(2006). AP-Sema6D-Fc, AP-Sema6A, or AP-Sema6C (gift of H. Fujisawa, Nagoya University) was transfected into HEK293 cells, and the protein was purified from culture supernatants. To assess binding, HEK293 cells were transiently transfected with expression vectors encoding Plexin-A1 (gift of A.W. Püschel), Neuropilin-1 (gift of R.J. Giger, University of Michigan), Nr-CAM, L1 (gift of D. Felsenfeld, Mount Sinai School of Medicine), MG-132 solubility dmso TAG-1 (gift of A. Furley, University of Sheffield), or

Neurofascin 186 (gift of V. Bennett, Duke University). AP-fusion protein binding to tissue sections was performed as described previously by Yoshida et al. (2006). All data were analyzed, and graphs were constructed using OpenLab imaging software, MetaMorph software,

or Microsoft Excel. All error bars represent the SEM, and statistical analysis was determined using one-way ANOVA followed by the Tukey’s post hoc test, where appropriate. In each figure the asterisk (∗) indicates p < 0.01, and N.S. indicates not significant (p > 0.05). We thank members of the C.M. lab, Jane this website Dodd, Jon Terman, and Alex Kolodkin for helpful comments on the experiments and manuscript. This work was supported by National Institutes of Health Grants EY12736 (to C.M.) and NS065048 (to Y.Y.), the Howard Hughes Medical Institute (to T.M.J.), Uehara Foundation (to T.K.), Ministry of Health, Labour and Welfare, Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation, and Target Protein Research Program of the Japan Science and Technology Agency (to A.K.), and Ministry of Education, Culture, Sports, Science and Technology of Japan, and the Japan Society for the Promotion of Science (to N.T.). “
“Early in development neurons make far more synaptic connections

than are maintained in the mature brain. Synaptic pruning is an activity-dependent developmental program in which a large number of synapses that form in early development are eliminated while a subset of synapses are maintained and strengthened (Hua and Smith, 2004, Katz and Shatz, 1996 and Sanes and Lichtman, 1999). While it is clear that neuronal activity plays a role, the precise cellular and molecular mechanisms underlying this developmental process remain to be elucidated. Microglia are the resident CNS immune cells which have long been recognized as rapid responders Terminal deoxynucleotidyl transferase to injury and disease, playing a role in a broad range of processes such as tissue inflammation and clearance of cellular debris (Hanisch and Kettenmann, 2007, Kreutzberg, 1996 and Ransohoff and Perry, 2009). In contrast to disease pathology, the function of microglia in the normal, healthy brain is far less understood. However, recent studies suggest that microglia may play a role in synaptic remodeling and plasticity in the healthy brain (Davalos et al., 2005, Nimmerjahn et al., 2005, Paolicelli et al., 2011, Schafer et al., 2012, Tremblay et al., 2010a and Wake et al., 2009).