Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens

Bessa, J M; Morais, M; Marques, F; Pinto, L; Palha, J A; Almeida, O F X; Sousa, N

doi:10.1038/tp.2013.39

Cited by 130Treatment of Major DepressionNeurotransmitter Receptor Influence on BehaviorStress Responses and Cortisol

Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens

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Bessa, J M, Morais, M, Marques, F, Pinto, L, Palha, J A, Almeida, O F X, Sousa, N·2013·Translational Psychiatry

DOI 10.1038/tp.2013.39PMC PMC3693402

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Abstract

There is accumulating evidence that the nucleus accumbens (NAc) has an important role in the pathophysiology of depression. As the NAc is a key component in the neural circuitry of reward, it has been hypothesized that anhedonia, a core symptom of depression, might be related to dysfunction of this brain region. Neuronal morphology and expression of plasticity-related molecules were examined in the NAc of rats displaying anhedonic behavior (measured in the sucrose-consumption test) in response to chronic mild stress. To demonstrate the relevance of our measurements to depression, we tested whether the observed changes were sensitive to reversal with antidepressants (imipramine and fluoxetine). Data show that animals displaying anhedonic behavior display an hypertrophy of medium spiny neurons in the NAc and, in parallel, have increased expression of the genes encoding for brain-derived neurotrophic factor, neural cell adhesion molecule and synaptic protein synapsin 1. Importantly, the reversal of stress-induced anhedonia by antidepressants is linked to a restoration of gene-expression patterns and dendritic morphology in the NAc. Using an animal model of depression, we show that stress induces anhedonic behavior that is associated with specific changes in the neuronal morphology and in the gene-expression profile of the NAc that are effectively reversed after treatment with antidepressants.

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The contribution of other brain regions, such as the nucleus accumbens, cannot be excluded from this anhedonic resilience.
“However, the contribution of other brain regions, such as the nucleus accumbens, cannot be excluded of this anhedonic resilience, given the previous association between stress-induced anhedonia and medium spiny neurons”
From Adult hippocampal neuroplasticity triggers susceptibility to recurrent depression (2017) · cites this paper as [25]
CUS increases dendritic length of NAc core MSNs, which is reversed by imipramine or fluoxetine treatment.
“In contrast, CUS increases dendritic length of NAc core MSNs, which is reversed by imipramine or fluoxetine treatment [154].”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [154]

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Authors: Bessa, J. M., Morais, M., Marques, F., Pinto, L., Palha, J. A., Almeida, O. F. X., & Sousa, N.
Affiliations: University of Minho (PT)
Max Planck Institute of Psychiatry (DE)
Corresponding author: Sousa, N
ORCID: Bessa, J M
Morais, M
Marques, F
Pinto, L
Palha, J A
Almeida, O F X
Sousa, N
Venue: Translational Psychiatry
Publisher: Springer Science and Business Media LLC
Published: 2013-06-04
Volume: 3
Issue: 6
Pages: e266-e266
ISSN: 2158-3188 (ISSN-L)
DOI: 10.1038/tp.2013.39
PMC: PMC3693402
OpenAlex: W2109873631
Cited by: 130
References: 34
Citations by year: 2026: 5 · 2025: 6 · 2024: 7 · 2023: 7 · 2022: 9 · 2021: 9 · 2020: 17 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 10 · 2015: 12 · 2014: 13 · 2013: 1
FWCI: 8.83
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc-sa
www.springer.com/tdm (unspecified)
Locations: Translational Psychiatry (publishedVersion, cc-by-nc-sa)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
MPG.PuRe (Max Planck Society) (submittedVersion, cc-by-nc-sa)
Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, cc-by-nc-nd)
Funders: Fundação para a Ciência e a Tecnologia (PTDC/SAU-NEU/105180/2008)
Topics: Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: nucleus accumbens, medium spiny neurons, neuronal hypertrophy, chronic mild stress, depression, imipramine, fluoxetine, brain-derived neurotrophic factor, CD56, synapsin-1, dendritic morphology, gene expression, reward systems, sucrose intake
MeSH terms: Animals, Antidepressive Agents, Behavior, Animal, Fluoxetine, Hypertrophy, Imipramine, Male, Nucleus Accumbens, Stress, Psychological, Rats, Wistar, Rats, Anhedonia, Real-Time Polymerase Chain Reaction

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Stress-induced anhedonia is associated with hypertrophy of medium spiny neurons of the nucleus accumbens

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