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. 2008 Dec 22;105(52):20953–20958. doi: 10.1073/pnas.0811025106

Fig. 2.

Fig. 2.

SAP102 mediates NMDA receptor synaptic trafficking during synaptogenesis in vivo. (A) Representative NMDAR EPSCs from untransfected and adjacent SAP102 overexpressing (SAP102 Ovxp) neurons from E16 to P6–P8. (B) SAP102 overexpression significantly increases NMDAR EPSC amplitudes relative to untransfected neurons. (D) Representative EPSCs in untransfected and neighboring neuron expressing SAP102 shRNA. (E) shRNA-mediated knockdown of SAP102 significantly reduces NMDAR EPSC amplitudes. Neither SAP102 overexpression (C: Top, sample traces; Bottom, summary bar graph) nor SAP102 knockdown (F: Top, sample traces; Bottom, summary bar graph) significantly affects the PPR [(C, control: 1.5 ± 0.19, n = 7; SAP102 Ovxp: 1.6 ± 0.16, n = 7; P = 0.82); (F, control: 1.5 ± 0.24, n = 8; SAP102 shRNA: 1.7 ± 0.16, n = 15; P = 0.89)]. (Error bars = SEM.) (G) Confocal image of transfected (SAP102 shRNA neuron, green) and untransfected neighbor (control, red) filled with Alexa Fluors. (H) High magnification of boxed area in G shows spines in both cells (white arrowheads). (I) Pair-wise comparison of the number of spines per unit length of apical dendrite between SAP102 shRNA-expressing and untransfected control neurons shows no significant difference in spine density. Open and filled circles represent spine densities for single pairs and the mean ± SEM, respectively. (Scale bars: A = 25 pA, 25 ms; D = 20 pA, 25 ms.)