Transsynaptic N-Cadherin Adhesion Complexes Control Presynaptic Vesicle and Bulk Endocytosis at Physiological Temperature

At mammalian glutamatergic synapses, most basic elements of synaptic transmission have been shown to be modulated by specific transsynaptic adhesion complexes. However, although crucial for synapse homeostasis, a physiological regulation of synaptic vesicle endocytosis by adhesion molecules has not...

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Bibliographic Details
Published in:Frontiers in cellular neuroscience 2021-10, Vol.15, p.713693-713693
Main Authors: Dagar, Sushma, Teng, Zenghui, Gottmann, Kurt
Format: Article
Language:English
Subjects:
Actin
actin filaments
bulk endocytosis
Cadherins
Cellular Neuroscience
Endocytosis
Filaments
Glutamatergic transmission
Homeostasis
Microscopy
Morphology
N-Cadherin
peri-active zone
physiological temperature
Physiology
Plasmids
Synaptic transmission
synaptic vesicle endocytosis
Synaptophysin
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Summary:At mammalian glutamatergic synapses, most basic elements of synaptic transmission have been shown to be modulated by specific transsynaptic adhesion complexes. However, although crucial for synapse homeostasis, a physiological regulation of synaptic vesicle endocytosis by adhesion molecules has not been firmly established. The homophilic adhesion protein N-cadherin is localized at the peri-active zone, where the highly temperature-dependent endocytosis of vesicles occurs. Here, we demonstrate an important modulatory role of N-cadherin in endocytosis at near physiological temperature by synaptophysin-pHluorin imaging. Different modes of endocytosis including bulk endocytosis were dependent on N-cadherin expression and function. N-cadherin modulation might be mediated by actin filaments because actin polymerization ameliorated the knockout-induced endocytosis defect. Using super-resolution imaging, we found strong recruitment of N-cadherin to glutamatergic synapses upon massive vesicle release, which might in turn enhance vesicle endocytosis. This provides a novel, adhesion protein-mediated mechanism for efficient coupling of exo- and endocytosis.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2021.713693