Limits...
Neuroligin 3 R451C mutation alters electroencephalography spectral activity in an animal model of autism spectrum disorders

View Article: PubMed Central - PubMed

ABSTRACT

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 Nlgn3R451C mutation 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 Nlgn3R451C knock-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.

No MeSH data available.


Time-of-day profile of vigilance states in WT and Nlgn3R451C mutant mice. The distribution profile of each vigilance state across the entire recording. Nlgn3R451C mutant mice exhibited a trend of less NREM sleep than WT (p = 0.051) (b), while the two groups did not differ from each other for wakefulness (a) and REM sleep (c) (genotype: both > 0.11)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC5384041&req=5

Fig3: Time-of-day profile of vigilance states in WT and Nlgn3R451C mutant mice. The distribution profile of each vigilance state across the entire recording. Nlgn3R451C mutant mice exhibited a trend of less NREM sleep than WT (p = 0.051) (b), while the two groups did not differ from each other for wakefulness (a) and REM sleep (c) (genotype: both > 0.11)

Mentions: We first analyzed if the proportion of time spent in each state differed between the first day and second day of recordings. As day 1 and day 2 did not differ significantly for any of the state (all p >0.098), the two days’ data were averaged for subsequent analysis. As patients with ASD often have shortened sleep duration, longer waking duration during the night, and altered circadian rhythm for sleep [3, 10, 14, 34], we analyzed the proportion of time that the mice spent in each vigilance state and their distribution during the light (ZT1-12 h) and dark (ZT13-24 h) periods. During both the light and dark periods, the Nlgn3R451C mutant mice did not differ significantly from their WT littermates in the proportion of time that they spent in wakefulness, NREM sleep, and REM sleep (all p >0.14) (Fig. 2). To determine the effect of Nlgn3R451C mutation on the distribution of vigilance states across the time-of-day, we analyzed the proportion of time spent during each hour over the 24 h recording period, and found no significant difference between genotypes for all three states (genotype: all p >0.05) (Fig. 3). As patients with ASD are often reported to have more fragmented sleep or more frequent awakenings after sleep onset than non-ASD subjects [3, 34], we also examined if Nlgn3R451C mutant mice had alterations in the number of episodes and the duration of each individual sleep-wake episode. As shown in Fig. 4, there were no significant differences between Nlgn3R451C mutant mice and WT controls in the number (all p >0.45) or the duration of sleep/wake episodes (all p >0.13) (Fig. 4). Taken together, these results suggest that Nlgn3R451C mutation does not significantly affect the overall sleep/wake duration or contribute to fragmentation of sleep.Fig. 2


Neuroligin 3 R451C mutation alters electroencephalography spectral activity in an animal model of autism spectrum disorders
Time-of-day profile of vigilance states in WT and Nlgn3R451C mutant mice. The distribution profile of each vigilance state across the entire recording. Nlgn3R451C mutant mice exhibited a trend of less NREM sleep than WT (p = 0.051) (b), while the two groups did not differ from each other for wakefulness (a) and REM sleep (c) (genotype: both > 0.11)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5384041&req=5

Fig3: Time-of-day profile of vigilance states in WT and Nlgn3R451C mutant mice. The distribution profile of each vigilance state across the entire recording. Nlgn3R451C mutant mice exhibited a trend of less NREM sleep than WT (p = 0.051) (b), while the two groups did not differ from each other for wakefulness (a) and REM sleep (c) (genotype: both > 0.11)
Mentions: We first analyzed if the proportion of time spent in each state differed between the first day and second day of recordings. As day 1 and day 2 did not differ significantly for any of the state (all p >0.098), the two days’ data were averaged for subsequent analysis. As patients with ASD often have shortened sleep duration, longer waking duration during the night, and altered circadian rhythm for sleep [3, 10, 14, 34], we analyzed the proportion of time that the mice spent in each vigilance state and their distribution during the light (ZT1-12 h) and dark (ZT13-24 h) periods. During both the light and dark periods, the Nlgn3R451C mutant mice did not differ significantly from their WT littermates in the proportion of time that they spent in wakefulness, NREM sleep, and REM sleep (all p >0.14) (Fig. 2). To determine the effect of Nlgn3R451C mutation on the distribution of vigilance states across the time-of-day, we analyzed the proportion of time spent during each hour over the 24 h recording period, and found no significant difference between genotypes for all three states (genotype: all p >0.05) (Fig. 3). As patients with ASD are often reported to have more fragmented sleep or more frequent awakenings after sleep onset than non-ASD subjects [3, 34], we also examined if Nlgn3R451C mutant mice had alterations in the number of episodes and the duration of each individual sleep-wake episode. As shown in Fig. 4, there were no significant differences between Nlgn3R451C mutant mice and WT controls in the number (all p >0.45) or the duration of sleep/wake episodes (all p >0.13) (Fig. 4). Taken together, these results suggest that Nlgn3R451C mutation does not significantly affect the overall sleep/wake duration or contribute to fragmentation of sleep.Fig. 2

View Article: PubMed Central - PubMed

ABSTRACT

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 Nlgn3R451C mutation 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 Nlgn3R451C knock-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.

No MeSH data available.