Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol

被引:6
作者
Bariselli, Sebastiano [1 ,2 ]
Lovinger, David M. [1 ]
机构
[1] NIAAA, Intramural Res Program, NIH, Bethesda, MD 20892 USA
[2] NIH, Ctr Compuls Behav, Bldg 10, Bethesda, MD 20892 USA
基金
瑞士国家科学基金会; 美国国家卫生研究院;
关键词
PRENATAL ETHANOL EXPOSURE; MEDIAL PREFRONTAL CORTEX; SPECTRUM DISORDERS; MOUSE MODEL; GABAERGIC INTERNEURONS; SYNAPTIC-TRANSMISSION; RESPONSE-INHIBITION; PROJECTION NEURONS; EXECUTIVE FUNCTION; LEARNING-DEFICITS;
D O I
10.1016/j.biopsych.2021.05.014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The term fetal alcohol spectrum disorder includes a group of diseases caused by fetal alcohol exposure (FAE). Patients with fetal alcohol spectrum disorder display heterogeneous socioemotional and cognitive deficits, particularly in the domain of executive function, that share symptoms with other neuropsychiatric disorders. Despite the availability of several preclinical models, the developmental brain defects causally linked to behavioral deficits induced by FAE remain poorly understood. Here, we first review the effects of FAE on corticostriatal development and its impact on both corticostriatal pathway function and cognitive abilities. We propose three non-mutually exclusive circuit models of corticostriatal dysfunctions to account for some of the FAE-induced cognitive deficits. One model posits that associative-sensorimotor imbalance causes hyper goal-directed behavior, and a second model implies that alteration of prefrontal-striatal behavioral suppression circuits results in loss of behavioral inhibition. A third model suggests that local striatal circuit deficits affect striatal neuronal ensemble function to impair action selection and performance. Finally, we discuss how preclinical approaches applied to these circuit models could offer potential rescue strategies for executive function deficits in patients with fetal alcohol spectrum disorder.
引用
收藏
页码:516 / 528
页数:13
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