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Neuron. 2008 Mar 27;57(6):930-41. doi: 10.1016/j.neuron.2008.01.032.

Food reward in the absence of taste receptor signaling.

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  • 1Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. iaraujo@jbpierce.org

Erratum in

  • Neuron. 2008 Apr 24;58(2):295.

Abstract

Food palatability and hedonic value play central roles in nutrient intake. However, postingestive effects can influence food preferences independently of palatability, although the neurobiological bases of such mechanisms remain poorly understood. Of central interest is whether the same brain reward circuitry that is responsive to palatable rewards also encodes metabolic value independently of taste signaling. Here we show that trpm5-/- mice, which lack the cellular machinery required for sweet taste transduction, can develop a robust preference for sucrose solutions based solely on caloric content. Sucrose intake induced dopamine release in the ventral striatum of these sweet-blind mice, a pattern usually associated with receipt of palatable rewards. Furthermore, single neurons in this same ventral striatal region showed increased sensitivity to caloric intake even in the absence of gustatory inputs. Our findings suggest that calorie-rich nutrients can directly influence brain reward circuits that control food intake independently of palatability or functional taste transduction.

Comment in

  • Tasteless food reward. [Neuron. 2008]
PMID:
18367093
[PubMed - indexed for MEDLINE]
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