We are living in a microbial world with our bodies having as many microbial cells as human cells. Growing evidence implicates these microbes, known collectively as the microbiome, as key regulators of brain function and behaviour [1]. One of the key findings from across many species is that the microbiome affects social behaviour [2]. We have shown that germ-free (GF) mice, which grow up in a sterile environment and thus have no bacteria in or on their bodies, are less sociable than normal mice[2]. Moreover, the amygdala, a brain region important for social behaviour, is particularly sensitive to changes in microbiome composition [3] and GF mice have widespread changes in amygdala neuronal morphology and function [4].

To this end we recently described dynamic regulation of several previously undescribed pathways in response to social stimulation. These include regulation of RNA-processing non-coding RNAs that are crucially involved in splicing regulation. Moreover, social stimulus evoked an increase in transcripts of genes involved in neuronal activity, which includes induction of several well established immediate early genes such as Fos or Arc, the MAP-K pathway and neurotrophic signalling via Bdnf. Moreover, we find upregulation of complement components, which have lately been established to be necessary for synaptic rearrangements and plasticity upon neuronal activity [6].

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