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The Journal of Neuroscience, July 11, 2007, 27(28):7508-7519; doi:10.1523/JNEUROSCI.0705-07.2007

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Development/Plasticity/Repair
Postsynaptic EphrinB3 Promotes Shaft Glutamatergic Synapse Formation

Jason Aoto,¹ Pamela Ting,¹ Bita Maghsoodi,¹ Nanjie Xu,³ Mark Henkemeyer,³ and Lu Chen^1,2

¹Department of Molecular and Cell Biology and ²Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720-3200, and ³Department of Developmental Biology and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390

Correspondence should be addressed to Lu Chen, Department of Molecular and Cell Biology, University of California, 201 LSA, MC 3200, Berkeley, CA 94720-3200. Email: luchen{at}berkeley.edu

Excitatory synapses in the CNS are formed on both dendritic spines and shafts. Recent studies show that the density of shaft synapses may be independently regulated by behavioral learning and the induction of synaptic plasticity, suggesting that distinct mechanisms are involved in regulating these two types of synapses. Although the molecular mechanisms underlying spinogenesis and spine synapse formation are being delineated, those regulating shaft synapses are still unknown. Here, we show that postsynaptic ephrinB3 expression promotes the formation of glutamatergic synapses specifically on the shafts, not on spines. Reducing or increasing postsynaptic ephrinB3 expression selectively decreases or increases shaft synapse density, respectively. In the ephrinB3 knock-out mouse, although spine synapses are normal, shaft synapse formation is reduced in the hippocampus. Overexpression of glutamate receptor-interacting protein 1 (GRIP1) rescues ephrinB3 knockdown phenotype by restoring shaft synapse density. GRIP1 knockdown prevents the increase in shaft synapse density induced by ephrinB3 overexpression. Together, our results reveal a novel mechanism for independent modulation of shaft synapses through ephrinB3 reverse signaling.

Key words: ephrin; shaft synapse; reverse signaling; excitatory synapses; hippocampal neurons; GRIP

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Received Feb. 15, 2007; revised May 11, 2007; accepted June 4, 2007.

Correspondence should be addressed to Lu Chen, Department of Molecular and Cell Biology, University of California, 201 LSA, MC 3200, Berkeley, CA 94720-3200. Email: luchen{at}berkeley.edu

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