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奖赏环路是脑内边缘系统的一部分,而奖赏系统则是愉快体验的核心,它可以促进人的学习,刺激和趋避行为.但奖赏系统的作用不仅局限于体验愉快,它同时也调节着人的认知与动机[1]. 弥散张量成像(Diffusion Tensor Imaging, DTI)由Basser等[2]在1996年首次提出,是目前唯一能在活体人脑组织的研究脑白质的非侵入性手段.DTI技术通过对水分子的自由热运动的各向异性进行量化分析,利用彩色图像显示白质纤维束的走行、方向、排列、紧密度、髓鞘化情况等信息[3],可以间接评价大脑白质纤维的完整性.DTI成像参数主要有两个:各向异性分数(Fractional Anisotropy,FA),反映细胞膜的完整性,受白质通道的调节,对纤维束的方向及一致性更加敏感;平均弥散率(Mean Diffusivity, MD),反映分子整体的弥散水平(平均椭球的大小)和弥散阻力的整体情况,MD越大,弥散阻力越大,信号传递速度越慢.本文对最近关于重性抑郁障碍(Major Depressive Disorder,MDD)奖赏环路的DTI的研究结果进行如下综述.  相似文献
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Background

Anhedonia, the diminished ability to experience pleasure, is an important dimensional entity linked to depression, schizophrenia, and other emotional disorders, but its origins and mechanisms are poorly understood. We have previously identified anhedonia, manifest as decreased sucrose preference and social play, in adolescent male rats that experienced chronic early-life adversity/stress (CES). Here we probed the molecular, cellular, and circuit processes underlying CES-induced anhedonia and tested them mechanistically.

Methods

We examined functional brain circuits and neuronal populations activated by social play in adolescent CES and control rats. Structural connectivity between stress- and reward-related networks was probed using high-resolution diffusion tensor imaging, and cellular/regional activation was probed using c-Fos. We employed viral-genetic approaches to reduce corticotropin-releasing hormone (Crh) expression in the central nucleus of the amygdala in anhedonic rats, and tested for anhedonia reversal in the same animals.

Results

Sucrose preference was reduced in adolescent CES rats. Social play, generally considered an independent measure of pleasure, activated brain regions involved in reward circuitry in both control and CES groups. In CES rats, social play activated Crh-expressing neurons in the central nucleus of the amygdala, typically involved in anxiety/fear, indicating aberrant functional connectivity of pleasure/reward and fear circuits. Diffusion tensor imaging tractography revealed increased structural connectivity of the amygdala to the medial prefrontal cortex in CES rats. Crh-short hairpin RNA, but not control short hairpin RNA, given into the central nucleus of the amygdala reversed CES-induced anhedonia without influencing other emotional measures.

Conclusions

These findings robustly demonstrate aberrant interactions of stress and reward networks after early-life adversity and suggest mechanistic roles for Crh-expressing amygdala neurons in emotional deficits portending major neuropsychiatric disorders.  相似文献
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