Department of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St, HSFII Building, Rm 265, Baltimore, MD, 21201, USA.
Sci Rep. 2020 Jul 24;10(1):12393. doi: 10.1038/s41598-020-69339-7.
Stress alters the structure and function of brain reward circuitry and is an important risk factor for developing depression. In the nucleus accumbens (NAc), structural and physiological plasticity of medium spiny neurons (MSNs) have been linked to increased stress-related and depression-like behaviors. NAc MSNs have opposing roles in driving stress-related behaviors that is dependent on their dopamine receptor expression. After chronic social defeat stress, NAc MSNs exhibit increased dendritic spine density. However, it remains unclear if the dendritic spine plasticity is MSN subtype specific. Here we use viral labeling to characterize dendritic spine morphology specifically in dopamine D2 receptor expressing MSNs (D2-MSNs). After chronic social defeat, D2-MSNs exhibit increased spine density that is correlated with enhanced social avoidance behavior. Together, our data indicate dendritic spine plasticity is MSN subtype specific, improving our understanding of structural plasticity after chronic stress.
压力改变了大脑奖励回路的结构和功能,是导致抑郁的重要风险因素。在伏隔核(NAc)中,中脑多巴胺神经元(MSNs)的结构和生理可塑性与应激相关和类似抑郁的行为增加有关。NAc MSNs 在驱动应激相关行为方面具有相反的作用,这取决于它们的多巴胺受体表达。慢性社会挫败应激后,NAc MSNs 的树突棘密度增加。然而,树突棘可塑性是否是 MSN 亚型特异性的仍不清楚。在这里,我们使用病毒标记来专门描述多巴胺 D2 受体表达的 MSNs(D2-MSNs)中的树突棘形态。慢性社会挫败后,D2-MSNs 的棘突密度增加,与增强的社交回避行为相关。总之,我们的数据表明树突棘可塑性是 MSN 亚型特异性的,这提高了我们对慢性应激后结构可塑性的理解。