TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
- University of Illinois at Chicago, United States
Abstract
TRPM7 contributes to a variety of physiological and pathological processes in many tissues and cells. With a widespread distribution in the nervous system, TRPM7 is involved in animal behaviors and neuronal death induced by ischemia. However, the physiological role of TRPM7 in CNS neuron remains unclear. Here, we identify endocytic defects in neuroendocrine cells and neurons from TRPM7 knockout (KO) mice, indicating a role of TRPM7 in synaptic vesicle endocytosis. Our experiments further pinpoint the importance of TRPM7 as an ion channel in synaptic vesicle endocytosis. Ca2+ imaging detects a defect in presynaptic Ca2+ dynamics in TRPM7 KO neuron, suggesting an importance of Ca2+ influx via TRPM7 in synaptic vesicle endocytosis. Moreover, the short-term depression is enhanced in both excitatory and inhibitory synaptic transmission from TRPM7 KO mice. Taken together, our data suggests that Ca2+ influx via TRPM7 may be critical for short-term plasticity of synaptic strength by regulating synaptic vesicle endocytosis in neurons.
Data availability
All data generated or analyzed during this study are included in the manuscript and supporting files.
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Funding
NIH Office of the Director (R01NS110533)
- Liang-Wei Gong
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: All animal experimental studies were approved by the Animal Care and Use Committee of the University of Illinois at Chicago and conformed to the guidelines of the National Institutes of Health.(animal protocol number 19-189).
Copyright
© 2021, Jiang et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
eLife 10:e66709.
https://doi.org/10.7554/eLife.66709
