Supplementary Materials

The PDF file includes:

  • Fig. S1. Structures of GSK inhibitors and commonly used mGluR5 NAMs.
  • Fig. S2. GSK3α- and GSK3β-selective inhibitors decrease phosphorylation of CRMP2 (in the PI3K/Akt signaling pathway) but do not stabilize β-catenin.
  • Fig. S3. Pharmacokinetics of new GSK3 inhibitors.
  • Fig. S4. Acute inhibition of GSK3α/β with BRD0320 ameliorates AGS incidence in Fmr1−/y mice.
  • Fig. S5. Chronic inhibition of GSK3β with BRD3731 has no effect on AGS incidence in Fmr1−/y mice.
  • Fig. S6. BRD3731 does not reduce evoked hyperexcitability in the Fmr1−/y visual cortex.
  • Fig. S7. BRD3731 does not reduce spontaneous hyperactivity in the Fmr1−/y visual cortex.
  • Fig. S8. CRMP2 phosphorylation is not a useful marker for GSK3 inhibition in vivo.
  • Fig. S9. Inhibition of GSK3α does not potentiate the locomotor effects of MK-801.
  • Fig. S10. Acute administration of the mGluR5 NAM CTEP ameliorates AGS in Fmr1−/y mice.
  • Fig. S11. Fmr1−/y mice develop tolerance to CTEP but not BRD0705 upon repeated dosing in the AGS assay.
  • Fig. S12. Inhibition of GSK3α does not affect Akt or ribosomal protein S6 phosphorylation.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Individual-level data for all figures.