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. 2012 Nov 23;6:90. doi: 10.3389/fncir.2012.00090

Figure 4.

Figure 4

The GluR δ2-Cbln1-NRXN trans-synaptic triad mediates synapse formation (modified from Uemura et al., 2010). (A) Suppression of Cbln1 synaptogenic activity by the extracellular domain of NRXN1β (NRXN1β-ECD) and the N-terminal domain of GluRδ2 (GluRδ2-NTD) in cultured cerebellar neurons. In primary cultures of cerebellar neurons, numerous punctate staining signals for VGluT1 were found on the dendrites of PCs from wild-type mice. VGluT1 signals were significantly reduced in PCs from Cbln1 KO mice. Addition of Cbln1 restored the intensity of VGluT1 signals. The restoring activity of Cbln1 was suppressed by addition of NRXN1β-ECD and GluRδ2-NTD. (B) Suppression of Cbln1 synaptogenic activity by NRXN1β-ECD and GluRδ2-NTD in vivo. Electron micrographs of cerebella from wild-type and Cbln1 KO mice and those from Cbln1 KO mice injected with Cbln1 together with or without NRXN1β-ECD and GluRδ2-NTD. In wild-type mice, all PC spines formed synaptic contacts with PFs. In Cbln1 KO mice, many PC spines lacked synaptic contacts (free spines). Injection of Cbln1 restored PF-PC connections in Cbln1 KO mice. The in vivo synatogenic activity of Cbln1 was suppressed by co-injection of NRXN1β-ECD and GluRδ2-NTD. n, normal synapses; f, free spines. Scale bars represent 5 μm in (A) and 0.5 μm in (B).