Physiologically relevant ethanol exposure alters NRXN expression in an isoform-, splice site-, and differentiation-dependent manner, prominently affecting NRXN3 and the SS4 site. These coordinated transcriptional and proteomic changes suggest that ethanol perturbs NRXN3β-NLGN2 interactions and inhibitory synapse stability, revealing a molecular pathway where alcohol may compromise cortical network excitatory-inhibitory balance.
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Lowe et al. (Wed,) studied this question.
www.synapsesocial.com/papers/69df2c62e4eeef8a2a6b16a5 — DOI: https://doi.org/10.1111/acer.70289
Clara C. Lowe
Kip D. Zimmerman
Rita Cervera‐Juanes
Alcohol Clinical and Experimental Research
Wake Forest University
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