4.8 Article

Distinct molecular pathways govern presynaptic homeostatic plasticity

期刊

CELL REPORTS
卷 37, 期 11, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.celrep.2021.110105

关键词

-

资金

  1. Forschungskredit grant of the University of Zurich [2018-06813]
  2. Swedish Research Council
  3. Swiss National Science Foundation Assistant Professor grant [PP00P3-15]
  4. European Research Council starting grant [679881]
  5. European Research Council (ERC) [679881] Funding Source: European Research Council (ERC)

向作者/读者索取更多资源

The study demonstrates that different receptor perturbations at the Drosophila neuromuscular junction result in different responses, with some receptor inhibitions not compensated by PHP while others induce compensatory PHP through distinct signaling pathways. This highlights the diversity of homeostatic signaling mechanisms, showing that synapses respond differentially to similar activity impairments and achieve homeostatic compensation via different pathways.
Presynaptic homeostatic plasticity (PHP) stabilizes synaptic transmission by counteracting impaired neurotransmitter receptor function through neurotransmitter release potentiation. PHP is thought to be triggered by impaired receptor function and to involve a stereotypic signaling pathway. However, here we demonstrate that different receptor perturbations that similarly reduce synaptic transmission result in different responses at the Drosophila neuromuscular junction. While receptor inhibition by the glutamate receptor (GluR) antagonist g-D-glutamylglycine (gDGG) is not compensated by PHP, the GluR inhibitors Philanthotoxin-433 (PhTx) and Gyki-53655 (Gyki) induce compensatory PHP. Intriguingly, PHP triggered by PhTx and Gyki involve separable signaling pathways, including inhibition of distinct GluR subtypes, differential modulation of the active zone scaffold Bruchpilot, and short-term plasticity. Moreover, while PHP upon Gyki treatment does not require genes promoting PhTx-induced PHP, it involves presynaptic protein kinase D. Thus, synapses not only respond differentially to similar activity impairments, but achieve homeostatic compensation via distinct mechanisms, highlighting the diversity of homeostatic signaling.

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。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据