Cited by 290Neuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on BehaviorMemory and Neural Mechanisms

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Reward behaviour is regulated by the strength of hippocampus–nucleus accumbens synapses

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LeGates, Tara A., Kvarta, Mark D., Tooley, Jessica R., Francis, T. Chase, Lobo, Mary Kay, Creed, Meaghan C., Thompson, Scott M.·2018·Nature

DOI 10.1038/s41586-018-0740-8PMC PMC6292781

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Abstract

Reward drives motivated behaviours and is essential for survival, and therefore there is strong evolutionary pressure to retain contextual information about rewarding stimuli. This drive may be abnormally strong, such as in addiction, or weak, such as in depression, in which anhedonia (loss of pleasure in response to rewarding stimuli) is a prominent symptom. Hippocampal input to the shell of the nucleus accumbens (NAc) is important for driving NAc activity 1,2 and activity-dependent modulation of the strength of this input may contribute to the proper regulation of goal-directed behaviours. However, there have been few robust descriptions of the mechanisms that underlie the induction or expression of long-term potentiation (LTP) at these synapses, and there is, to our knowledge, no evidence about whether such plasticity contributes to reward-related behaviour. Here we show that high-frequency activity induces LTP at hippocampus-NAc synapses in mice via canonical, but dopamine-independent, mechanisms. The induction of LTP at this synapse in vivo drives conditioned place preference, and activity at this synapse is required for conditioned place preference in response to a natural reward. Conversely, chronic stress, which induces anhedonia, decreases the strength of this synapse and impairs LTP, whereas antidepressant treatment is accompanied by a reversal of these stress-induced changes. We conclude that hippocampus-NAc synapses show activity-dependent plasticity and suggest that their strength may be critical for contextual reward behaviour.

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The reward integrator
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Self-citation
Glutamatergic projections from ventral hippocampus to nucleus accumbens cholinergic neurons are altered in a mouse model of depressionPreprint
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Authors: LeGates, T. A., Kvarta, M. D., Tooley, J. R., Francis, T. C., Lobo, M. K., Creed, M. C., & Thompson, S. M.
Affiliations: University of Maryland, Baltimore (US)
Corresponding author: Thompson, Scott M.
ORCID: LeGates, Tara A.
Kvarta, Mark D.
Tooley, Jessica R.
Francis, T. Chase
Lobo, Mary Kay
Creed, Meaghan C.
Thompson, Scott M.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2018-11-26
Volume: 564
Issue: 7735
Pages: 258-262
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/s41586-018-0740-8
PMC: PMC6292781
OpenAlex: W2900803145
Cited by: 290
References: 23
Citations by year: 2026: 36 · 2025: 33 · 2024: 41 · 2023: 36 · 2022: 41 · 2021: 45 · 2020: 25 · 2019: 30 · 2018: 1
FWCI: 11.49
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: National Institute of Mental Health (R01MH106500, R01MH086828)
National Institute on Drug Abuse (R01DA038613)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords: hippocampus, nucleus accumbens, long-term potentiation, synaptic plasticity, conditioned place preference, anhedonia, chronic stress, antidepressant treatment, goal-directed behavior
MeSH terms: Animals, Chronic Disease, Conditioning, Psychological, Dopamine, Female, Goals, Hippocampus, Male, Neuronal Plasticity, Nucleus Accumbens, Reward, Stress, Psychological, Synapses, Long-Term Potentiation, Mice, Anhedonia

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Reward behaviour is regulated by the strength of hippocampus–nucleus accumbens synapses

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