The soluble neurexin-1β ectodomain causes calcium influx and augments dendritic outgrowth and synaptic transmission.

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 presyn

SUBMITTER: Wierda KDB 

PROVIDER: S-EPMC7582164 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature