Nature: A textbook discovery!

Click on the blue word to pay attention to our strict control of energy intake is a necessary ability for all animals to survive
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The key to energy balance is the need to sense the energy state, take in the energy needed for physiological activities, and avoid excessive consumption of food
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The combination of internal state (feeling hunger) and environmental factors (scent of food or visual attractiveness) affect eating behavior
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There is a delicate balance between promoting the urge to eat and suppressing the urge to eat in the brain.
After the neural circuit that regulates the feeding behavior is disturbed, this balance is also broken, which will cause unhealthy eating habits: loss of appetite (anorexia nervosa) Or increased appetite
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Prader-Willi syndrome (PWS) is a rare genetic disease characterized by mental retardation, hypotonia, lethargy, hyperappetite, and hypothalamic dysfunction
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On November 17, 2021, the J.
Nicholas Betley research team of the University of Pennsylvania revealed through nuclear magnetic resonance and single-cell sequencing that there is a type of neuron group in the cerebellum that inhibits excessive feeding.
This inhibition depends on dopamine
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Researchers used MRI technology to find that the deep cerebellar nucleus (DCN) activity of PWS patients is reduced when facing food cues after fasting, and food activity is seen to increase after being full
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In situ hybridization further confirmed that neurons in the DCN region of mice were activated after eating
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The deep cerebellar nucleus (DCN) is composed of three nuclei: the parietal (medial) nucleus, the intermediate nucleus, and the dentate (lateral) nucleus
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After activating the medial nucleus, lateral nucleus and intermediate nucleus of DCN by chemical genetics technology, only the neurons of the lateral nucleus are activated and inhibit feeding behavior (simulating the feeling of fullness), even in a rewarding high-sugar and high-fat diet Down is also inhibited; and inhibiting neurons in this area (simulating a hungry state) promotes feeding behavior
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Furthermore, two types of glutamatergic neurons in the DCN region were defined by single-cell sequencing technology: type I neurons express Spp1, Miat and Crhr1, and type II neurons express Celf4, Dpp10 and Unc5d
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Selective activation of type I neurons in the DCN area can significantly inhibit eating behavior, but activation of type II neurons has no effect on eating behavior
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On the one hand, eating behavior depends on the demand for energy homeostasis (perception of hypothalamic hunger neurons), and on the other hand, it also depends on the value of food (rewarding, such as a high-fat and high-sugar diet)
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Researchers found that AgRP neurons, which activate hypothalamic starvation-related peptides, can promote eating in mice, but at the same time, activating AgRP neurons and class I neurons in the DCN region can inhibit the eating behavior of mice
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This indicates that the type I neurons in the DCN area do not depend on the hypothalamus to regulate feeding behavior
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The relationship between dopamine signals and food intake is complex and vague: the levels of dopamine are all related to the increase in eating behavior 
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Researchers found that ventral striatal dopamine release increased after activating class I neurons in the DCN area, and this increase was strongly correlated with decreased feeding behavior
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Chemical activation of dopaminergic neurons in the ventral striatum also inhibits eating behavior
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In order to further confirm the relationship between them, the researchers inhibited the activity of dopaminergic neurons while activating type I neurons.
However, the mice did not show the behavior of stopping eating, which indicates that type I neurons in the DCN area inhibited eating behavior.
The effect of this depends on the dopamine signal
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The cerebellum is known for regulating body balance, coordinating voluntary and fine movements
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This article finds that the cerebellum has a new "responsibility" that is responsible for regulating satiety and stopping eating
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This brain area may be a candidate brain area for the treatment of appetite disorders through deep brain stimulation techniques
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[References] https://doi.
org/10.
1038/s41586-021-04143-5 The pictures in the article are from the references