Experiments using zebrafish identify a novel sleep-promoting neuronal circuit in which hypothalamic NPVF neurons promote sleep via the hindbrain serotonergic raphe nuclei, which promote sleep in both zebrafish and mice.
Kinetic interactions between sodium channels and auxiliary factors create a molecular computational engine that can sense and regulate cellular excitability.
The dorsal raphe nucleus contains transcriptionally diverse cell classes that include subtypes of serotonergic neurons with distinct molecular and anatomical signatures.
Dorsal raphe Pet1 neurons are molecularly heterogeneous, comprising as many as fourteen distinct subtypes that show biased cell body distributions across dorsal raphe subdomains.
Pet1 neurons actively maintain cardiorespiratory tone and dynamic range in mouse neonates and critically support the recovery response to apneas, informing brain findings in the sudden infant death syndrome.
Serotonin-releasing neurons show tonic firing-rate changes correlating with global reward value in addition to phasic firing-rate changes correlating with local task events.
Serotonin neurons in chronically isolated mice become less responsive to excitatory stimulation, but inhibiting a distinctive calcium-activated potassium channel can restore both neuronal activity and behavior.
When the neuropeptide orexin is peripherally administered in mice with septic shock, it penetrates the blood-brain barrier and acts in the brain to improve survival through multiple autonomic and neuroendocrine pathways.
The collective action of six transcription factors selects and activates the regulatory regions of the HSN serotonergic neuron effector genes constituting a signature that can be used for the novo identification of HSN expressed genes.