Skip to main content
. 2013 Apr 25;14(7):810–822. doi: 10.1111/tra.12071

Figure 7. Increased GluK2 recycling requires metabotropic actions of KARs.

Figure 7

A) Representative immunoblots showing GluK2 surface expression after kainate treatment. BAPTA-AM (lanes 5 and 6) but not EDTA 3,4 blocked the kainate-induced increase of KARs in the plasma membrane. Preincubation with the phospholipase C inhibitor (U73122, lanes 7 and 8) or the G-protein inhibitor pertussis toxin PTS (lanes 9 and 10) blocked the kainate-induced increase of KARs in the surface. n = 3 (note that PTS increased GluK2 in the total fraction and in the plasma membrane). n = 4. B) Histogram showing quantification of normalized data represented in A. C) Immunoblots showing that replacing extracellular Na+ with N-methyl-d-glucamine does not block the kainate-induced increase of KARs in the plasma membrane. n = 3. D) Histogram of quantified data represented in C. E) Immunolocalization of GluK2 (red) and PSD95 (green) in control neurons and neurons 20 min after kainate application (KA). Also shown are neurons treated with EDTA ± KA, BAPTA-AM ± KA, U73122 ± KA, chelerythrine (CLT) ± KA and pertussis toxin (PTS) ± KA. F) Histogram indicating Pearson's coefficient for the degree of colocalization of GluK2 and PSD95 under the conditions shown in A–B. Mean ± SEM. p < 0.001, n = 11–15 neurons. G) Percentage of spines with TfR-A495-positive endosomes in the spine head or in the dendritic shaft at the spine base. Mean ± SEM, p < 0.001 for control versus kainate and EDTA versus EDTA kainate and p > 0.1 for the rest of the treatments. n = 18–20 spines per neuron from 10 to 12 neurons.