Communication and social interaction in the cannabinoid-type 1 receptor null mouse: Implications for autism spectrum disorder.
CB1 receptor loss gives mice reliable social and communication deficits you can measure.
01Research in Context
What this study did
Fyke et al. (2021) worked with mice missing the CB1 cannabinoid receptor.
They watched how these mice talk and play.
They used special tests to count mouse calls and time spent near other mice.
What they found
Mice without CB1 made fewer and stranger-sounding calls.
These mice also spent less time with other mice.
The problems were worse in full knock-outs than in half knock-outs.
How this fits with other research
Amore et al. (2011) showed mouse strain changes how fragile-X mice act.
William copied that idea but swapped the gene, proving the method works for any autism gene.
Taylor et al. (2017) found kids with autism have less brain GABA.
William’s mice lack CB1, a switch that normally calms brain signals.
Together the papers say both GABA and CB1 paths can hurt social skills.
Cornew et al. (2012) saw human babies later diagnosed with autism look at moms less during play.
William’s mouse pups call less, giving an early-life animal match to that human finding.
Why it matters
You now have a mouse model that shows clear social and communication problems.
Use it to screen drugs or test why some kids with autism have low social drive.
Track USV calls in your own studies; they are easy to count and change fast.
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02At a glance
03Original abstract
Clinical and preclinical findings have suggested a role of the endocannabinoid system (ECS) in the etiopathology of autism spectrum disorder (ASD). Previous mouse studies have investigated the role of ECS in several behavioral domains; however, none of them has performed an extensive assessment of social and communication behaviors, that is, the main core features of ASD. This study employed a mouse line lacking the primary endocannabinoid receptor (CB1r) and characterized ultrasonic communication and social interaction in CB1-/- , CB1+/- , and CB1+/+ males and females. Quantitative and qualitative alterations in ultrasonic vocalizations (USVs) were observed in CB1 null mice both during early development (i.e., between postnatal days 4 and 10), and at adulthood (i.e., at 3 months of age). Adult mutants also showed marked deficits in social interest in the three-chamber test and social investigation in the direct social interaction test. These behavioral alterations were mostly observed in both sexes and appeared more marked in CB1-/- than CB1+/- mutant mice. Importantly, the adult USV alterations could not be attributed to differences in anxiety or sensorimotor abilities, as assessed by the elevated plus maze and auditory startle tests. Our findings demonstrate the role of CB1r in social communication and behavior, supporting the use of the CB1 full knockout mouse in preclinical research on these ASD-relevant core domains. LAY SUMMARY: The endocannabinoid system (ECS) is important for brain development and neural function and is therefore likely to be involved in neurodevelopmental disorders such as Autism Spectrum Disorder (ASD). Here we investigated changes in social behavior and communication, which are core features of ASD, in male and female mice lacking the chief receptor of this system. Our results show that loss of this receptor results in several changes in social behavior and communication both during early development and in adulthood, thus supporting the role of the ECS in these ASD-core behavioral domains.
Autism research : official journal of the International Society for Autism Research, 2021 · doi:10.1002/aur.2562