Summary: A new study has revealed how brains circuits and neurotransmitters manage food introduction, offering insights into fat control.
Researchers identified serotonin neurons in the midbrain’s dorsal Raphe nucleus ( DRN ) as key players, inhibited by GABA and dopamine when hunger strikes. This restriction lowers dopamine levels, triggering feeding habits, while hunger reverses the process. Importantly, GABA and serotonin synergize for more serious effects on norepinephrine suppression.
These results provide more information about feeding rules and help develop fatness treatments. Future analysis will look into how different feeding phases are controlled by neural circuits.
Important Information:
- Neurotransmitter Synergy: GABA and serotonin harmoniously limit serotonin cells during poverty, promoting food introduction.
- Serotonin’s Role: Serotonin levels rise post-meal to curb more serving, highlighting its double role in hunger and satiety.
- Obesity Insight: Recognizing these methods might lead to more effective treatments for obesity that target particular feeding stages.
Origin: Baylor College of Medicine
The head performs the necessary actions to consume a meal when it is feeling thirsty.
Many of these methods are not well known, but a recent study by researchers at Baylor College of Medicine and the University of Texas Health Science Center in Houston found that brain wires and chemical messengers are involved in food introduction and food intake rules.
The results have an impact on the development of better treatments to treat obesity, a global epidemic.
” It’s also known that serotonin, a neurotransmitter in the mind, can reduce food intake. This finding led to the development of drugs that interact with norepinephrine or its receptors to manage food intake and obesity”, said related author , Dr. Yong Xu, teacher of , pediatrics , – nourishment and associate director of basic sciences at the , USDA/ARS Children’s Nutrition Research Center , at Baylor.
” However, some of these drugs have unwanted side effects, and they are no longer offered to patients. To improve drug design, there is a need to better understand how the brain regulates food intake.
The , Xu lab , and colleagues have been studying the role of serotonin on feeding control for quite a long time. In this study, they focused on a little-known component of the serotonin regulation of food intake.
They looked for brain regions and neurotransmitters that, when activated or unactivated, act appropriately to maintain a balanced diet of food.
” We asked, how can we leverage this system to regulate feeding”? Xu said.
The dorsal Raphe nucleus ( DRN ) in the middlebrain is where the majority of the serotonin is synthesized by neurons. The arcuate of the hypothalamus ( ARH) is one of the many brain regions that serotonin neurons in the DRN project to.
The team showed that the ARH circuit and two neurotransmitters, GABA and dopamine, play a key role in meal initiation.
” Working with animal models, we found that when the animals are hungry, serotonin-producing neurons in the DRN are inhibited by GABA and dopamine. This reduces the levels of serotonin in the brain, which allows the initiation of a meal”, Xu explained.
” As the animals feed and become satiety-free, the inhibitory signals on serotonin neurons are decreased, and more serotonin is created to impede feeding through ARH projections,” says the statement.
” What’s unique about this is that GABA and dopamine act synergistically , – , when both are present, serotonin neurons appear to be more inhibited than when only one of the neurotransmitters is present”, Xu said.
This research is significant because it advances our understanding of how the brain handles body weight and food, and specifically the roles of neurotransmitters in a particular feeding behavior phase, meal initiation. This information can be used to create more effective anti-obesity medications.
” Looking forward, we are interested in identifying signals that regulate the other phases of feeding”, Xu said.
Other contributors to this work include Kristine M. Conde, Huey Zhong Wong, Shuzheng Fang, Yongxiang Li, Meng Yu, Yue Deng, Qingzhuo Liu, Xing Fang, Mengjie Wang, Yuhan Shi, Olivia Z. Ginnard, Yuxue Yang, Longlong Tu, Hesong Liu, Hailan Liu, Na Yin, Jonathan C. Bean, Junying Han, Megan E. Burt, Sanika V. Jossy, Yongjie Yang, Qingchun Tong, Benjamin R. Arenkiel, Chunmei Wang and Yang He. The authors have affiliations with Houston’s University of Texas Health Science Center or Baylor College of Medicine.
Funding: This work was supported by USDA/CRIS ( grants 51000-064-01S, 3092-51000-062-04 ( B ) S), National Institutes of Health ( grants R01DK120858, F32DK134121, R01DK131446 ) and American Heart Association ( grant 23POST1030352 ).
About this news about hunger and neuroscience
Author: Taylor Barnes
Source: Baylor College of Medicine
Contact: Taylor Barnes – Baylor College of Medicine
Image: The image is credited to Neuroscience News
Original Research: Open access.
Yong Xu and colleagues ‘ study” Serotonin neurons integrate GABA and dopamine inputs to control meal initiation.” Metabolism
Abstract
GABA and dopamine inputs are integrated into serotonin neurons to control meal initiation.
With limited orally administered medications, obesity is a growing global health epidemic.
Serotonin (5-HT) is one neurotransmitter that is still a top target for new weight-loss medications, but research is still needed to understand how 5-HT is produced in the dorsal Raphe nucleus ( DRN ) and how it affects meal initiation.
Using an optogenetic feeding paradigm, we showed that the 5-HTDRN➔arcuate nucleus ( ARH) circuit plays a role in meal initiation.
Incorporating electrophysiology and ChannelRhodopsin-2-Assisted Circuit Mapping, we demonstrated that 5-HTDRN , neurons receive inhibitory input partially from GABAergic neurons in the DRN, and the 5-HT response can be enhanced by hunger.
Additionally, deletion of the GABAA , receptor subunit in 5-HT neurons inhibits meal initiation with no effect on the satiation process.
Finally, we demonstrated that the dopaminergic inputs via the dopamine receptor D2 contribute to enhancing the GABA-induced feeding response.
Thus, our results indicate that 5-HTDRN , neurons are inhibited by synergistic inhibitory actions of GABA and dopamine, for the initiation of a meal.
