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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: J Neurosci. 2010 Sep 1;30(35):11565–11575. doi: 10.1523/JNEUROSCI.1746-10.2010

Figure 4. GI-LTP-induced surface trafficking of GluA1 requires CaMKK.

Figure 4

A, Immunofluorescence images of hippocampal dendritic spines transfected with mRFP-βactin (left) or superimposed with surface GluA1 pseudo colored in green (right) for control and GI-LTP treated neurons. Scale bar is 15 μm and 2.5 μm for panel and inset, respectively. B, Quantification of spine head area and surface GluA1 (n = 75 – 100 spines per neuron; 6 – 8 neurons per coverslip) for control and GI-LTP treated neurons (n = 8 coverslips per condition from 2 independent cultures). C, Scatter plot of surface GluA1 and spine head area for control and GI-LTP treated cover slips. D, Representative western blots of biotinylated surface GluA1 (GluA1bio) and total GluA1 (GluA1tot) for conditions shown. E, Quantification of the ratio of surface biotinylated to total GluA1 for each condition indicated (n = 8 from 5 independent experiments). For GI-LTP treated cultures, neurons were fixed or biotinylated 40 minutes post GI-LTP. Error bars indicate SEM. * p<0.05 by Student's t-test.