Hungry? A Newly Discovered Neural Circuit May Be to Blame

Summary: Researchers have identified a subset of neurons in a region of the hypothalamus that play a critical role in regulating feeding and appetite in mice.

Source: AAAS.

A particular subset of neurons located in an enigmatic region of the hypothalamus plays a central role in regulating feeding and body weight in mice, a new study reveals. The results illuminate a previously unknown neural mechanism of feeding regulation and offer new perspectives on understanding changes in appetite.

Knowledge of the function of a region of the hypothalamus called the nucleus tuberalis lateralis, or NTL, is scarce, though scientists seek to better understand it as damage to this brain region in patients results in marked declines in appetite, and in rapid loss in body weight.

To further explore any role the NTL may have in regulation of feeding and body weight, Sarah Xinwei Luo and colleagues observed the behavior of somatostatin (SST) neurons in the NTL using a mouse model.

The authors found that the SST neurons were activated by both hunger (following overnight food deprivation) and after administration of the hunger hormone, ghrelin. Selective activation and deactivation of the neurons, using both drugs and optogenetics, demonstrated that eating behavior could be controlled – activation increased eating behavior, while inhibition significantly reduced it.

Total elimination of the neurons altogether resulted in decreased daily food intake as well as gradual weight gain.

a brain made of food icons

According to the study’s findings, SST neurons are required for controlling healthy eating and body weight. NeuroscienceNews.com image is in the public domain.

According to the study’s findings, SST neurons are required for controlling healthy eating and body weight.

In a related Perspective, Sabrina Diano notes that Luo et al.’s results are highly relevant – efforts to affect body weight and other physiological impairments associated with aberrant feeding behaviors, like obesity or anorexia nervosa, have been futile.

Despite the translational uncertainty between the neural circuitry of mice and humans, Luo et al.’s results are novel and warrant further investigation, says Diano.

About this neuroscience research article

Source: AAAS
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Regulation of feeding by somatostatin neurons in the tuberal nucleus” by Sarah Xinwei Luo, Ju Huang, Qin Li, Hasan Mohammad, Chun-Yao Lee, Kumar Krishna, Alison Maun-Yeng Kok, Yu Lin Tan, Joy Yi Lim, Hongyu Li, Ling Yun Yeow, Jingjing Sun, Miao He, Joanes Grandjean, Sreedharan Sajikumar, Weiping Han, and Yu Fu in Science. Published July 5 2018.
doi:10.1126/science.aar4983

Cite This NeuroscienceNews.com Article
AAAS”Hungry? A Newly Discovered Neural Circuit May Be to Blame.” NeuroscienceNews. NeuroscienceNews, 5 July 2018.
<http://neurosciencenews.com/sst-neurons-hunger-9520/>.
AAAS(2018, July 5). Hungry? A Newly Discovered Neural Circuit May Be to Blame. NeuroscienceNews. Retrieved July 5, 2018 from http://neurosciencenews.com/sst-neurons-hunger-9520/
AAAS”Hungry? A Newly Discovered Neural Circuit May Be to Blame.” http://neurosciencenews.com/sst-neurons-hunger-9520/ (accessed July 5, 2018).

Abstract

Regulation of feeding by somatostatin neurons in the tuberal nucleus

The tuberal nucleus (TN) is a surprisingly understudied brain region. We found that somatostatin (SST) neurons in the TN, which is known to exhibit pathological or cytological changes in human neurodegenerative diseases, play a crucial role in regulating feeding in mice. GABAergic tuberal SST (TNSST) neurons were activated by hunger and by the hunger hormone, ghrelin. Activation of TNSST neurons promoted feeding, whereas inhibition reduced it via projections to the paraventricular nucleus and bed nucleus of the stria terminalis. Ablation of TNSST neurons reduced body weight gain and food intake. These findings reveal a previously unknown mechanism of feeding regulation that operates through orexigenic TNSST neurons, providing a new perspective for understanding appetite changes.

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