Neurexin-Neuroligin Disruption in Psychiatric Disease

Neurodevelopmental and psychiatric disorders repeatedly converge on synaptic dysfunction. But presynaptic and postsynaptic failures are not interchangeable. Here, we examine two studies that perturb opposite poles of the neurexin-neuroligin adhesion axis:

Postsynaptic Neuroligin 2 (NGLN2) C-terminal truncation reduced GABAergic synaptic density and inhibitory transmission, producing obsessive–compulsive disorder (OCD)-like and social deficits in mice.

Presynaptic Neurexin 1a (NRXN1a ) autoantibodies, detected in a subset of schizophrenia patients, disrupted NRXN1a-neuroligin binding, reduced excitatory transmission, and induced schizophrenia-like behaviors reversible upon antibody removal.

Together, these data revealed that synaptic polarity matters, and which side of the adhesion bridge fails determines which circuit shifts.

The studies also highlight how validated antibody markers—Anti-Neuroligin-2 (#ANR-036) and Anti-Neurexin-1α (#ANR-031)—can be used to probe synaptic architecture and link molecular disruptions to functional changes in neural circuits.

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Two Psychiatric Disorders, One Synaptic Bridge.

New studies show how opposite disruptions of the neurexin–neuroligin adhesion complex link inhibitory deficits to OCD and excitatory disruption to schizophrenia.

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