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. Author manuscript; available in PMC: 2010 Jun 1.
Published in final edited form as: Curr Opin Neurobiol. 2009 May 4;19(3):319–326. doi: 10.1016/j.conb.2009.03.011

Figure 2. Proposed mechanisms by which newly synthesis proteins mediate persistent decrease in surface AMPA receptors during mGluR-LTD.

Figure 2

Brief activation of mGluR1/5 triggers rapid endocytosis of AMPARs that requires activity of the Tyr phosphatase STEP and basal levels of Arc. Tyr dephosphorylation of the GluR2 subunit of the AMPAR is correlated with mGluR-triggered AMPAR endocytosis, suggesting that this is the relevant phosphatase substrate. MGluRs also rapidly increase translation of Step, Map1b and Arc mRNA. MAP1B is required for mGluRs to induce long-term decreases in surface AMPARs perhaps by sequestering the AMPAR binding protein GRIP. New synthesis of Arc, and perhaps STEP, may maintain mGluR-LTD by causing persistent increases in AMPAR endocytosis rate.