Chunk #0 — Figure 1

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PDZ binding of TARPγ-8 controls synaptic transmission but not synaptic plasticity.

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TARP©-8 PDZ binding is necessary for synaptic localization of AMPARs. (a) diagram of the synaptic AMPAR/TARP/PSD-95 complex. The PDZ ligand (–TTPV) is deleted. (b) The anti-©-8 antibody recognized ©-8 in both γ-8+/+ and γ-8Δ4/Δ4, whereas anti-TTPV antibody recognized ©-8 only in WT. Brain lysates were immunoprecipitated with normal rabbit IgG (control) or anti ©-8 antibody, followed by western blotting. All full and uncropped blots are shown in Supplementary Figure 7. (c) PSD-95 is not associated with ©-8⊗4 in vivo. PSD-95 was co-immunoprecipitated with ©-8 in γ-8+/+, but not in γ-8Δ4/Δ4 mice. (d) Protein levels of ©-8, GluA1, and GluA2/3 were somewhat decreased in hippocampi in a ©-8⊗4 gene dosage-dependent manner (n=4). (e, f) Protein levels of ©-8, GluA1, and GluA2/3 in the PSD fraction from hippocampus were reduced in γ-8Δ4/Δ4 mice, but not in the Triton X-100-solublized synaptosome fraction (Syn/Tx). In contrast, expression of ©-8, GluA1, and GluA2/3 in the Syn/Tx fraction was significantly reduced in γ-8−/− mice, but not in γ-8Δ4/Δ4 mice. (f) Protein levels were normalized to those from γ-8+/+ mice (n=4). Synaptophysin (Sph) was used as a non-PSD protein. All data are given as mean ± s.e.m.; * P < 0.05.