If I could fall asleep and wake up on command, I probably wouldn’t resort to watching Netflix’s second-string comedy specials at 3 a.m. or disperse foghorn-like alarm clocks around my room. It’s safe to say I’m jealous of anyone with a more easily programmed body clock.
Apparently, that means I’m jealous of a petri-dish of brain cells. WSU News reports that neuroscientists at Washington State University have grown a minuscule bundle of brain cells that can be induced to conk out, get up and even catch up on rebound sleep after extended periods of wakefulness.
The research, recently published in the European Journal of Neuroscience, provides the first tangible evidence that sleep begins in small neural networks. The tiny group of cells is the smallest “unit” of sleep ever identified. Figuring out how to create sleep in a dish — outside any animal — is a big step in the research arms race to understand, with greater clarity, the genetic and neural bases of sleep disorders.
To create the “sleep-unit,” a research team, led by James Krueger, spent two weeks culturing neurons and glial cells (the two types of brain cells) to grow into an independent neural network. To determine the cells’ state of consciousness, Krueger’s team used EEG to measure electrical brain activity, in the same way scientists record sleep in real animals. Eventually, the network exhibited similar EEG patterns to those seen in animal brains.
The sleep-unit’s normal state, according to Krueger, is comparable to non-deep sleep. To induce deeper sleep, researchers added a sleep-regulating protein called TNF to the petri dish. The TNF didn’t kick in immediately, but, as the sleep-unit grew, researchers saw deep-sleep activity spontaneously flare up.
“There was little delta power (aka deep sleep waves) during the first few days of culture,” Krueger told Van Winkle’s, “but as the cells connected to each other delta wave power increased. Delta wave power is a key measure to characterize sleep in whole animals.”
To reverse the effects of TNF — i.e., to wake up the neurons — researchers applied electrical stimulation to the petri dish. Subsequently, the neurons exhibited EEG patterns indicating wakefulness. They then hazed the poor neurons, using extended simulation to force the equivalent of an all-nighter. In response, the sleep-unit did what animals do to maintain homeostasis: They slept in.
Neurons and glia — they’re just like us.
Some studies tell us what we already know — they’re more “no shit” than “mind blown.” Others furnish findings so theoretically abstruse that it’s difficult to attach real-life relevance. This one is different: It is both pointy-headed and grounded. Building on this research, scientists can study sleep outside the body without having to address how other physiological processes (e.g., fluctuating body temperature) may affect results. Isolating sleep, Krueger said, will enhance the speed and specificity of research on such hairy topics as the genetics of sleep and drug actions. The findings also reinforce the idea that different brain networks run on different sleep-and-wakefulness schedules.
“It appears that parts of the brain can be asleep while, simultaneously, parts may be awake.”
According to Krueger, this helps explain:
- sleep inertia;
- graded levels of wakefulness and sleep;
- some sleep pathologies such as insomnia; and
- changes in brain performance, as small units are involved in different specific tasks.
For Krueger, the next step is to understand if (and how) sleep deprivation alters the behavior of brain cells. In this case, from mice. What’s more, now that they’ve determined that TNF puts brain cells to sleep, Krueger’s team can explore how the drowsiness-inducing protein actually works.