I recently read an article called Integrating GABA and Dopamine Signals to Regulate Meal Initiation. In this article, Dr. Yong Xu, a professor of pediatrics, as well as other colleagues find a better understanding on how to control the release of serotonin in order to regulate the intake of food as well as appetite for food. Drugs that interact with serotonin in order to regulate food consumption, which were prescribed to help prevent obesity, are no longer offered to patients because of unwanted side effects though.
Serotonin is mostly synthesized in the Dorsal Raphe Nucleus (DRN) and these neurons then get projected to other regions of the brain. The DRN is located in the brainstem in the middle of the brain. One of the regions is the arcuate of the hypothalamus (ARH). ARH is located at the base of the hypothalamus, directly above the brainstem.
By experimenting on animals, Xu Labs discovered that hunger is caused by the prevention of serotonin-producing neurons in the DRN by neurotransmitters such as GABA, which means Gamma-Aminobutyric, and dopamine. Neurotransmitters are signaling molecules that carry messages from one nerve cell to another. When these neurons are suppressed, the levels of serotonin in the brain are also suppressed, and an animal can then start to eat a meal. As the meal progresses, the signals that restrain serotonin levels lessen, and more serotonin is produced in order for the animal to reach satiety. This serotonin is produced through projections to the ARH. They also discovered that when both GABA and dopamine are present, serotonin neurons are more inhibited than if there was just one of the neurotransmitters.
While writing about this article, I found it interesting how one of the most important indicators for when we are full is just the release of serotonin. And it’s intriguing how just by producing more serotonin when eating could cause someone’s appetite to completely disappear.
Find the Article here: https://www.sciencedaily.com/releases/2024/12/241220132846.htm
