LRRTM2 interacts with Neurexin1 and regulates excitatory synapse formation. (2004), this study uncovers regulation of Neurexin synaptogenic activity by alternative splicing.ĭe Wit, J. Alternative splicing controls selective trans-synaptic interactions of the Neuroligin–Neurexin complex. Neurexins induce differentiation of GABA and glutamate postsynaptic specializations via neuroligins. EphB receptors interact with NMDA receptors and regulate excitatory synapse formation. Neuroligin expressed in nonneuronal cells triggers presynaptic development in contacting axons. Scheiffele, P., Fan, J., Choih, J., Fetter, R. Neurexin mediates the assembly of presynaptic terminals. Understanding axon guidance: are we nearly there yet? Development (2018).ĭean, C. Synaptic specificity, recognition molecules, and assembly of neural circuits. Synaptic Neurexin complexes: a molecular code for the logic of neural circuits. Beyond molecular codes: simple rules to wire complex brains. Assembly of excitatory synapses in the absence of glutamatergic neurotransmission. Formation and maintenance of functional spines in the absence of presynaptic glutamate release. The cell-autonomous role of excitatory synaptic transmission in the regulation of neuronal structure and function. Finally, we propose a conceptual framework for how combinations of synaptic protein isoforms act as ‘senders’ and ‘readers’ to instruct synapse formation and the acquisition of cell type-specific and synapse-specific functional properties. We then discuss the mechanisms and logic of the cell type-specific regulation of Neurexin isoforms, in particular at the level of alternative mRNA splicing. In this Review, we first summarize insights into Neurexin function obtained from various model organisms. Recent studies on the Neurexin protein family and its ligands provide fundamental insight into how synapses are assembled and remodelled, how synaptic properties are specified and how single gene mutations associated with neurodevelopmental and psychiatric disorders might modify the operation of neuronal circuits and behaviour. We propose that a substantial degree of synapse formation and function is instructed by molecular codes resulting from transcriptional programmes. The function of neuronal circuits relies on the properties of individual neuronal cells and their synapses.
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