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No one wants to eat when they have an upset stomach. To pinpoint exactly where in the brain this distaste for eating originates, scientists studied nauseated mice.
The work, published in Cell Reports on 27 March1, describes a previously uncharacterized cluster of brain cells that fire when a mouse is made to feel nauseous, but don’t fire when the mouse is simply full. This suggests that responses to satiety and nausea are governed by separate brain circuits.
“With artificial activation of this neuron, the mouse just doesn’t eat, even if it is super hungry,” says Wenyu Ding at the Max Planck Institute for Biological Intelligence in Martinsried, Germany, who led the study.
Ding and colleagues suspected that this group of neurons was involved in processing negative experiences, such as feeling queasy, so they injected the mice with a chemical that induces nausea and then scanned the animals’ brains. This confirmed that the neurons are active when mice feel nauseous.
Light bites
Using a light-based technique called optogenetics, the team artificially activated the neurons of mice that had been deprived of food in the hours before the experiment. When the neurons were ‘off’, the mice ate. When the researchers turned them on, the mice walked away mid-chow.
These brain cells could influence how fast you eat — and when you stop
Researchers also blocked the activity of these neurons in nauseated mice that were hungry and found that the mice overcame their nausea to eat.
Understanding the brain circuits that control nausea is an important part of researching dysregulated eating, such as that seen in people with obesity and anorexia, says Haijiang Cai, a neuroscientist at the University of Arizona in Tucson.
A previous study2 described neurons near those characterized by the authors that also regulate eating, but that don’t differentiate between feelings of fullness and nausea. With their results, Ding and colleagues show that the two experiences are controlled by separate brain circuits.
“It’s going to be exciting in the future if we can target the neurocircuitry that controls satiation to suppress appetite, but not to cause nausea,” says Cai. For example, this information might assist in controlling the nausea caused by some appetite-suppressant drugs.
The same could be true in reverse, allowing someone to eat when they are nauseated. Nausea is a common side effect of many cancer treatments and makes it difficult for patients to stay properly nourished.
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