EphB maintains dendritic spine morphology through focal adhesion kinase.

Editor's Note: These short, critical reviews of recent papers in the Journal, written exclusively by graduate students or postdoctoral fellows, are intended to summarize the important findings of the paper and provide additional insight and commentary. For more information on the format and purpose of the Journal Club, please see The postsynaptic components of excita-tory synapses are located at specialized structures called dendritic spines, small protrusions along neuronal dendrites. Den-dritic spines are not static, and changes in spine size, shape, and density are believed to be associated with synaptic plasticity and memory. A plethora of molecules have been found to regulate dendritic spine morphogenesis, including cytoplas-mic kinases, scaffold proteins, cell surface receptors, and ion channels. Eph receptors, including EphAs and EphBs, form the largest family of receptor tyrosine kinases. Their membrane-attached ligands ephrins, not only activate Eph receptors on the opposing cell membrane and transduce forward signaling, but also elicit reverse signaling cascades in ephrin-expressing cells upon binding to the receptors. Ephs and ephrins have been well studied in axon pathfinding and topo-graphic mapping. In recent years, accumulating evidence demonstrate that Eph receptors play important roles in the mor-phogenesis of dendritic spines (Pasquale, 2005; Chen et al., 2009). For example, activation of EphB signaling induces the formation of dendritic spines. In contrast, EphA4 triggers dendritic spine retraction in mature neurons, and knockout of EphA4 in hippocampal neurons results in aberrant dendritic spine morphology. Although the mechanisms by which EphB receptors regulate spine formation have been extensively studied, it is not clear whether EphB receptors play a role in the maintenance of dendritic spines and how they exert their actions. An early study on EphB1-3 triple-knockout mice revealed that the loss of EphB receptors reduces spine number in mature neurons, suggesting that EphBs either promote spine formation or are required for maintaining mature dendritic spines (Henkemeyer et al., 2003). It was recently demonstrated that knockdown of EphB2 by shRNA during the third week in vitro causes a shift of spine morphology from mushroom-shaped to long filopodia-like protrusions, supporting a role of EphB2 in stabilizing mature den-dritic spines (Kayser et al., 2008). Thus, it would be of interest to elucidate how EphB receptors maintain the shape of mature dendritic spines. In a recent issue of The Journal of Neuroscience, Shi et al. (2009) addressed this question by demonstrating that EphB2 maintains the morphology of mature den-dritic spines by suppressing the actin-destabilizing activity …