Data from: Hypothalamic circuitry underlying stress-induced insomnia and peripheral immunosuppression

The neural substrates of insomnia/hyperarousal induced by stress remain
unknown. Here, we show that restraint stress leads to hyperarousal
associated with strong activation of corticotropin-releasing hormone
neurons in the paraventricular nucleus of hypothalamus (CRHPVN) and
hypocretin neurons in the lateral hypothalamus (HcrtLH). CRHPVN neurons
directly innervate HcrtLH neurons and optogenetic stimulation of
LH-projecting CRHPVN neurons elicits hyperarousal. CRISPR-Cas9-mediated
knockdown of the crh gene in CRHPVN neurons abolishes hyperarousal induced
by stimulating LH-projecting CRHPVN neurons. Genetic ablation of Hcrt
neurons or crh gene knockdown significantly counteracts restraint
stress-induced hyperarousal. As stress is further associated with changes
in immune function, we used single-cell mass cytometry by time of flight
(CyTOF) to analyze peripheral blood and found extensive changes to immune
cell distribution and functional responses during wakefulness upon
optogenetic stimulation of CRHPVN neurons. Our findings suggest both
central and peripheral systems are synergistically engaged in the response
to stress via CRHPVN circuitry.