Introducing the brain: satiation is in the cerebellum (Introduction)

by David Turell , Saturday, November 20, 2021, 20:14 (1097 days ago) @ David Turell

Mouse studies:

https://www.sciencedaily.com/releases/2021/11/211117211610.htm

"Chen, an associate professor at the Scintillion Institute, in San Diego, used clues from Prader Willi patients to guide investigations in mice that uncovered a subset of cerebellar neurons that signals satiation after eating.

"When the researchers activated these neurons, the magnitude of the effect "was enormous," accordingly to Betley. The animals ate just as often as typical mice, but each of their meals was 50-75% smaller.

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"Turning to the mice, single-cell transcriptomic analysis confirmed that a small subset of glutamatergic neurons in the aDCN were the ones being activated upon eating. Activating only these aDCN neurons led the animals to dramatically constrain their meal size, whether they had been deprived of food or given as much food as they wanted previously. When the researchers did the reverse, inhibiting these same neurons, the mice ate larger-than-normal meals. While reducing food intake can often lead people and animals to compensate by eating more food later, the aDCN-stimulated animals did not do so, and measures of metabolic activity remained steady.

"The findings were remarkable but didn't reveal what exactly the neurons were doing. Were they simply causing the animals to eat less, or were they involved in helping them predict how much to eat or regulate eating based on other feedback?

"The work, shared in the journal Nature, suggests that neurons in the cerebellum's anterior deep cerebellar nuclei (aDCN) are involved in helping animals regulate their meal size.

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"Feeding behaviors can also be driven by the reward and pleasure of eating, and thus Betley, Low, and colleagues next looked to see if dopamine signaling in the brain's ventral striatrum -- associated with neural "reward" pathways -- was affected by aDCN activation. They found that when the aDCN neurons associated with reduced feeding were activated dopamine flooded the ventral striatum. This was perplexing, as increased dopamine signaling generally drives animals to seek more reward.

"To better understand the relationship between dopamine signaling and aDCN activity, the researchers activated the mice's aDSC neurons for an hour prior to feeding them. While mice normally have a spike in dopamine levels upon being given food, the aDCN-activated mice had a severely hindered dopamine increase.

"'Other people have seen that when you activate dopaminergic neurons with dopamine, or take away dopamine, the animal will eat less," says Betley. "There may be a Goldilocks principle, making sure you eat just enough." Too much dopamine blocks the subsequent dopamine spike to rewards, ultimately changing behavior, he says."

Comment: Keep eating and stop eating controls must be present to maintain body size, and must be present in all new species from the beginning of animal evolution. Only design can do this.