Lrfn2-Mutant Mice Display Suppressed Synaptic Plasticity and Inhibitory Synapse Development and Abnormal Social Communication and Startle Response

Journal: Journal of Neuroscience

Published: 2018-06-27

DOI: 10.1523/jneurosci.3321-17.2018

Affiliations: 8

Authors: 16

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Research Highlight

Synaptic changes explain genetic link to psychiatric disease



A mouse study has revealed how a mutant gene linked to autism and other neuropsychiatric disorders alters synaptic activity in the brain.

Synaptic adhesion molecules regulate the development and function of synapses, which in turn govern the functions of neural circuits and the brain.

Now, a team led by researchers from the Institute for Basic Sciences created mice deficient in Lrfn2, a gene that encodes a synaptic adhesion molecule. These mice showed changes in both inhibitory and excitatory synaptic function, and displayed abnormal behaviours connected to social communication and startled responses.

The human version of Lrfn2 has been implicated in autism spectrum disorder, schizophrenia, working memory deficits and antisocial personality disorders. The findings reveal some of the neural impairments that likely underpin these neuropsychiatric problems — and suggest pathways that could be targeted therapeutically to correct synaptic defects.

Supported content

  1. Journal of Neuroscience 38, 5872–5887 (2018). doi: 10.1523/JNEUROSCI.3321-17.2018
Institutions Share
Center for Synaptic Brain Dysfunctions, IBS, South Korea 0.22
KAIST Department of Biological Sciences, South Korea 0.22
Department of Oral Anatomy and Neurobiology, KNU, South Korea 0.13
Department of Physiology, SNU, South Korea 0.13
Department of Brain and Cognitive Sciences, DGIST, South Korea 0.13
KAIST Graduate School of Medical Science and Engineering, South Korea 0.06
Department of Anatomy, Korea University, South Korea 0.06
Department of Biomedical Sciences, Korea University, South Korea 0.06