Regulation of GluD1 receptor expression across a protracted ethanol withdrawal time course

When subjected to chronic ethanol exposure, the brain undergoes neuroadaptive changes in the glutamatergic receptor system. Alterations include changes in both function and expression of glutamatergic receptor proteins, which are associated with long term propensity to relapse to drug use. In this study, we quantified the expression of GluD1, a delta type glutamate receptor subunit, across a withdrawal time course following chronic intermittent ethanol exposure. We hypothesized that GRID1 expression would increase in a withdrawal dependent, sex specific manner during protracted withdrawal. Tissue collected from the basolateral amygdala was biotinylated, allowing us to characterize surface expression and total protein fractions in the same samples. Western blots were then performed on the tissue fractions across withdrawal times and sex. Our current data indicates no significant alterations in the expression of GluD1 protein in basolateral amygdala tissue in either surface or total protein samples. The current data set is incomplete in that group values need to be increased as dictated by a priori power analysis. However, GluD1 expression does not appear to be differentially regulated across protracted withdrawal from a chronic intermittent ethanol exposure. This work was funded by NIAAA (NIH) Grant # R03AA031063. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.