First your brain makes you crave. Then it makes you eat
A recent study with rats on a cookie dough diet suggests the brain circuit that causes us to crave food may be separate from the one that makes us eat it.
Scientists are eager to understand why we eat when we’re not hungry—called non-homeostatic eating—and how it works in the brain.
“Non-homeostatic eating can be thought of as eating dessert after you’ve eaten an entire meal,” says Kyle Parker, a former grad student and investigator in the University of Missouri Bond Life Sciences Center. “I may know that I’m not hungry, but this dessert is delicious so I’m going to eat it anyway. We’re looking at what neural circuitry is involved in driving that behavior.”
Matthew J. Will, an associate professor of psychological sciences and Parker’s adviser, says for behavior scientists, eating is described as a two-step process called the appetitive and consummatory phases.
“I think of the neon sign for a donut shop—the logo and the aroma of warm glazed donuts are the environmental cues that kick start the craving, or appetitive, phase,” Will says. “The consummatory phase is after you have that donut in hand and eat it.”
Why the rats stopped binge eating
Parker studied the behavior patterns of laboratory rats by activating the brain’s pleasure center, a hotspot in the brain that processes and reinforces messages related to reward and pleasure. He then fed the rats a cookie dough-like diet to exaggerate their feeding behaviors and found that the rats ate twice as much as usual.
When he simultaneously inactivated another part of the brain called the basolateral amygdala, the rats stopped binge eating. They kept returning to their food baskets in search of more, but only consumed a normal amount.
“It seemed as if the rats still craved the dough,” Will says. “They kept going back for food but simply didn’t eat. We found that we had interrupted the part of the brain that’s specific to feeding—the circuit attached to actual eating—but not the craving. In essence, we left that craving intact.”
“It seemed as if the rats still craved the dough. They kept going back for food but simply didn’t eat.”
To find out what was happening in the brain during cravings, Parker set up a spin-off experiment. Like before, he switched on the region of the brain associated with reward and pleasure and inactivated the basolateral amygdala in one group of rats but not the other. This time, however, he limited the amount of the high fat diet the rats had access to so that both groups ate the same amount.
Outwardly, both groups of rats displayed the same feeding behaviors. They ate a portion of food, but kept going back and forth to their food baskets. However, inside the brain, Parker saw clear differences. Rats with activated nucleus accumbens showed increased dopamine neuron activity, which is associated with motivated approach behavior.
The team also found that the state of the basolateral amygdala had no effect on dopamine signaling levels. However, in a region of the brain called the hypothalamus, Parker saw elevated levels of orexin-A, a molecule associated with appetite, only in rats with activated basolateral amygdala.
“We showed that what could be blocking the consumption behavior is this block of the orexin behavior,” Parker says.
“The results reinforced the idea that dopamine is involved in the approach—or the craving phase—and orexin-A in the consumption,” Will says.
The team believes that these findings could lead to a better understanding of the different aspects of overeating and drug addiction. By revealing the independent circuitry of craving vs. the actual consumption or drug taking, this could lead to potential drug treatments that are more specific and have less unwanted side effects.
Their study was recently was published in Behavioral Neuroscience and funded in part by the National Institute of Drug Abuse.
Source: University of Missouri