“Nonhedonic” food motivation in humans involves dopamine in the dorsal striatum and methylphenidate amplifies this effect

Synapse - Tập 44 Số 3 - Trang 175-180 - 2002
Nora D. Volkow1,2, G. J. Wang1, Joanna S. Fowler1, Jean Logan1, Millard Jayne1, Dinko Franceschi1, Cristopher Wong1, S. John Gatley1, Andrew N. Gifford1, Yu‐Shin Ding1, Naomi Pappas1
1Brookhaven National Laboratory, Upton, New York 11973
2Department of Psychiatry, State University of New York at Stony Brook, Stony Brook, New York, 11794

Tóm tắt

AbstractThe drive for food is one of the most powerful of human and animal behaviors. Dopamine, a neurotransmitter involved with motivation and reward, its believed to regulate food intake in laboratory animals by modulating its rewarding effects through the nucleus accumbens (NA). Here we assess the involvement of dopamine in “nonhedonic” food motivation in humans. Changes in extracellular dopamine in striatum in response to nonhedonic food stimulation (display of food without consumption) were evaluated in 10 food‐deprived subjects (16–20 h) using positron emission tomography (PET) and [11C]raclopride (a D2 receptor radioligand that competes with endogenous dopamine for binding to the receptor). To amplify the dopamine changes we pretreated subjects with methylphenidate (20 mg p.o.), a drug that blocks dopamine transporters (mechanism for removal of extracellular dopamine). Although the food stimulation when preceded by placebo did not increase dopamine or the desire for food, the food stimulation when preceded by methylphenidate (20 mg p.o.) did. The increases in extracellular dopamine were significant in dorsal (P < 0.005) but not in ventral striatum (area that included NA) and were significantly correlated with the increases in self‐reports of hunger and desire for food (P < 0.01). These results provide the first evidence that dopamine in the dorsal striatum is involved in food motivation in humans that is distinct from its role in regulating reward through the NA. In addition it demonstrates the ability of methylphenidate to amplify weak dopamine signals. Synapse 44:175–180, 2002. © 2002 Wiley‐Liss, Inc.

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Synapse

Tập 44 Số 3

175-180

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