D2 dopamine receptor gene polymorphism discriminates two kinds of novelty seeking

D2 dopamine receptor gene polymorphism discriminates two kinds of novelty seeking
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DOI:
10.1016/s0191-8869(01)00197-0
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发表时间:
2002-10-19
影响因子:
4.3
通讯作者:
Noble, EP
Noble, EP
中科院分区:
心理学3区
文献类型:
--
作者:
Berman, S;Ozkaragoz, T;Noble, EP

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Cloninger的人格心理生物学模型应用于物质滥用,得到了褒贬不一的支持。与该模型相反,最近的数据表明,高度追求新颖性(NS)和高度避免伤害(HA)的组合代表着严重物质滥用的发展的重大风险。对203名青春期男孩的D2多巴胺受体(DRD2)基因A1等位基因与NS和HA的关系进行了研究。具体地说,我们假设携带A1+等位基因(A1/A1和A1/A2基因)的受试者会报告更强的NS,并且与A1-等位基因(A2/A2基因)的受试者相比,NS与HA之间的关系更正。这些预测得到了支持。81例A1+等位基因男童NS与HA的相关性(r=0.27,P=0.02),122例A1+等位基因男童NS与HA的相关性(r=-0.15,P=0.09),表明这种关系因等位基因状态不同而不同(F=8.52,P<0:004)。在那些携带A1等位基因的人中,目前的结果与传统观点一致,即寻求新奇可以提供积极的强化,或满足食欲驱动。相比之下,那些携带A1+等位基因的人寻求新奇似乎包括一种负面的强化或自我调节功能。(C)2002爱思唯尔科学有限公司。保留所有权利。
Cloninger's psychobiological model of personality as applied to substance misuse has received mixed support. Contrary to the model, recent data suggest that a combination of high novelty seeking (NS) and high harm avoidance (HA) represents a significant risk for the development of severe substance misuse. A genetic polymorphism previously implicated in severe substance dependence, the A1 allele of the D2 dopamine receptor (DRD2) gene, was examined in relation to NS and HA amongst 203 adolescent boys. Specifically, we hypothesized that subjects with the A1 + allele (A1/A1 and A1/A2 genotypes) would report stronger NS and would exhibit a more positive relationship between NS and HA than those with the A1-allele (A2/A2 genotypes). These predictions were supported. The correlation between NS and HA in 81 A1 + allelic boys (r = 0.27, P = 0.02), and that in the 122 A1- allelic boys (r = -0.15, P = 0.09), indicated that this relationship differed according to allelic status (F = 8.52, P < 0:004). Among those with the A1-allele, the present results are consistent with the traditional view that novelty seeking provides positive reinforcement, or the fulfillment of appetitive drives. In contrast, novelty seeking in those with the A1 + allele appears to include a negative reinforcement or self-medicating function. (C) 2002 Elsevier Science Ltd. All rights reserved.