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Rats With Part of Brain Deactivated Move Toward Food But Do Not Eat

Date:
September 9, 2009
Source:
University of Missouri-Columbia
Summary:
Using an animal model of binge eating, researchers discovered that deactivating the basolateral amygdala, a brain region involved in regulating emotion, specifically blocked consumption of a fatty diet. Surprisingly, it had no effect on the rat wanting to look for the food repeatedly.

Scientists led a rat to fatty food, but they couldn’t make it eat. Using an animal model of binge eating, University of Missouri researchers discovered that deactivating the basolateral amygdala, a brain region involved in regulating emotion, specifically blocked consumption of a fatty diet. Surprisingly, it had no effect on the rat wanting to look for the food repeatedly.
Credit: iStockphoto/Larysa Dodz

Scientists led a rat to the fatty food, but they couldn’t make it eat. Using an animal model of binge eating, University of Missouri researchers discovered that deactivating the basolateral amygdala, a brain region involved in regulating emotion, specifically blocked consumption of a fatty diet. Surprisingly, it had no effect on the rat wanting to look for the food repeatedly.

“It appears that two different brain circuits control the motivation to seek and consume,” said Matthew Will, assistant professor of psychological sciences in the MU College of Arts and Science and investigator in the Christopher S. Bond Life Sciences Center. “Understanding how this circuit in the brain works may provide insight into the exact networks and chemicals in our brain that determine the factors influencing our feeding habits.”

The release of opioids, pleasure chemicals that can lead to euphoria, into the brain produces binge eating in non-hungry rats. Will and his team of researchers determined that deactivating the basolateral amygdala blocked this type of binge eating.

“A key to curbing the obesity epidemic in America is controlling the desire to binge eat,” Will said. “Humans have more programming to start and continue eating than to stop eating, especially when they have a bowl of ice cream in front of them. Most of us would finish it even if we weren’t hungry.”

Deactivating the basolateral amygdala had no effect on feeding in rats that were simply deprived of food for 24 hours. This suggests that the basolateral amygdala is specifically involved in the overconsumption of food based on its palatability or pleasure driven by opioids, rather than the level of hunger.

“The finding that the basolateral amygdala only appears involved in the opioid produced consumption was the most surprising part of the study,” Will said. “Normally, if a rat stops eating, they will go lay down and take it easy. In this case, they showed all signs of still wanting to eat, but didn’t.”

In the past when food availability was scarce, humans may have needed this “binge eating” regulation to eat enough food when it was available. Now, when humans have access to foods high in sugar and fat 24 hours a day, this regulation can cause humans to overeat.


Story Source:

The above story is based on materials provided by University of Missouri-Columbia. Note: Materials may be edited for content and length.


Journal Reference:

  1. Will et al. Behavioral characterization of amygdala involvement in mediating intra-accumbens opioid-driven feeding behavior.. Behavioral Neuroscience, 2009; 123 (4): 781 DOI: 10.1037/a0016060

Cite This Page:

University of Missouri-Columbia. "Rats With Part of Brain Deactivated Move Toward Food But Do Not Eat." ScienceDaily. ScienceDaily, 9 September 2009. <www.sciencedaily.com/releases/2009/09/090908151334.htm>.
University of Missouri-Columbia. (2009, September 9). Rats With Part of Brain Deactivated Move Toward Food But Do Not Eat. ScienceDaily. Retrieved April 18, 2014 from www.sciencedaily.com/releases/2009/09/090908151334.htm
University of Missouri-Columbia. "Rats With Part of Brain Deactivated Move Toward Food But Do Not Eat." ScienceDaily. www.sciencedaily.com/releases/2009/09/090908151334.htm (accessed April 18, 2014).

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