Figure 15.

Molecular model of LAR-RPTP and Nrxn actions in shaping trans-synaptic signaling pathways. LAR-RPTPs directly interact with Nrxns and act as their coreceptors to mediate presynaptic differentiation (A). Notably, combinations of distinct molecular components in presynaptic neurons underlie different actions of PTPσ and PTPδ at excitatory and inhibitory synapses, respectively. α-Nrxns might negatively modulate the interaction affinity of PTPσ with its respective postsynaptic ligands (e.g., TrkC or Slitrk2) by increasing local HS concentrations to orchestrate postsynaptic assembly (B). Abl, Abelson tyrosine kinase; β-Cat, β-catenin; CASK, calcium/calmodulin-dependent serine protein kinase; CASKIN, CASK interacting protein; ELKS, glutamine, leucine, lysine, and serine-rich protein; Ena, enabled; MIM-B, missing-in-metastasis B; N-cad, N-cadherin; RIM1, Rab3-interacting molecule 1; RIM-BP, RIM-binding protein; Slitrk, Slit- and Trk-like protein; SYDE1, synapse-defective Rho GTPase homolog 1; TrkC, tropomyosin receptor kinase C.