Summary: Researchers have identified how specialized neurons in fruit fly brains trigger the key steps in falling asleep.
Source: Oxford University.
Researchers have now shown how specialist nerve cells in the brains of fruit flies trigger several key steps of falling asleep.
The team at Oxford University’s Centre for Neural Circuits and Behaviour worked with a small cluster of neurons that had previously been shown to put flies to sleep when activated. When the flies are awake the sleep-control neurons are turned off. The longer the flies are awake, the more tired they become, which eventually reaches a tipping point and activates the neurons.
But the fact that the sleep-inducing neurons are only a tiny minority of all nerve cells posed a puzzle. Sleep entails some of the most profound and widespread changes our brains experience on a daily basis. How could so few cells control so much?
The team have found that the sleep-inducing cells ‘gate’ – or regulate the flow of electrical signals through – a node in the brain that is critical for all aspects of sleep: the fly’s motor system – controlling movement – was disconnected, preventing the animal from sleep-walking; the insect’s sensory thresholds were increased, making it less aware of its surroundings; and the ‘sleep debt’ or tiredness that had accumulated during waking was cleared.
Fruit flies are widely used by scientists as a model organism to understand how biological mechanisms work in larger, more complex organisms like humans. The 2017 Medicine Nobel Prize was awarded for discoveries concerning the body clock in flies.
Professor Gero Miesenboeck, Director of the Centre for Neural Circuits and Behaviour, said: ‘The sleep-inducing neurons act as a brake on the very brain cells whose activity causes tiredness. A beautifully simple system thus keeps sleep need and sleep in the balance.
‘We still don’t know why sleep debt builds up, what it consists of physically, how it triggers the switch to sleep and how the accumulated sleep debt is cleared. Finding the answers will help us solve the mystery of sleep.’
Source: Oxford University
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Original Research: Full open access research for “Recurrent Circuitry for Balancing Sleep Need and Sleep” by Jeffrey M. Donlea, Diogo Pimentel, Clifford B. Talbot, Anissa Kempf, Jaison J. Omoto, Volker Hartenstein, and Gero Miesenböck in Neuron. Published online January 4 2018 doi:10.1016/j.neuron.2017.12.016
Recurrent Circuitry for Balancing Sleep Need and Sleep
•Sleep-promoting dFB neurons inhibit helicon cells of the central complex
•Helicon cells transmit visual signals to R2 ring neurons and gate locomotion
•Neurons generating sleep need and sleep-inducing neurons are recurrently connected
•A unified mechanism accounts for sensory, motor, and homeostatic features of sleep
Sleep-promoting neurons in the dorsal fan-shaped body (dFB) of Drosophila are integral to sleep homeostasis, but how these cells impose sleep on the organism is unknown. We report that dFB neurons communicate via inhibitory transmitters, including allatostatin-A (AstA), with interneurons connecting the superior arch with the ellipsoid body of the central complex. These “helicon cells” express the galanin receptor homolog AstA-R1, respond to visual input, gate locomotion, and are inhibited by AstA, suggesting that dFB neurons promote rest by suppressing visually guided movement. Sleep changes caused by enhanced or diminished allatostatinergic transmission from dFB neurons and by inhibition or optogenetic stimulation of helicon cells support this notion. Helicon cells provide excitation to R2 neurons of the ellipsoid body, whose activity-dependent plasticity signals rising sleep pressure to the dFB. By virtue of this autoregulatory loop, dFB-mediated inhibition interrupts processes that incur a sleep debt, allowing restorative sleep to rebalance the books.
“Recurrent Circuitry for Balancing Sleep Need and Sleep” by Jeffrey M. Donlea, Diogo Pimentel, Clifford B. Talbot, Anissa Kempf, Jaison J. Omoto, Volker Hartenstein, and Gero Miesenböck in Neuron. Published online January 4 2018 doi:10.1016/j.neuron.2017.12.016