%0 Journal Article %T Thrombospondin receptor ¦Á2¦Ä-1 promotes synaptogenesis and spinogenesis via postsynaptic Rac1 %A Cagla %A Cagla Eroglu %A Choi %A Debra L. %A Debra L. Silver %A Dongqing %A Dongqing Wang %A Erin F. %A Erin F. Spence %A Eroglu %A Feng %A Guoping %A Guoping Feng %A Henry H. %A Henry H. Yin %A Ji-Eun %A Ji-Eun Choi %A Kim %A Koh %A Louis-Jan %A Louis-Jan Pilaz %A Mitev %A Namsoo %A Namsoo Kim %A Petar %A Petar Mitev %A Pilaz %A Risher %A Scott H. %A Scott H. Soderling %A Sehwon %A Sehwon Koh %A Silver %A Soderling %A Spence %A W. Christopher %A W. Christopher Risher %A Wang %A Yin %J JCB | The Journal of Cell Biology %D 2018 %R 10.1083/jcb.201802057 %X Astrocytes control excitatory synaptogenesis by secreting thrombospondins (TSPs), which function via their neuronal receptor, the calcium channel subunit ¦Á2¦Ä-1. ¦Á2¦Ä-1 is a drug target for epilepsy and neuropathic pain; thus the TSP¨C¦Á2¦Ä-1 interaction is implicated in both synaptic development and disease pathogenesis. However, the mechanism by which this interaction promotes synaptogenesis and the requirement for ¦Á2¦Ä-1 for connectivity of the developing mammalian brain are unknown. In this study, we show that global or cell-specific loss of ¦Á2¦Ä-1 yields profound deficits in excitatory synapse numbers, ultrastructure, and activity and severely stunts spinogenesis in the mouse cortex. Postsynaptic but not presynaptic ¦Á2¦Ä-1 is required and sufficient for TSP-induced synaptogenesis in vitro and spine formation in vivo, but an ¦Á2¦Ä-1 mutant linked to autism cannot rescue these synaptogenesis defects. Finally, we reveal that TSP¨C¦Á2¦Ä-1 interactions control synaptogenesis postsynaptically via Rac1, suggesting potential molecular mechanisms that underlie both synaptic development and pathology. %U http://jcb.rupress.org/content/217/10/3747