期刊
JOURNAL OF NEUROSCIENCE
卷 27, 期 28, 页码 7508-7519出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0705-07.2007
关键词
ephrin; shaft synapse; reverse signaling; excitatory synapses; hippocampal neurons; GRIP
资金
- NIMH NIH HHS [MH66332, MH069792, R01 MH066332, R01 MH069792] Funding Source: Medline
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.
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