is a wealth of information regarding the proteomic architecture of excitatory synapses and initiators of excitatory synaptogenesis (Scannevin and Huganir, 2000; Brose 2009), equivalent understanding of inhibitory synapses lags far behind. The postsynaptic scaffold of inhibitory synapses, gephyrin, is known to cluster GABA receptors, interact with the actin cytoskeleton and frans-synaptic adhesion molecules, and be targeted by intracellular signaling cascades (Tyagara-jan and Fritschy, 2014). Yet, we know little regarding the mechanisms of inhibitory synapse formation and the molecules involved. In this issue of Neuron, Fossati and colleagues identify an unexpected regulator of inhibitory synaptogenesis and use it as an entry point to a mechanistic reveal and a treasure trove of interacting extracellular and intracellular molecular players that regulate inhibitory synapse formation (Fossati et al., 2019).
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  • 来源
    《Neuron》 |2019年第6期|共3页
  • 作者

    Katherine L. Villa; Elly Nedivi;

  • 作者单位

    Picower Institute for Learning and Memory Departments of Biology and Brain and Cognitive Sciences;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经病学;
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