Figure 8.

Surface expression of neuronal CNIH-2 requires γ-8. A, In wild-type mouse hippocampus, GluA1, GluA2, TARPs, and CNIH-2 occur on the surface. Knock-out of γ-8 (γ-8/γ-8) reduced total levels of GluA1, GluA2, and CNIH-2 while selectively depleting CNIH-2 from the surface in hippocampal slices. B, In cerebella from stargazer mice (stg/stg), CNIH-2 resides almost exclusively within cells, whereas GluA1, GluA2, and γ-7 are present on the surface. The asterisk (*) denotes a nonspecific band in biotinylated lysates that reacts with the secondary antibody. C, Quantification reveals a reduction in the surface expression of CNIH-2 in extracts from the γ-8 knock-out hippocampus, whereas surface GluA isoform expression remains equivalent, relative to wild-type hippocampus. D, CNIH-2 surface expression in stargazer cerebellum is absent, whereas GluA isoforms and γ-7 are present at the plasma membrane. For both hippocampal and cerebellar surface biotinylation experiments, β-tubulin and synaptophysin served as internal controls for surface expression.