Winter sleepiness has a biological circuit in the brain

Seasonal affective disorder (SAD), commonly called winter depression, affects millions of people. One of its most common symptoms is excessive sleepiness during short winter days. Until now, the mechanism behind that winter sleepiness was unclear.

Researchers studied the fruit fly Drosophila and found that a protein called cryptochrome (CRY) plays a key role. CRY is a circadian photoreceptor, a protein that detects light and helps set the internal biological clock. Under short, winter-like days, CRY remains active, and that has direct consequences for sleep. The study was published in eLife.

GABA as the switch between sleep and wakefulness

CRY acts in neurons that produce GABA, the brain’s main inhibitory neurotransmitter. Active CRY suppresses GABA release in those neurons. This reduces inhibition of nearby wake-promoting neurons (the large ventral lateral neurons) via GABA-A receptors, keeping them more active. When light levels are low, CRY is degraded, GABA suppression lifts, and the wake-promoting cells are strongly inhibited, leading to more sleep.

Flies in which the CRY gene was switched off slept more under short, winter-like conditions than normal flies. That pattern resembles the excessive sleep seen in human seasonal depression.

Relevance for aging and sleep

Sleep quality and the biological clock change with age. Older adults more frequently experience disrupted circadian rhythms, which is associated with a higher risk of cognitive decline and other health problems. Understanding the molecular switches that regulate seasonal sleep may eventually contribute to better treatments for sleep disorders in later life. Whether this circuit operates similarly in humans requires further research.

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