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. Author manuscript; available in PMC: 2015 Mar 5.
Published in final edited form as: Neuron. 2014 Mar 5;81(5):1070–1083. doi: 10.1016/j.neuron.2014.01.022

Figure 2. NR2B phosphorylation at Ser1116 regulates NMDAR function.

Figure 2

(A) Increased cell surface NR2B correlates with reduced P-S1116 in hippocampal slices. Levels of cell surface-biotinylated NR2B pulled-down from lysates of hippocampal slices incubated in the absence (−) or presence (+) of the Cdk5 inhibitor CP681301 are shown with blots and quantitation (n = 4). Prior to pull-down, lysates were tested for NR2B Load and P-S1116 (bottom panel). (B) Effect of Cdk5 inhibition on the NR2B component of NMDAR-EPSC. Voltage-clamp EPSC recordings of total NMDAR-EPSC (INMDA) in the absence or presence of the specific NR2B inhibitor ifenprodil from pyramidal neurons within the hippocampal area CA1 pretreated with vehicle (control) or the Cdk5 inhibitor CP681301 are shown. (C and D) Quantitation of NMDAR EPSC recordings showing an increase of ifenprodil-sensitive NR2B component (C) and prolonged decay kinetics (D) of NMDAR EPSC in cells incubated in the absence (−) or presence (+) of CP681301 (n = 6–7). Data are represented as mean ± SEM. See also Figure S2A and B.