Summary
A bioRxiv preprint reports that vagus nerve stimulation recruited neurons in the default mode network in mice. Selectively activating or silencing those neurons reproduced or abolished stimulation-related changes in cognitive behaviours.
A bioRxiv preprint reports that stimulating the vagus nerve activated neuronal groups in the default mode network (DMN) in mice, and that manipulating those groups changed cognitive behaviours associated with the stimulation. The findings point to a brain circuit that may help explain how signals carried by the vagus nerve influence cognition. They are from animal research, not evidence of a cognitive benefit in people.
From vagus nerve signals to brain networks
The vagus nerve carries sensory information from the body to the brain, among other functions. To examine how its signals affect brain activity, the researchers analysed responses across the mouse brain. They report that vagus nerve stimulation activated neuronal ensembles—groups of neurons that respond together—in the DMN. By contrast, mechanisms independent of vagal signalling predominantly affected the salience network, another set of connected brain regions.
The researchers also identify subpopulations of neurons in the locus coeruleus, a brainstem region, as mediating the association between vagal signals and the DMN. This suggests a route by which stimulation-related signals may be relayed into brain networks involved in cognitive processing.
Manipulating the network affected behaviour
The study reports that selectively activating the vagus-responsive DMN ensembles reproduced stimulation-related enhancements in cognitive behaviours and progressive problem-solving behaviours. Silencing those ensembles abolished the reported effects of vagus nerve stimulation. These interventions suggest the identified neurons had a functional role in the behavioural changes in the mice, rather than simply becoming active alongside them.
The work is a preprint posted on bioRxiv and has not yet been peer reviewed. Its findings provide a mechanistic result in mice; they do not establish that the same pathway improves cognition in humans.