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1 n, revealing a novel cellular pathway in the brain reward system.
2 for interaction between hypothalamus and the brain reward system.
3 ddition to during gestation, can program the brain reward system.
4 leus accumbens (NAc), a key component of the brain reward system.
5 ggested to be linked to a dysfunction of the brain reward system.
6 at results from contingent activation of the brain reward system.
7 together lead to altered homeostasis of the brain reward system.
8 easing neurons appear to be important in the brain reward system.
9 that ADX does not affect sensitivity of the brain reward system.
10 nd used to control prediction updates in the brain reward system.
11 (ICSS) test is sensitive to the function of brain reward systems.
12 hibitory effects of higher nicotine doses on brain reward systems.
13 lecular manipulations affect the function of brain reward systems.
14 nucleus accumbens (NAc), a key component of brain reward systems.
15 ion of dopaminergic neurotransmission in the brain reward systems.
16 tering dopaminergic neurotransmission in the brain reward systems.
17 ral tegmental area (VTA) are the origin of a brain reward system and are critically involved in drug
19 esis that insulin modulates sensitivity of a brain reward system and that hypoinsulinemia may be the
20 pioid system is widely known to modulate the brain reward system and thus affect the behavior of huma
21 tualized as a cycle of decreased function of brain reward systems and recruitment of antireward syste
23 icotine dependence, long-term alterations in brain reward systems, and nicotine receptor regulation i
25 mate signaling in pain states and define the brain reward system as an important region for the regul
26 to promote addiction in part by "hijacking" brain reward systems, but the underlying mechanisms rema
27 thermore, similar genetic vulnerabilities in brain reward systems can increase predisposition to drug
28 cond) cellular and chemical responses in the brain reward system during drug-seeking and drug-taking
30 hat addictive drugs often render an addict's brain reward system hypersensitive, leaving the individu
31 n order to evaluate the effect of ADX on the brain reward system in general, and cocaine reward in pa
32 partly from the inappropriate activation of brain reward systems in response to aggressive or violen
33 ed whether ADX decreases sensitivity of the 'brain reward system' in general, or its response to coca
34 tic effect via functional changes within the brain reward system, including the ventral striatum.
35 nt mechanism by which normal function of the brain reward system may be impaired during substance abu
36 ce for fatty foods, regulated in part by the brain reward system, may contribute to the development o
37 al tegmental area (VTA), the main hub of the brain reward system, remains only partially characterize
38 accumbens (nAc) is a critical region in the brain reward system since it integrates abundant synapti
39 a cycle of progressive dysregulation of the brain reward system that results in the compulsive use a
40 or miRNAs in drug-induced neuroplasticity in brain reward systems that drive the emergence of compuls
41 ed as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resul
42 ed activation in one of the core hubs of the brain reward system (the ventral striatum), better rewar
43 ltaFosB influences the responsiveness of the brain reward system to rewarding and aversive drugs.
44 evealing how social interactions can recruit brain reward systems to drive changes in affiliative beh
46 g psychostimulant-elicited plasticity in the brain reward system, we undertook a phenotype-driven app