Defects in an early developmental process, involving the removal of extra connections between neurons, are associated with alterations in social behavior in mice. The results, reported this week in Nature Neuroscience, may shed light on the neurobiology of social behavior and have implications for our understanding of social deficits in autism or obsessive compulsive disorder.
The developmental process synaptic pruning is mediated by microglia, a non-neuronal cell type in the brain that also functions in immune responses. Mice with compromised microglia have previously been shown to have deficits in learning and memory. These findings add support to the idea that altered social and cognitive behaviors, symptoms of many psychiatric disorders, may be caused by altered development of the connections between neurons.
Cornelius Gross and colleagues studied genetically-modified mice in which there was a transient decrease in the number of microglia in the brain. These mice showed decreased social interaction with other mice, as well as increased grooming behavior, which has been suggested to be analogous to repetitive behaviors seen in disorders like OCD and autism spectrum disorders. Looking at brain samples, the authors also found that these mice showed deficient synaptic pruning, and reduced functional connectivity between the hippocampus and prefrontal cortex, two regions of the brain implicated in cognitive and social behaviors.