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An excitatory synapse hypothesis of depression
Open accessAbstract
Depression is a common cause of mortality and morbidity, but the biological bases of the deficits in emotional and cognitive processing remain incompletely understood. Current antidepressant therapies are effective in only some patients and act slowly. Here, we propose an excitatory synapse hypothesis of depression in which chronic stress and genetic susceptibility cause changes in the strength of subsets of glutamatergic synapses at multiple locations, including the prefrontal cortex (PFC), hippocampus, and nucleus accumbens (NAc), leading to a dysfunction of corticomesolimbic reward circuitry that underlies many of the symptoms of depression. This hypothesis accounts for current depression treatments and suggests an updated framework for the development of better therapeutic compounds.
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“It appears that increased strength of excitatory neurotransmission, in particular involving AMPARs, represents a common downstream target that is necessary for antidepressant efficacy among classical and rapid-acting antidepressants (Alt et al., 2006; Gould et al., 2019; Thompson et al., 2015).”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Thompson et al., 2015
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“Collectively, these patterns observed in human patients are consistent with the premise that neuronal and molecular plasticity deficits may feed forward to impairments in the coordinated function of prefrontal and limbic regions 66 , resulting in impaired PFC regulation and unchecked stimulus-driven responses to salient negative stimuli.”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [66]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Although stress-induced structural changes in the PFC are equally important in their contribution to the pathophysiology of neuropsychiatric conditions [256–262]”
From Development of prefrontal cortex (2022) · cites this paper as [259]
Experimental — accuracy not yet measuredIn the citing paper
“Conventional antidepressant therapeutics including selective serotonin reuptake inhibitors (SSRIs) or non-typical therapeutics, including ketamine and brain stimulation, may alleviate depression symptoms by acting on excitatory brain systems (33).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [33]
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“Stress-induced dysfunction in forebrain excitatory transmission has led to the development of the excitatory synaptic transmission hypothesis of depression (22, 32, 33).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [33]
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“As glutamate clearance modulates neuronal excitability [200] and glutamatergic synapse strength contributes to depression [202], how astrocytic glutamate clearance contributes to excitatory synapse strength and subsequent depressive behavior is also worth further investigation in the reward circuit.”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [202]
In the citing paper
“Indeed, a net result of all these processes is a sustained potentiation of excitatory synapses in cortico-mesolimbic brain circuits involved in the maintenance of mood and stress-reactivity 190.”
From Mechanisms of ketamine action as an antidepressant (2018) · cites this paper as [190]
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Metadata
- Authors
- Thompson, S. M., Kallarackal, A. J., Kvarta, M. D., Van Dyke, A. M., LeGates, T. A., & Cai, X.
- Affiliations
- University of Maryland, Baltimore (US)
- Southern Illinois University Carbondale (US)
- Corresponding author
- Thompson, Scott M.
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 38
- Issue
- 5
- Pages
- 279-294
- ISSN
- 0166-2236 (ISSN-L)
- PMC
- PMC4417609
- OpenAlex
- W2088861514
- Cited by
- 265
- References
- 203
- Citations by year
- 2026: 5 · 2025: 17 · 2024: 23 · 2023: 34 · 2022: 23 · 2021: 33 · 2020: 29 · 2019: 28 · 2018: 20 · 2017: 22 · 2016: 17 · 2015: 14
- FWCI
- 3.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (2t32ns063391-21)
- National Institute of Mental Health (R01MH086828)
- National Institute of General Medical Sciences (T32GM008181, T32GM092237)
- National Institute of Neurological Disorders and Stroke (T32NS007375, T32-NS063391)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- depression, glutamatergic synapses, chronic stress, genetic susceptibility, prefrontal cortex, hippocampus, nucleus accumbens, antidepressant treatment, synaptic plasticity
- MeSH terms
- Animals, Antidepressive Agents, Brain, Depression, Humans, Synapses, Excitatory Postsynaptic Potentials
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