Circuits Regulating Pleasure and Happiness-Mechanisms of Depression.
Circuits Regulating Pleasure and Happiness-Mechanisms of Depression.
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DOI：
10.3389/fnhum.2016.00571
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发表时间：
2016
影响因子：
2.9
通讯作者：
Ivanova SA
中科院分区：
文献类型：
--
作者：
Loonen AJ;Ivanova SA
根据我们的食欲搜索与痛苦回避行为的调节模型，显示这些基本行为的动机是由两个平行的皮质-纹状体-丘脑-皮质，再进入回路，包括核心和壳部分的丘脑核，分别。从一侧的尾状核到另一侧的中央杏仁核的一系列基底神经节通过刺激（前）额叶和边缘皮质的活动来控制这些寻求奖励和逃避痛苦行为的强度。过度活跃的动机表现出可能导致奖励的行为，诱导渴望的感觉（救济导致快乐）。过度活跃的动机表现出与避免痛苦有关的行为，导致焦虑（救济导致幸福）。这两个系统以互惠的方式合作。在临床抑郁症中，这两个回路的活动之间存在不匹配：平衡被转移到避免痛苦的一侧。抑郁性心境障碍的发病机制主要有单胺学说、生物节律学说、神经内分泌学说、神经免疫学说和点燃/神经可塑性学说。本文描述了这些理论的关系模型（上述）的监管奖励寻求与痛苦避免行为。慢性应激导致的结构变化可能导致两个系统之间的不匹配。这种不匹配一方面导致缺乏快乐、精力不足和优柔寡断，另一方面导致烦躁不安、持续担忧和负面期望。单胺类、皮质醇和细胞因子的神经可塑性作用可能介导这些结构改变的诱导。长期暴露于压力的情况下（特别是在儿童时期经历的）可能会导致发展这种情况的易感性增加。这一假说为用心理疗法治疗抑郁症提供了可能性。遗传和其他生物因素（毒性、感染性或创伤性）可能会增加对相关神经可塑性变化诱导的敏感性。这些神经可塑性调节的恢复或补偿可以解释生物疗法治疗抑郁症的效果。
According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with psychotherapy. Genetic and other biological factors (toxic, infectious, or traumatic) may increase sensitivity to the induction of relevant neuroplastic changes. Reversal or compensation of these neuroplastic adjustments may explain the effects of biological therapies in treating depression.
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