GluA1 Phosphorylation Contributes to Postsynaptic Amplification of Neuropathic Pain in the Insular Cortex

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Figure 7.
Figure 7.

AC1 determines the upregulation of synaptic GluA1 and translocation of AKAP79/150 and PKA in the insular cortex. A, On day 7 after nerve ligation, the abundance of GluA1 and its phosphorylation at the Ser845 site in the PSD fraction from AC1−/− mice with nerve ligation showed no change compared with sham control (n = 4 mice for each group). B, No upregulation of AKAP79/150, PKA RIIβ, or PKA Cα was observed in the PSD fraction of the insular cortex from AC1−/− mice with nerve ligation compared with sham control (n = 5 mice for each group). C, In the non-PSD fraction of the insular cortex from AC1−/− mice, the abundance of AKAP79/150 or phosphorylation of GluA1 at the Ser845 site showed no change on day 7 after nerve ligation compared with sham control (n = 5–6 mice for each group).

  1. The Journal of Neuroscience vol. 34 no. 40 13505-13515
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