Overview

• Mark Wu’s team at Johns Hopkins published in Science on June 19 that a subgroup of neurons in the thalamic nucleus reuniens (mRE) tracks and recovers sleep debt in mice.
• Chemogenetic stimulation of mRE neurons roughly doubled non-REM sleep and triggered nesting and grooming behaviors typical of pre-sleep preparation.
• In sleep-deprived mice, deactivation of mRE cells increased activity levels, reduced nesting and cut non-REM sleep by about 10 percent.
• Neuronal recordings revealed that mRE firing rates climb during enforced wakefulness and subside during recovery sleep, underscoring their homeostatic function.
• mRE neurons act on zona incerta cells through CaMKII-dependent plasticity to consolidate deep recovery sleep, pointing to potential targets for hypersomnia and other sleep-disorder therapies.