The neuroscience of positive memory deficits in depression

Adults with unipolar depression typically show poor episodic memory for positive material, but the neuroscientific mechanisms responsible for this deficit have not been characterized. I suggest a simple hypothesis: weak memory for positive material in depression reflects disrupted communication betw...

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Main Author: Daniel Gerard Dillon
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-09-01
Series:Frontiers in Psychology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fpsyg.2015.01295/full
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spelling doaj-30e310f2851d4dacad1be4b31d131b3c2020-11-25T00:53:51ZengFrontiers Media S.A.Frontiers in Psychology1664-10782015-09-01610.3389/fpsyg.2015.01295158950The neuroscience of positive memory deficits in depressionDaniel Gerard Dillon0McLean HospitalAdults with unipolar depression typically show poor episodic memory for positive material, but the neuroscientific mechanisms responsible for this deficit have not been characterized. I suggest a simple hypothesis: weak memory for positive material in depression reflects disrupted communication between the mesolimbic dopamine pathway and medial temporal lobe (MTL) memory systems during encoding. This proposal draws on basic research showing that dopamine release in the hippocampus is critical for the transition from early- to late-phase long-term potentiation (LTP) that marks the conversion of labile, short-term memories into stable, long-term memories. Neuroimaging and pharmacological data from healthy humans paint a similar picture: activation of the mesolimbic reward circuit enhances encoding and boosts retention. Unipolar depression is characterized by anhedonia--loss of pleasure--and reward circuit dysfunction, which is believed to reflect negative effects of stress on the mesolimbic dopamine pathway. Thus, I propose that the MTL is deprived of strengthening reward signals in depressed adults and memory for positive events suffers accordingly. Although other mechanisms are important, this hypothesis holds promise as an explanation for positive memory deficits in depression.http://journal.frontiersin.org/Journal/10.3389/fpsyg.2015.01295/fullAnhedoniaDepressionHippocampusMemoryReward
collection DOAJ
language English
format Article
sources DOAJ
author Daniel Gerard Dillon
spellingShingle Daniel Gerard Dillon
The neuroscience of positive memory deficits in depression
Frontiers in Psychology
Anhedonia
Depression
Hippocampus
Memory
Reward
author_facet Daniel Gerard Dillon
author_sort Daniel Gerard Dillon
title The neuroscience of positive memory deficits in depression
title_short The neuroscience of positive memory deficits in depression
title_full The neuroscience of positive memory deficits in depression
title_fullStr The neuroscience of positive memory deficits in depression
title_full_unstemmed The neuroscience of positive memory deficits in depression
title_sort neuroscience of positive memory deficits in depression
publisher Frontiers Media S.A.
series Frontiers in Psychology
issn 1664-1078
publishDate 2015-09-01
description Adults with unipolar depression typically show poor episodic memory for positive material, but the neuroscientific mechanisms responsible for this deficit have not been characterized. I suggest a simple hypothesis: weak memory for positive material in depression reflects disrupted communication between the mesolimbic dopamine pathway and medial temporal lobe (MTL) memory systems during encoding. This proposal draws on basic research showing that dopamine release in the hippocampus is critical for the transition from early- to late-phase long-term potentiation (LTP) that marks the conversion of labile, short-term memories into stable, long-term memories. Neuroimaging and pharmacological data from healthy humans paint a similar picture: activation of the mesolimbic reward circuit enhances encoding and boosts retention. Unipolar depression is characterized by anhedonia--loss of pleasure--and reward circuit dysfunction, which is believed to reflect negative effects of stress on the mesolimbic dopamine pathway. Thus, I propose that the MTL is deprived of strengthening reward signals in depressed adults and memory for positive events suffers accordingly. Although other mechanisms are important, this hypothesis holds promise as an explanation for positive memory deficits in depression.
topic Anhedonia
Depression
Hippocampus
Memory
Reward
url http://journal.frontiersin.org/Journal/10.3389/fpsyg.2015.01295/full
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