Thanks for the recommendation! Just started on it. Perfect read for a snowy Sunday morning :)

Our results suggest that a common set of neuromodulators are recruited across different physiological states, acting from distinct neural sources and in distinct combinations to drive state-dependent behaviors.

We found that infection-induced quiescence involves the neuron ASI and DAF-7/TGF-beta, which control satiety-induced quiescence in uninfected animals.

Using the incredible imaging setup established in the lab by Jungsoo Kim and Adam Atanas, we characterized this novel form of quiescence using brain-wide imaging in freely moving animals.

Using cell-specific genetic perturbations we found that the neurons that release FLP-13 to delay quiescence in infected animals are distinct from ALA.

Interestingly, the ALA neuropeptide FLP-13 which is somnogenic upon other forms of stress instead acts to delay quiescence and death in infected animals.

The ALA neuron and its neuropeptides FLP-7, FLP-24, and NLP-8, which control stress-induced sleep in uninfected animals, are required for the pathogen-induced feeding reduction.

We found that chronic (days-long) infection by a bacterial pathogen induce classic hallmarks of sickness — like loss of appetite and a novel form of quiescence akin to lethargy, and eventually death.