New research finds that this scenario involves a fight between two neighboring groups of brain cells in which the brain’s opioid system also plays a key role. The study, which is presented in the Proceedings of the National Academy of Sciences , was conducted in mice, but scientists believe the findings will help us better understand similar mechanisms in humans.
“Our work shows that satiety signals are not powerful enough to work against the strong urge to eat, which has strong evolutionary value,” explains Huda Akil, a neuroscientist in the Department of Psychiatry at the Institute for Molecular and Behavioral Neuroscience. the University of Michigan and leader of the work.
The researchers focused on two small groups of adjacent nerve cells in the hypothalamus , which is a small region of the brain that is involved in various functions, such as controlling “motivated behaviors.”
The two cell groups are called pro-opiomelanocortin (POMC) and r-agouti protein (AgRP). They reside in a region of the hypothalamus known as the arcuate nucleus (Arch).
Scientists already knew that the two groups and the arcuate nucleus were somehow involved in “feeding control.”
In fact, in previous work, some team members had already revealed that, upon receiving certain signals, POMC neurons act “like a brake” when eating and AgRP neurons act like the accelerator pedal, especially when a long time has elapsed. since the last meal.
What was not clear, however, was how these two groups interacted. Optogenetics helped the researchers map the signals of this mechanism by using laser light to turn selected cells on and off in mice that were overeating.
They revealed that when they activated the POMC cells, this also activated the nearby AgRP cells, which meant that the accelerator pedal and the power brake were connected at the same time, and the result was that the accelerator pedal won the battle.
“When both are stimulated at the same time, AgRP takes the cake,” explains Akil.
Using a different optogenetic method, the scientists saw that they could trigger POMC cells without activating nearby AgRP cells. This led to a rapid and “significant” decrease in the mice’s intake.
The role of the opioid system
In another series of experiments, the scientists found that activating AgRP also activated the brain’s pleasure center. Giving the rodents the opioid receptor blocker naloxone stopped this behavior.
“This suggests that the brain’s own endogenous opioid system may play an important role in the desire to eat beyond what is needed,” Akil notes.
These findings, however, suggest that brain circuits, or “neural systems,” also appear to play an important role, as they may be reacting to emotional, social, and perceptual cues in the face of overeating.
“There is a whole industry built that attracts you to eat, whether you need it or not, through visual cues, packaging, smells, emotional associations. People are hungry just by looking at them, and we need to study the neural signals involved in those attentions, the perceptual mechanisms that drive us to eat, “concludes Akil.
Reference: Uneven balance of power between hypothalamic peptidergic neurons in the control of feeding. Qiang Wei, David M. Krolewski, Shannon Moore, Vivek Kumar, Fei Li, Brian Martin, Raju Tomer, Geoffrey G. Murphy, Karl Deisseroth, Stanley J. Watson Jr., and Huda Akil PNAS published ahead of print 2018 https: / /doi.org/10.1073/pnas.1802237115 Proceedings of the National Academy of Sciences
