Food reward in the absence of taste receptor signaling

被引:333
作者
de Araujo, Ivan E. [1 ,5 ]
Oliveira-Maia, Albino J. [1 ,6 ,7 ]
Sotnikova, Tatyana D. [4 ]
Gainetdinov, Raul R. [4 ]
Caron, Marc G. [4 ]
Nicolelis, Miguel A. L. [1 ,3 ,5 ]
Simon, Sidney A. [1 ,2 ,5 ]
机构
[1] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA
[3] Duke Univ, Med Ctr, Dept Biomed Engn, Durham, NC 27710 USA
[4] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA
[5] Duke Univ, Med Ctr, Ctr Neuroengn, Durham, NC 27710 USA
[6] Univ Porto, Inst Histol & Embriol, Fac Med, P-4200319 Oporto, Portugal
[7] Univ Porto, IBMC, Inst Cell & Mol Biol, P-4200319 Oporto, Portugal
关键词
D O I
10.1016/j.neuron.2008.01.032
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:930 / 941
页数:12
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