ArticleAlcohol, clinical & experimental research2026
Ethanol Alters the Neurexin Landscape in Human Neuroblastoma Cells.
Article in Alcohol, clinical & experimental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNeurexins (NRXNs) are presynaptic adhesion molecules essential for synaptic organization and the regulation of excitatory-inhibitory balance. The molecular diversity of NRXNs arises from alternative promoters and splicing, particularly at splice site 4 (SS4), which dictates ligand binding. Dysregulation of NRXNs has been linked to substance use disorders, but it remains unclear how the expression of NRXN isoforms responds to physiologically relevant amounts of ethanol.
methodsHuman IMR-32 neuroblastoma cells were maintained in an undifferentiated (UnDiff) state or differentiated (Diff) with trans-retinoic acid (tRA) to promote an enrichment in parvalbumin (PV) expression. Cells were exposed to physiologically relevant ethanol concentrations (0, 7, or 35 mM) in vapor chambers. Quantitative polymerase chain reaction (qPCR) quantified mRNA levels of major NRXN transcripts (NRXN1, NRXN2, and NRXN3) and SS4 variants (+SS4, -SS4). Immunocytochemistry (ICC) was used to measure protein expression and overlap with neuroligin2 (NLGN2) and PV.
resultsDifferentiation increased basal expression of several NRXN transcripts, including NRXN2α, NRXN2 +SS4, NRXN3α, NRXN3β, and NRXN3 -SS4. In Diff cells, ethanol-induced dose-dependent downregulation of NRXN2α, NRXN3α, NRXN3β, and NRXN3 -SS4 transcripts, while NRXN1 remained stable. In Diff cells, ICC confirmed isoform-specific protein reductions without changes in other markers (Tuj1 and PV). NRXN3β decreased at 7 and 35 mM; and NRXN1 and NRXN2 at 35 mM. Ethanol significantly reduced overall expression of NRXN3β at 7 and 35 mM; and NRXN1 and NRXN2 at 35 mM, along with NRXN3β-NLGN2 spatial overlap and NRXN1, 2, and 3β signal within PV-positive cells, indicating targeted disruption of inhibitory synaptic organization.
conclusionsPhysiologically 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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