Postsynaptic ephrinB3 promotes shaft glutamatergic synapse formation

Jason Aoto, Pamela Ting, Bita Maghsoodi, Nanjie Xu, Mark Henkemeyer, Lu Chen

Research output: Contribution to journalArticlepeer-review

68 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)7508-7519
Number of pages12
JournalJournal of Neuroscience
Volume27
Issue number28
DOIs
StatePublished - Jul 11 2007

Keywords

  • Ephrin
  • Excitatory synapses
  • GRIP
  • Hippocampal neurons
  • Reverse signaling
  • Shaft synapse

ASJC Scopus subject areas

  • Neuroscience(all)

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