Amygdala EphB2 signaling regulates glutamatergic neuron maturation and innate fear

Xiao Na Zhu, Xian Dong Liu, Hanyi Zhuang, Mark Henkemeyer, Jing Yu Yang, Nan Jie Xu

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


The amygdala serves as emotional center to mediate innate fear behaviors that are reflected through neuronal responses to environmental aversive cues. However, the molecular mechanism underlying the initial neuron responses is poorly understood. In this study, we monitored the innate defensive responses to aversive stimuli of either elevated plus maze or predator odor in juvenile mice and found that glutamatergic neurons were activated in amygdala. Loss of EphB2, a receptor tyrosine kinase expressed in amygdala neurons, suppressed the reactions and led to defects in spine morphogenesis and fear behaviors. We further found a coupling of spinogenesis with these threat cues induced neuron activation in developing amygdala that was controlled by EphB2. A constitutively active form of EphB2 was sufficient to rescue the behavioral and morphological defects caused by ablation of ephrin-B3, a brain-enriched ligand to EphB2. These data suggest that kinase-dependent EphB2 intracellular signaling plays a major role for innate fear responses during the critical developing period, in which spinogenesis in amygdala glutamatergic neurons was involved.

Original languageEnglish (US)
Pages (from-to)10151-10162
Number of pages12
JournalJournal of Neuroscience
Issue number39
StatePublished - Sep 28 2016


  • Amygdala
  • EphB2
  • Ephrin-B3
  • Glutamatergic neuron
  • Innate fear
  • Spine

ASJC Scopus subject areas

  • Neuroscience(all)


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