Transsynaptic Signaling of Ephs in Synaptic Development, Plasticity, and Disease

formation between neurons is critical for proper circuit and brain function. Prior to activity -dependent refinement of connections between neurons, activity-independent cues regulate the contact and recognition of potential synaptic partners. Formation of a synapse results in molecular recognition events that initiate the process of synaptogenesis. Synaptogenesis requires contact between axon and dendrite, selection of correct and rejection of incorrect partners, and recruitment of appropriate pre-and postsynaptic proteins needed for the establishment of functional synaptic contact. Key regulators of these events are families of transsynaptic proteins, where one protein is found on the presynaptic neuron and the other is found on the post -synaptic neuron. Of these families, the EphBs and ephrin-Bs are required during each phase of synaptic develop-ment from target selection, recruitment of synaptic proteins, and formation of spines to regulation of synaptic plasticity at glutamatergic spine synapses in the mature brain. These roles also place EphBs and ephrin-Bs as important regulators of human neurological diseases. This review will focus on the role of EphBs and ephrin-Bs at synapses.(c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

Automated summary

The formation between neurons is crucial for proper circuit and brain function. Prior to activity-dependent refinement, activity-independent cues regulate the recognition and contact of potential synaptic partners. The formation of a synapse initiates molecular recognition events and requires contact, selection, and recruitment of synaptic proteins for functional synaptic contact. Key regulators of synaptogenesis include the EphBs and ephrin-Bs, which play important roles in target selection, synaptic protein recruitment, spine formation, and synaptic plasticity. EphBs and ephrin-Bs are also implicated in human neurological diseases. This review focuses on their role at synapses.