Abstract：
:Classically, neurexins are thought to mediate synaptic connections through trans interactions with a number of different postsynaptic partners. Neurexins are cleaved by metalloproteases in an activity-dependent manner, releasing the soluble extracellular domain. Here, we report that in both immature (before synaptogenesis) and mature (after synaptogenesis) hippocampal neurons, the soluble neurexin-1β ectodomain triggers acute Ca2+-influx at the dendritic/postsynaptic side. In both cases, neuroligin-1 expression was required. In immature neurons, calcium influx required N-type calcium channels and stimulated dendritic outgrowth and neuronal survival. In mature glutamatergic neurons the neurexin-1β ectodomain stimulated calcium influx through NMDA-receptors, which increased presynaptic release probability. In contrast, prolonged exposure to the ectodomain led to inhibition of synaptic transmission. This secondary inhibition was activity- and neuroligin-1 dependent and caused by a reduction in the readily-releasable pool of vesicles. A synthetic peptide modeled after the neurexin-1β:neuroligin-1 interaction site reproduced the cellular effects of the neurexin-1β ectodomain. Collectively, our findings demonstrate that the soluble neurexin ectodomain stimulates growth of neurons and exerts acute and chronic effects on trans-synaptic signaling involved in setting synaptic strength.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Wierda KDB,Toft-Bertelsen TL,Gøtzsche CR,Pedersen E,Korshunova I,Nielsen J,Bang ML,Kønig AB,Owczarek S,Gjørlund MD,Schupp M,Bock E,Sørensen JBdoi
10.1038/s41598-020-75047-zsubject
Has Abstractpub_date
2020-10-22 00:00:00pages
18041issue
1issn
2045-2322pii
10.1038/s41598-020-75047-zjournal_volume
10pub_type
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