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. 2011 Apr 6;31(14):5353–5364. doi: 10.1523/JNEUROSCI.0282-11.2011

Figure 1.

Figure 1.

EphB2 regulates localization of NMDAR receptors to synapses in mature cortical neurons. A–C, Confocal microscopy maximum projection images of cultured cortical neurons at 21 DIV expressing eGFP and shRNA vector (control), EphB2.1 shRNA, or EphB2.1 shRNA plus “rescue” EphB2 (functional EphB2 OE), immunostained for GFP (green), NR1 (red), and the presynaptic marker vGlut (blue). The magnified sections (top) of high-contrast image with arrows show spine (yellow arrows) and shaft (white arrows) synapses, defined as the locations where NR1, GFP, and vGlut immunostaining colocalize. The bottom panels show same region with anti-NR1 staining in red. D–F, Cumulative probability histograms of synaptic NR1, NR1 at spine synapses, and NR1 at shaft synapses. Functional EphB2 OE using a rescue construct in the context of endogenous EphB2 knockdown caused a significant increase in the amount of NR1 colocalizing with vGlut, whereas knockdown of EphB2 resulted in a decrease (Kolmogorov–Smirnov test, p < 0.001). Amount of NR1 for each condition is normalized to the maximum intensity observed from all three conditions. Control, n = 27 cells, 432 synapses; EphB2.1 shRNA, n = 27, 359; functional EphB2 OE, n = 21, 319.