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Lrfn2-Mutant Mice Display Suppressed Synaptic Plasticity and Inhibitory Synapse Development and Abnormal Social Communication and Startle Response
- Lrfn2-Mutant Mice Display Suppressed Synaptic Plasticity and Inhibitory Synapse Development and Abnormal Social Communication and Startle Response
- Li, Yan; Kim, Ryun Hee; Cho, Yi Sul; Song, Woo Seok; Kim, Do Youn; Kim, Kyung Deok; Roh, Junyeop Daniel; Chung, Changuk; Park, Han Wool; Yang, Esther; Kim, Soo Jeong; Ko, Jaewon; Kim, Hyun; Kim, Myoung Hwan; Bae, Yong Chul; Kim, Eun Joon
- DGIST Authors
- Ko, Jaewon
- Issue Date
- Journal of Neuroscience, 38(26), 5872-5887
- Article Type
- excitatory synaptic function; GABAergic neurons; inhibitory synapses; Lrfn2; NMDA receptor; social communication; ADHESION-LIKE MOLECULES; ULTRASONIC VOCALIZATIONS; NMDA RECEPTOR; MOUSE MODELS; SALM/LRFN FAMILY; LAR-RPTPS; ORGANIZERS; DISORDERS; COMPLEXES; PROTEINS
- SALM1 (SALM (synaptic adhesion-like molecule), also known as LRFN2 (leucine rich repeat and fibronectin type III domain containing), is a postsynaptic density (PSD)-95-interacting synaptic adhesion molecule implicated in the regulation of NMDA receptor (NMDAR) clustering largely based on in vitro data, although its in vivo functions remain unclear. Here, we found that mice lacking SALM1/LRFN2 (Lrfn2-/- mice) show a normal density of excitatory synapses but altered excitatory synaptic function, including enhanced NMDAR-dependent synaptic transmission but suppressed NMDAR-dependent synaptic plasticity in the hippocampal CA1 region. Unexpectedly, SALM1 expression was detected in both glutamatergic and GABAergic neurons and Lrfn2-/- CA1 pyramidal neurons showed decreases in the density of inhibitory synapses and the frequency of spontaneous inhibitory synaptic transmission. Behaviorally, ultrasonic vocalization was suppressed in Lrfn2-/- pups separated from their mothers and acoustic startle was enhanced, but locomotion, anxiety-like behavior, social interaction, repetitive behaviors, and learning and memory were largely normal in adult male Lrfn2-/- mice. These results suggest that SALM1/LRFN2 regulates excitatory synapse function, inhibitory synapse development, and social communication and startle behaviors in mice. © 2018 the authors.
- Society for Neuroscience
- Related Researcher
Laboratory of Synapse Formation and Function
Synapse Formation and Function; Neural Circuits; 뇌질환; animal model
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- Department of Brain and Cognitive SciencesLaboratory of Synapse Formation and Function1. Journal Articles
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