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Updated 13 April 2011 E-mail discussion
Printable version

Live Discussion: Neurexin—From Basic Biology to Cognitive Diseases


Thomas Südhof

Steven Clapcote

On 23 March 2011, SRF held a live online discussion about neurexin with Thomas Südhof of Stanford University and Steven Clapcote of the University of Leeds.

From its humble beginnings as the identified target of a toxin in black widow venom, to its current status as suspected culprit in some cases of schizophrenia and autism, neurexin fascinates basic scientists and clinicians alike.

Anchored in the tip of an axon, neurexin binds to molecules on the receiving end of the synapse. This interaction across the synaptic cleft assembles the working parts of synapses and influences how they work. Because miniscule changes in synapse function can cascade into substantial changes in how signals are routed through the brain, mutations of neurexin and its associated molecules can aid us in understanding the basics of communication across the synapse, and what goes wrong in brain disorders like schizophrenia.

Using Clapcote's recent review article (Reichelt et al., 2011) as a starting point, Clapcote and Südhof guided a discussion of this multifaceted molecule that boasts thousands of isoforms and multiple binding partners. How might neurexin participate in specifying the different synapse types in the brain, and how might it shape our understanding of brain disorders like autism and schizophrenia as "synaptopathies" stemming from dysfunctional synapses?

Suggested Reading: Reichelt AC, Rodgers RJ, Clapcote SJ. The role of neurexins in schizophrenia and autistic spectrum disorder. Neuropharmacology. 2011 Jan 22. Abstract

View Transcript of Live Discussion — Posted 13 April 2011

View Comments By:
Tristram Lett, James L. Kennedy — Posted 22 March 2011



Comments on Online Discussion
Comment by:  Tristram LettJames L. Kennedy (SRF Advisor) (Disclosure)
Submitted 22 March 2011 Posted 22 March 2011

Accumulating evidence suggests that heterozygous deletions in the neurexin-1 (NRXN1) gene pose a significant risk to autism spectrum disorders and schizophrenia. In contrast, no common variant in NRXN1 has been associated with either disorder, suggesting that the risk created by these markers is limited. However, this does not exclude the possibility that common variants could be important in alternate phenotypes. For instance, a genetic change that does not result in truncated or dysfunctional protein, but likely in aberrant gene regulation at critical times of development, may have greater relevance in a more homogeneous subgroup of schizophrenia patients.

Recent evidence suggests that NRXN1 modulates post-synaptic differentiation of glutamatergic synapses potentially through neuroligin or leucine-rich repeat transmembrane proteins. Considering some antipsychotic medications’ potential action on glutamate regulation, dysregulation of NRXN1 by common variants (or haplotypes) could potentially alter antipsychotic efficacy. We have found that common alleles in NRXN1 are...  Read more


View all comments by Tristram Lett
View all comments by James L. Kennedy
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