September 20th, 2012 in Medical research
Extracellular enkephalin levels surged when rats began to eat milk chocolate M&Ms. Onset of eating coincided with a robust increase in extracellular enkephalin (met and leu), which remained sustained during eating and gradually tapered off as eating declined. The magnitude of the enkephalin increase in individuals correlated with their latency to eat their first M&M: higher enkephalin increase for the fastest eaters.
Credit: Current Biology, DOI: 10.1016/j.cub. 2012.08.014
“This means that the brain has more extensive systems to make individuals want to overconsume rewards than previously thought,” said Alexandra DiFeliceantonio of the University of Michigan, Ann Arbor. “It may be one reason why overconsumption is a problem today.”
DiFeliceantonio’s team made the discovery by giving rats an artificial boost with a drug delivered straight to a brain region called the neostriatum. Those animals gorged themselves on more than twice the number of M&M chocolates than they would otherwise have eaten. The researchers also found that enkephalin, the natural drug-like chemical produced in that same brain region, surged when rats began to eat the candy-coated morsels, too.
It’s not that enkephalins or similar drugs make the rats like the chocolates more, the researchers say, but rather that the brain chemicals increase their desire and impulse to eat them.
The findings reveal a surprising extension of the neostriatum’s role, as DiFeliceantonio notes that the brain region had primarily been linked to movement. And there is reason to expect that the findings in rats can tell us a lot about our own binge-eating tendencies.
“The same brain area we tested here is active when obese people see foods and when drug addicts see drug scenes,” she says. “It seems likely that our enkephalin findings in rats mean that this neurotransmitter may drive some forms of overconsumption and addiction in people.”
The researchers now hope to unravel a related phenomenon that some of us might wish we could do more to control: what happens in our brains when we pass by our favorite fast food restaurant and feel that sudden desire to stop.
More information: DiFeliceantonio et al.: “Enkephalin surges in dorsal neostriatum as a signal to eat.” DOI: 10.1016/j.cub.2012.08.014
“Brain study reveals the roots of chocolate temptations.” September 20th, 2012. http://medicalxpress.com/news/2012-09-brain-reveals-roots-chocolate-temptations.html
Enkephalin surges in dorsal neostriatum as a signal to eat.
Current Biology, 20 September 2012
Copyright © 2012 Elsevier Ltd All rights reserved.
- Enkephalin surges in neostriatum are triggered by eating sweet rewards
- Intense eating is generated specifically by anteromedial part of dorsal neostriatum
- Neostriatum opioid stimulation causes more eating but not “liking” for sweetness
Compulsive overconsumption of reward characterizes disorders ranging from binge eating to drug addiction. Here, we provide evidence that enkephalin surges in an anteromedial quadrant of dorsal neostriatum contribute to generating intense consumption of palatable food. In ventral striatum, mu opioid circuitry contributes an important component of motivation to consume reward [1,2,3,4]. In dorsal neostriatum, mu opioid receptors are concentrated within striosomes that receive inputs from limbic regions of prefrontal cortex [5,6,7,8,9,10,11,12,13]. We employed advanced opioid microdialysis techniques that allow detection of extracellular enkephalin levels. Endogenous >150% enkephalin surges in anterior dorsomedial neostriatum were triggered as rats began to consume palatable chocolates. In contrast, dynorphin levels remained unchanged. Furthermore, a causal role for mu opioid stimulation in overconsumption was demonstrated by observations that microinjection in the same anterior dorsomedial quadrant of a mu receptor agonist ([D-Ala2, N-MePhe4, Gly-ol]-enkephalin; DAMGO) generated intense >250% increases in intake of palatable sweet food (without altering hedonic impact of sweet tastes). Mapping by “Fos plume” methods confirmed the hyperphagic effect to be anatomically localized to the anteromedial quadrant of the dorsal neostriatum, whereas other quadrants were relatively ineffective. These findings reveal that opioid signals in anteromedial dorsal neostriatum are able to code and cause motivation to consume sensory reward.