TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis

Transient receptor potential melastatin 7 (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 physiolog...

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Autores principales: Zhong-Jiao Jiang, Wenping Li, Li-Hua Yao, Badeia Saed, Yan Rao, Brian S Grewe, Andrea McGinley, Kelly Varga, Simon Alford, Ying S Hu, Liang-Wei Gong
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Publicado: eLife Sciences Publications Ltd 2021
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Acceso en línea:https://doaj.org/article/06beb57d36444a1a84531c47103de50b
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spelling oai:doaj.org-article:06beb57d36444a1a84531c47103de50b2021-11-15T06:05:31ZTRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis10.7554/eLife.667092050-084Xe66709https://doaj.org/article/06beb57d36444a1a84531c47103de50b2021-09-01T00:00:00Zhttps://elifesciences.org/articles/66709https://doaj.org/toc/2050-084XTransient receptor potential melastatin 7 (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 central nervous system (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 transmissions 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.Zhong-Jiao JiangWenping LiLi-Hua YaoBadeia SaedYan RaoBrian S GreweAndrea McGinleyKelly VargaSimon AlfordYing S HuLiang-Wei GongeLife Sciences Publications Ltdarticlesynaptic vesicle endocytosisshort-term synaptic depressioncell-attached capacitance recordingsSyGCaMP6fiGluSnFRpHluorinMedicineRScienceQBiology (General)QH301-705.5ENeLife, Vol 10 (2021)
institution DOAJ
collection DOAJ
language EN
topic synaptic vesicle endocytosis
short-term synaptic depression
cell-attached capacitance recordings
SyGCaMP6f
iGluSnFR
pHluorin
Medicine
R
Science
Q
Biology (General)
QH301-705.5
spellingShingle synaptic vesicle endocytosis
short-term synaptic depression
cell-attached capacitance recordings
SyGCaMP6f
iGluSnFR
pHluorin
Medicine
R
Science
Q
Biology (General)
QH301-705.5
Zhong-Jiao Jiang
Wenping Li
Li-Hua Yao
Badeia Saed
Yan Rao
Brian S Grewe
Andrea McGinley
Kelly Varga
Simon Alford
Ying S Hu
Liang-Wei Gong
TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
description Transient receptor potential melastatin 7 (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 central nervous system (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 transmissions 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.
format article
author Zhong-Jiao Jiang
Wenping Li
Li-Hua Yao
Badeia Saed
Yan Rao
Brian S Grewe
Andrea McGinley
Kelly Varga
Simon Alford
Ying S Hu
Liang-Wei Gong
author_facet Zhong-Jiao Jiang
Wenping Li
Li-Hua Yao
Badeia Saed
Yan Rao
Brian S Grewe
Andrea McGinley
Kelly Varga
Simon Alford
Ying S Hu
Liang-Wei Gong
author_sort Zhong-Jiao Jiang
title TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
title_short TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
title_full TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
title_fullStr TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
title_full_unstemmed TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
title_sort trpm7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis
publisher eLife Sciences Publications Ltd
publishDate 2021
url https://doaj.org/article/06beb57d36444a1a84531c47103de50b
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