title: Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors.
abstract: 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 postsynaptic 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.
authors.affiliation: Department of Life Science, Pohang University of Science and Technology, Pohang, Gyungbuk 790-784, Korea.
authors.forename: Sang-Yong
authors.initials: SY
authors.lastname: Jung
authors.forename: Juhyun
authors.initials: J
authors.lastname: Kim
authors.forename: Oh Bin
authors.initials: OB
authors.lastname: Kwon
authors.forename: Jung Hoon
authors.initials: JH
authors.lastname: Jung
authors.forename: Kyongman
authors.initials: K
authors.lastname: An
authors.forename: A Young
authors.initials: AY
authors.lastname: Jeong
authors.forename: C Justin
authors.initials: CJ
authors.lastname: Lee
authors.forename: Yun-Beom
authors.initials: YB
authors.lastname: Choi
authors.forename: Craig H
authors.initials: CH
authors.lastname: Bailey
authors.forename: Eric R
authors.initials: ER
authors.lastname: Kandel
authors.forename: Joung-Hun
authors.initials: JH
authors.lastname: Kim
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials; D000679:Amygdala / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D015153:Blotting, Western; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D002460:Cell Line; D016291:Dizocilpine Maleate / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials; D006801:Humans; D017774:Long-Term Potentiation; D051379:Mice; D018345:Mice, Knockout; D009473:Neuronal Plasticity / Q000502:physiology*; D034622:RNA Interference; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*; D013788:Thalamus / Q000378:metabolism / Q000502:physiology
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; C093438:neuroligin 1; D016291:Dizocilpine Maleate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione