Microbiota and social behavior: a possible treatment

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Dr. Noèlia Fernàndez Castillo
About the Author

Dr. Noelia Fernández Castillo is a postdoctoral researcher of the Centre of Biomedical Network Research on Rare Diseases (CIBERER) at the Genetics Department of the Universitat de Barcelona (Spain). She works in the fields of psychiatric genetics and neurogenetics, specifically on substance use disorders, migraine, and episodic diseases.

Dr. Judit Cabana Dominguez
About the Author

Dr. Judit Cabana Dominguez works at the Department of Genetics, Microbiology & Statistics, University of Barcelona in Spain.


Increasing evidences are showing that the gut microbiota can alter brain and behavior, and thus may play a role in the development of psychiatric and neurodevelopmental disorders, such as autism and schizophrenia. Animal models are a useful tool to study this mechanism. For example, germ-free (GF) mice, which have never been exposed to microorganisms, are usually compared to the exposed ones, known as conventional colonized mice (CC). Recent studies have reported that GF animals show increased response to stress, reduced anxiety and memory. In most cases, these alterations are restricted to males, in which there are higher incidence rates of neurodevelopmental disorders compared to females.

Mice, like humans, are social species and are used to study social behavior. A recent study compared GF and CC mice using different sociability tests. GF mice showed impairments in social behavior compared with CC, particularly in males. Interestingly, they demonstrate that social deficits can be reverted by bacterial colonization of GF gut (GFC), achieving normal social behavior.

Microbiota seem to be crucial for social behaviors, including social motivation and preference for social novelty, and regulate repetitive behaviors, characteristic of several disorders such as autism and schizophrenia. Bacterial colonization can revert these alterations, suggesting that microbial-based interventions in later life could improve the social impairments and could be a useful for the symptomatology of these disorders.

Reference

Desbonnet et al. Molecular Psychiatry (2014) 19, 146–148; doi:10.1038/mp.2013.65