|Alternative Title||Cognitive dysfunction and underlying neural basis in substance addiction|
|赵海潮1; 黄小路1; 何清华1,2|
As one of the most serious public health problems that extract a high toll on individuals and the society as a whole, substance abuse/addiction has attracted much attention from both researchers and the public. According to the DSM-5, substance addiction is a chronically relapsing psychiatric disorder that has been characterized by compulsion to seek and use drugs, loss of control in limiting intake despite serious negative consequences. However, more than 80% of the individuals with addiction fail to seek treatment, perhaps reflecting their cognitive function impairments. Previous studies have showed that most drugs of abuse exert their reinforcing effects and produce euphoria by inducing dopamine surges in limbic regions, which then have cascading effects on other neurotransmitter systems, leading to characteristic plastic adaptions; significant changes in neural circuits implicated in reward, attention, inhibitory control, decision making and interoception; and cognitive dysfunctions. However, much is still to be learned about the neural mechanisms involved in drugs' effects on cognitive functions and the vicious cycle of “drug abuse - withdrawal - recovery - relapse". For a better understanding of the causes of substance addiction and its underlying neural mechanisms, we provide an integrative review of behavioral and neuroimaging studies in substance addiction, introduce a neurobiological model of substance addiction, and finally propose future directions for research and clinical treatment. First, we summarize the research on the cognitive and neural mechanisms involved in substance addiction. (1) Drug-related cues can enhance the activities in the mesocorticolimbic system implicated in reward and drug motivation, which then result in increased attention to the drug-related stimuli. Thus, the neural changes in the frontolimbic system may be a potential neural basis for attentional bias toward drugs in individuals with addiction. (2) The deficit in inhibitory control typically observed in individuals with substance addiction may be due to a dysfunction in their prefrontal cortex-striatothalamic circuitry. (3) These individuals' poor decision making may be a product of an imbalance between three separate, but interacting, neural systems: the amygdala-striatum (an impulsive system); the prefrontal cortex (a reflective system); and the insula (the interoceptive system). (4) Emerging evidence shows that individuals with drug addiction have interoceptive processing deficits, perhaps due to dysfunctions in brain systems such as the insula and the anterior cingulate cortex. Second, we introduce a neurobiological model of substance addiction that depicts addiction as a result of an imbalance of six interactive circuits (i.e., reward, motivation/drive, memory, executive control, mood, and interoception). These brain circuits interact with one another to attain proper inhibitory control and hence good decision making. During addiction, however, the enhanced activities of six circuits (i.e., reward, motivation, memory, executive control, mood, and interoception) overwhelm the PFC's inhibitory control and hence lead to craving. Finally, we propose that future studies should (1) use multi-modal imaging techniques, (2) pay attention to comorbidity and clarify the association between addiction and other psychiatric disorders, (3) discover more biomarkers and optimize the diagnostic system using both behavioral and neuroimaging information, and (4) develop brain-based intervention techniques. Such studies should deepen our understanding of substance addiction and provide insights to its treatment.
|Keyword||物质成瘾 注意 抑制控制 决策 内感受|
|Funding Organization||国家自然科学基金 ; 中央高校基本科研业务费专项资金 ; 北京师范大学认知神经科学与学习国家重点实验室开放课题基金 ; 中国科学院心理健康重点实验室开放课题基金|
|Corresponding Author Affilication||Key Laboratory of Mental Health, CAS|
|赵海潮,黄小路,何清华. 物质成瘾所伴随的认知功能缺陷及其神经基础[J]. 科学通报,2016,61(34):3672-3683.|
|MLA||赵海潮,et al."物质成瘾所伴随的认知功能缺陷及其神经基础".科学通报 61.34(2016):3672-3683.|
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