Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors

Sang Yong Jung, Juhyun Kim, Oh Bin Kwon, Hoon Jung, Kyongman An, A. Young Jeong, C. Justin Lee, Yun Beom Choi, Craig H. Bailey, Eric R. Kandel, Joung Hun Kim

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72 Citations (Scopus)


Despite considerable evidence for a critical role of neuroligin-1 in the specification of excitatory synapses, the cellular mechanisms and physiological roles of neuroligin-1 in mature neural circuits are poorly understood. In mutant mice deficient in neuroligin-1, or adult rats in which neuroligin-1 was depleted, we have found that neuroligin-1 stabilizes the NMDA receptors residing in the post-synaptic membrane of amygdala principal neurons, which allows for a normal range of NMDA receptor-mediated synaptic transmission. We observed marked decreases in NMDA receptor-mediated synaptic currents at afferent inputs to the amygdala of neuroligin-1 knockout mice. However, the knockout mice exhibited a significant impairment in spike-timing-dependent long-term potentiation (STD-LTP) at the thalamic but not the cortical inputs to the amygdala. Subsequent electrophysiological analyses indicated that STD-LTP in the cortical pathway is largely independent of activation of postsynaptic NMDA receptors. These findings suggest that neuroligin-1 can modulate, in a pathway-specific manner, synaptic plasticity in the amygdala circuits of adult animals, likely by regulating the abundance of postsynaptic NMDA receptors.

Original languageEnglish
Pages (from-to)4710-4715
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number10
Publication statusPublished - 2010 Mar 9


  • Autism
  • Cortical pathway
  • Thalamic pathway

ASJC Scopus subject areas

  • General


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