Scientists at the Max Planck Institute for Biological Intelligence have made a significant breakthrough in understanding how the brain regulates appetite, especially in conditions of nausea. This discovery could improve our understanding of eating disorders and other conditions involving dysregulated eating behaviors, reports SciTech Daily.
The study published in Cell Reports involved detailed experiments on mice and identified a specific group of nerve cells in the amygdala, a region of the brain normally associated with emotional responses. These cells are activated during episodes of nausea and actively suppress the desire to eat. Unlike other cells in the amygdala that inhibit appetite due to satiety, these newly discovered cells respond specifically to nausea.
These cells, when activated artificially, can prevent even hungry mice from eating. On the other hand, deactivating these cells allows mice to eat regardless of nausea. This suggests a direct and powerful control of eating behavior through these specific cells.
The research team also investigated the pathway by which these cells work. They found that when a rat feels nauseous, signals are sent to the brain that reach the amygdala, activating these cells. These cells then project their inhibitory signals to other brain areas, including the parabrachial nucleus, a key part of the brainstem involved in processing internal bodily states.
This finding contrasts with other appetite-related pathways in the amygdala, which interact mainly with nearby cells and are activated by fullness after eating. This distinction highlights the complexity of the brain's regulation of appetite, showing that the mechanisms regulating loss of appetite due to nausea are different from those activated by satiety.
The importance of this study lies not only in the elucidation of a critical brain function, but also in its potential implications for the treatment of eating disorders. Understanding the specific brain circuits that inhibit food intake under certain conditions could lead to more effective treatments for diseases in which appetite regulation is disturbed.
