Since Aaron Beck proposed his cognitive model of depression, biased attention, biased processing, and biased rumination (different phases of biased cognition) have been considered as the key elements consistently linked with depression. Increasing evidence suggests that the functional failures in the “emotional processing system (EPS)” underlie the neurological foundation of the biased cognition of depression. Light therapy, a non-intrusive approach, exerts powerful effects on emotion and cognition and affects the activity, functional connectivity, and plasticity of multiple brain structures. Although numerous studies have reported its effectiveness in treating depression, the findings have not been integrated with Beck’s cognitive model and EPS, and the neurobiological mechanisms of antidepressant light therapy remain largely unknown. In this review, integrated with the classical theories of Beck’s cognitive model of depression and EPS, we identified the key neural circuits and abnormalities involved in the cognitive bias of depression and, accordingly, identified and depicted several light-sensitive circuits (LSCs, neural circuits in the EPS that are responsive to light stimulation) that may underlie the antidepressant neural targets of light therapy, as listed below:

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Retina (rods/cones)–thalamic regions (LGN, pulvinar, and SC)–visual cortex.

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ipRGCs hypothalamic (SCN, PVN, DMH, SPVZ, LH)–preoptic areas (DMH–VLPO)–brainstem (DMH–LC)/other regions (pituitary and pineal gland).

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ipRGCs–limbic regions (LHb and amygdala).

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ipRGCs–thalamic regions (vLGN/IGL and OPN)–LHb.

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Thalamic region/brainstem region/hypothalamic region–amygdala, amygdala–mPFC–PFC, amygdala–ACC–PFC, brainstem (VTA/LC)–ACC–PFC.

In summary, the LSCs above narrow down the research scope of identifying the neural targets of antidepressant light therapy and help elucidate the neuropsychological mechanism of antidepressant light therapy.

自从 Aaron Beck 提出他的抑郁认知模型以来，偏向注意力、偏向处理和偏向沉思（偏向认知的不同阶段）一直被认为是与抑郁症相关的关键因素。越来越多的证据表明，“情绪处理系统（EPS）”的功能障碍是抑郁症偏见认知的神经基础。光疗法是一种非侵入性方法，对情绪和认知产生强大的影响，并影响多个大脑结构的活动、功能连接和可塑性。尽管许多研究报告了其治疗抑郁症的有效性，但这些发现并未与贝克的认知模型和 EPS 相结合，抗抑郁光疗法的神经生物学机制仍然很大程度上未知。

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视网膜（视杆/视锥细胞）-丘脑区域（LGN、丘脑和 SC）-视觉皮层。

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ipRGCs 下丘脑（SCN、PVN、DMH、SPVZ、LH）-视前区（DMH-VLPO）-脑干（DMH-LC）/其他区域（垂体和松果体）。

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ipRGCs-边缘区域（LHb 和杏仁核）。

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ipRGCs-丘脑区域（vLGN/IGL 和 OPN）-LHb。

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丘脑区/脑干区/下丘脑区-杏仁核、杏仁核-mPFC-PFC、杏仁核-ACC-PFC、脑干(VTA/LC)-ACC-PFC。

综上所述，上述LSCs缩小了识别抗抑郁光疗法神经靶点的研究范围，有助于阐明抗抑郁光疗法的神经心理学机制。