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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: Neuropharmacology. 2016 Oct 25;113(Pt A):426–433. doi: 10.1016/j.neuropharm.2016.10.025

Figure 2. GRIP is required for a Li+ treatment-induced increase in surface GluA2.

Figure 2

Schematic diagrams show the binding properties of MycGluA2 and its mutants (Greger et al, 2002) a) GluA2-SVKI (WT) binds to PICK1 and GRIP; b) GluA2-SVKE is unable to bind to either PICK1 or GRIP, and c) GluA2-AVKI is able to bind to PICK1 but not GRIP. Also given are representative confocal images of cultured hippocampal neurons expressing the various mutants of MycGluA2 from Sindbis virus vectors and treated with NaCl or LiCl showing surface GluA2 (green) and total GluA2 (red). Scale bar indicates 10μm. Higher magnification images of highlighted dendrites are shown below. Summary graphs show that: a) LiCl treatment was able to increase surface GluA2-SVKI (WT) levels in cultured hippocampal neurons (n=12 neurons, *p<0.05, unpaired two-tailed Student’s t tests), but b–c) LiCl treatment was unable to alter surface levels of mutant GluA2 (n=30 neurons in b) and 50 neurons in c)), suggesting that the ability of MycGluA2 to bind to GRIP is required for a Li+ treatment-induced increase in surface GluA2 in cultured hippocampal neurons.