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Neuroligins and neurexins link synaptic function to cognitive disease


The brain processes information by transmitting signals at synapses, which connect neurons into vast networks of communicating cells. In these networks, synapses not only transmit signals but also transform and refine them. Neurexins and neuroligins are synaptic cell-adhesion molecules that connect presynaptic and postsynaptic neurons at synapses, mediate signalling across the synapse, and shape the properties of neural networks by specifying synaptic functions. In humans, alterations in genes encoding neurexins or neuroligins have recently been implicated in autism and other cognitive diseases, linking synaptic cell adhesion to cognition and its disorders.

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Figure 1: Architecture of the trans-synaptic neurexin–neuroligin complex.
Figure 2: Atomic model of the trans-synaptic complex formed by NRXN1β and NLGN1.
Figure 3: Differential effects of deletion of the gene encoding NLGN1 and NLGN2 on inhibitory synapses in the somatosensory cortex.
Figure 4: The Arg451Cys substitution in NLGN3 impairs NLGN3 synthesis but enhances inhibitory synaptic transmission.


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I thank D. Arac, A. Brunger, X. Liu, J. Gibson and K. Huber for advice and help with figures. Work in my laboratory on NRXNs and NLGNs is supported by the National Institute of Mental Health and the Simon Foundation.

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Südhof, T. Neuroligins and neurexins link synaptic function to cognitive disease. Nature 455, 903–911 (2008).

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