抑郁症患者对积极材料记忆不良的神经科学假说

D. Dillon
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引用次数: 0

摘要

抑郁症会破坏情景记忆;与抑郁症相关的压力和过度的负面情绪在很大程度上是罪魁祸首。成年抑郁症患者反复回想负面情绪的倾向是有案可查的,这在该疾病的认知模型中占有显著地位。然而,只专注于增强对消极材料的记忆,忽略了一个事实,即抑郁会损害对积极情绪材料的记忆。导致这种积极记忆缺陷的神经机制尚不清楚,但来自非人类动物和健康成年人的数据提出了一个简单的假设。每天面对无数的输入,大脑已经进化出了区分信息的信号,以保留信息和安全丢弃信息。多巴胺的释放就是这样一个信号。当多巴胺撞击海马体中的受体时,它会触发一系列分子过程,加强突触之间的联系,巩固对多巴胺释放附近事件的记忆。因为多巴胺神经元对意外的、有益的事件(即高度兴奋的、积极的经历)做出强烈的反应,这种机制应该支持对积极经历的持久记忆。越来越多的文献将抑郁症与压力引起的中脑多巴胺神经元抑制联系起来。本章提出,抑郁症中的积极记忆缺陷反映了上述机制的失败:积极事件不会引起抑郁症成年人的强烈多巴胺反应,导致海马多巴胺受体激活减弱,突触强化受损,最终导致记忆力下降。本章详细介绍了这一建议,以评估其作为抑郁症积极记忆缺陷的解释的前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Neuroscientific Hypothesis Concerning Poor Memory for Positive Material in Depression
Depression can disrupt episodic memory; stress and excessive negative emotion associated with depressive illness are largely to blame. The tendency of depressed adults to repeatedly retrieve and elaborate on emotionally negative memories is well documented and figures prominently in the disorder’s cognitive models. Focusing exclusively on enhanced memory for negative material, however, misses the fact that depression impairs memory for emotionally positive material. The neural mechanisms responsible for this positive memory deficit are not well understood, but data from nonhuman animals and healthy adults suggest a simple hypothesis. Confronted daily with innumerable inputs, the brain has evolved signals that distinguish information to retain from information to safely discard. Dopamine release is such a signal. When dopamine impinges on receptors in the hippocampus, it triggers a sequence of molecular processes that strengthen the connection between synapses, solidifying memory for the events proximal to dopamine release. Because dopamine neurons fire robustly in response to unexpected, rewarding events (i.e., highly arousing, positive experiences), this mechanism should support lasting memories for positive experiences. A growing literature links depression to stress-induced inhibition of midbrain dopamine neurons. The chapter proposes that the positive memory deficit in depression reflect failure of the aforementioned mechanism: Positive events do not elicit robust dopamine responses in depressed adults, leading to weak activation of hippocampal dopamine receptors, compromised synaptic strengthening, and—ultimately—poor memory. The chapter presents this proposal in detail to evaluate its promise as an explanation for positive memory deficits in depression.
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