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date: 23 October 2019

Abstract and Keywords

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.

Keywords: unipolar depression, emotional memory, episodic memory, cognitive theories of depression, interactions between mood and memory, hippocampus, consolidation, dopamine, reinforcement learning, incentive salience, anhedonia, long-term potentiation

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