Molecular brainApr 8, 2017

Neuroligin 3 R451C mutation changes brain electrical activity in an animal model of autism

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Updated Apr 5, 2026

Abstract

Nlgn3 knock-in mice exhibited significantly altered electroencephalography (EEG) power spectral profiles during wake and sleep.

Sleep duration and distribution in Nlgn3 knock-in mice were normal.
Alterations in EEG power spectral profiles suggest potential disruptions in sleep architecture.
The study highlights the need to investigate the relationship between synaptic imbalances and sleep impairments in autism spectrum disorders.

Simplified

Human studies demonstrate that sleep impairment is a concurrent comorbidity of autism spectrum disorders (ASD), but its etiology remains largely uncertain. One of the prominent theories of ASD suggests that an imbalance in synaptic excitation/inhibition may contribute to various aspects of ASD, including sleep impairments. Following the identification of Nlgn3mutation in patients with ASD, its effects on synaptic transmission and social behaviours have been examined extensively in the mouse model. However, the contributory role of this mutation to sleep impairments in ASD remains unknown. In this study, we showed that Nlgn3knock-in mice, an established genetic model for ASD, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep. R451C R451C

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Neuroligin 3 R451C mutation changes brain electrical activity in an animal model of autism

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