Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (639 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Collection of pleomorphic cells in the caudal part of the anterior horn of the lateral ventricle, in the region of the olfactory tubercle, lying between the head of the caudate nucleus and the anterior perforated substance. It is part of the so-called ventral striatum, a composite structure considered part of the basal ganglia.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Accumbens, Nucleus; Nucleus Accumbens Septi; Accumbens Septi, Nucleus; Accumbens Septus, Nucleus; Nucleus Accumbens Septus; Septi, Nucleus Accumbens; Septus, Nucleus Accumbens; Accumbens Nucleus.
Where it fits in the MeSH classification
- Broader topics
- Ventral Striatum
Related concepts
- Lateral Ventricle
- Olfactory Tubercle
- Caudate Nucleus
- Anterior Perforated Substance
- Ventral Striatum
- Basal Ganglia
Research landscape
PubMed indexes 13,595 records tagged with the MeSH heading “Nucleus Accumbens” (counts retrieved 2026-10-29). 2,533 of them (18.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 4,237 records.
Reviews account for 659 records (4.8%) and meta-analyses for 12. Randomized controlled trials number 65 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,557 |
| 2000-2009 | 3,268 |
| 2010-2019 | 4,237 |
| 2020 onward | 2,533 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 659 | 4.8% |
| Meta-analyses | 12 | 0.1% |
| Randomized controlled trials | 65 | 0.5% |
Method: PubMed query "Nucleus Accumbens"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Drugs of abuse hijack a mesolimbic pathway that processes homeostatic need | 2024 | Research article Design not recorded in structured metadata | 58 | cc by PMID 38669575 · DOI · PMC11077477 |
| Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure | 2024 | Research article Design not recorded in structured metadata | 56 | cc by PMID 38514654 · DOI · PMC10958053 |
| Dorsal hippocampus to nucleus accumbens projections drive reinforcement via activation of accumbal dynorphin neurons | 2024 | Research article Design not recorded in structured metadata | 40 | cc by PMID 38286800 · DOI · PMC10825206 |
| FGF21 analogue PF-05231023 on alcohol consumption and neuronal activity in the nucleus accumbens | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 40419727 · DOI · PMC12708781 |
Drugs of abuse hijack a mesolimbic pathway that processes homeostatic need [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Drugs of abuse are thought to promote addiction in part by "hijacking" brain reward systems, but the underlying mechanisms remain undefined.
- Closing excerpt
- These findings characterize the dynamic, molecular and circuit basis of a common reward pathway, wherein drugs of abuse interfere with the fulfillment of innate needs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (129 words)
Drugs of abuse are thought to promote addiction in part by "hijacking" brain reward systems, but the underlying mechanisms remain undefined. Using whole-brain FOS mapping and in vivo single-neuron calcium imaging, we found that drugs of abuse augment dopaminoceptive ensemble activity in the nucleus accumbens (NAc) and disorganize overlapping ensemble responses to natural rewards in a cell type-specific manner. Combining FOS-Seq, CRISPR-perturbation, and single-nucleus RNA sequencing, we identified Rheb as a molecular substrate that regulates cell type-specific signal transduction in NAc while enabling drugs to suppress natural reward consumption. Mapping NAc-projecting regions activated by drugs of abuse revealed input-specific effects on natural reward consumption. These findings characterize the dynamic, molecular and circuit basis of a common reward pathway, wherein drugs of abuse interfere with the fulfillment of innate needs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38669575 · DOI · PMC11077477
Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Accumulating evidence points to dysregulations of the Nucleus Accumbens (NAc) in eating disorders (ED), however its precise contribution to ED symptomatic dimensions remains unclear.
- Closing excerpt
- These results suggest that dysregulations of NAc dopaminoceptive neurons might be at the core of EDs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Accumulating evidence points to dysregulations of the Nucleus Accumbens (NAc) in eating disorders (ED), however its precise contribution to ED symptomatic dimensions remains unclear. Using chemogenetic manipulations in male mice, we found that activity of dopamine D1 receptor-expressing neurons of the NAc core subregion facilitated effort for a food reward as well as voluntary exercise, but decreased food intake, while D2-expressing neurons have opposite effects. These effects are congruent with D2-neurons being more active than D1-neurons during feeding while it is the opposite during running. Chronic manipulations of each subpopulations had limited effects on energy balance. However, repeated activation of D1-neurons combined with inhibition of D2-neurons biased behavior toward activity-related energy expenditure, whilst the opposite manipulations favored energy intake. Strikingly, concomitant activation of D1-neurons and inhibition of D2-neurons precipitated weight loss in anorexia models. These results suggest that dysregulations of NAc dopaminoceptive neurons might be at the core of EDs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38514654 · DOI · PMC10958053
Dorsal hippocampus to nucleus accumbens projections drive reinforcement via activation of accumbal dynorphin neurons [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The hippocampus is pivotal in integrating emotional processing, learning, memory, and reward-related behaviors.
- Closing excerpt
- Our findings unveil a pathway governing reinforcement, advancing our understanding of the hippocampal circuity's role in reward-seeking behaviors.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
The hippocampus is pivotal in integrating emotional processing, learning, memory, and reward-related behaviors. The dorsal hippocampus (dHPC) is particularly crucial for episodic, spatial, and associative memory, and has been shown to be necessary for context- and cue-associated reward behaviors. The nucleus accumbens (NAc), a central structure in the mesolimbic reward pathway, integrates the salience of aversive and rewarding stimuli. Despite extensive research on dHPC→NAc direct projections, their sufficiency in driving reinforcement and reward-related behavior remains to be determined. Our study establishes that activating excitatory neurons in the dHPC is sufficient to induce reinforcing behaviors through its direct projections to the dorso-medial subregion of the NAc shell (dmNAcSh). Notably, dynorphin-containing neurons specifically contribute to dHPC-driven reinforcing behavior, even though both dmNAcSh dynorphin- and enkephalin-containing neurons are activated with dHPC stimulation. Our findings unveil a pathway governing reinforcement, advancing our understanding of the hippocampal circuity's role in reward-seeking behaviors.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38286800 · DOI · PMC10825206
FGF21 analogue PF-05231023 on alcohol consumption and neuronal activity in the nucleus accumbens [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Fibroblast growth factor 21 (FGF21) is a liver-derived hormone known to suppress alcohol consumption in mice and non-human primates.
- Closing excerpt
- Mechanistically, the observed reductions in alcohol consumption following PF-05231023 may involve diminished alcohol palatability and modulation of neuronal activity from distinct subsets of Acb neurons.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (213 words)
Fibroblast growth factor 21 (FGF21) is a liver-derived hormone known to suppress alcohol consumption in mice and non-human primates. However, the role of FGF21 in modulating environmental and behavioural factors driving alcohol consumption-such as cue-driven responses and effortful actions to obtain alcohol-and its effects on neural activity related to consumption, remain unclear. Here, we evaluated the impact of PF-05231023, a long-acting FGF21 analogue, across multiple dimensions of alcohol consumption and motivation and examined consumption-related activity in the nucleus accumbens. PF-05231023 reduced alcohol intake and preference in a dose- and sex-specific manner; diminished approach behaviours following an alcohol but not sucrose cue; and decreased lever-pressing under a progressive-ratio schedule, both alone and when combined with the Glucagon-like peptide-1 (GLP-1) agonist Exendin-4; it did not reduce lever-pressing for sucrose in alcohol-naïve mice. Additionally, PF-05231023 altered the microstructure of alcohol consumption by shortening drinking bouts and increased the recruitment of nucleus accumbens (Acb) neurons associated with bout termination as determined by micro-endoscopy of GCaMP7f. These findings demonstrate that PF-05231023 broadly suppresses alcohol-motivated behaviours without impacting natural reward and that targeting FGF21 signaling in combination with GLP-1 agonists may enhance therapeutic efficacy. Mechanistically, the observed reductions in alcohol consumption following PF-05231023 may involve diminished alcohol palatability and modulation of neuronal activity from distinct subsets of Acb neurons.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40419727 · DOI · PMC12708781
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The mysterious motivational functions of mesolimbic dopamine [5]
- Research article The nucleus accumbens: an interface between cognition, emotion, and action [6]
- Research article Nucleus accumbens shell and core dopamine: differential role in behavior and addiction [7]
- Research article Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits [8]
- Research article Mesolimbocortical and nigrostriatal dopamine responses to salient non-reward events [9]
- Research article Dopamine and drug addiction: the nucleus accumbens shell connection [10]
References
- Tan B, Browne CJ, Nöbauer T, Vaziri A, Friedman JM, Nestler EJ. Drugs of abuse hijack a mesolimbic pathway that processes homeostatic need. . 2024. PMID 38669575 · DOI · PMC11077477
- Walle R, Petitbon A, Fois GR, Varin C, Montalban E, Hardt L, et al.. Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure. . 2024. PMID 38514654 · DOI · PMC10958053
- Ibrahim KM, Massaly N, Yoon HJ, Sandoval R, Widman AJ, Heuermann RJ, et al.. Dorsal hippocampus to nucleus accumbens projections drive reinforcement via activation of accumbal dynorphin neurons. . 2024. PMID 38286800 · DOI · PMC10825206
- Cooley BJ, Occelli Hanbury-Brown CV, Choi EA, Heller WA, Lim AW, Lawrence AJ, et al.. FGF21 analogue PF-05231023 on alcohol consumption and neuronal activity in the nucleus accumbens. . 2026. PMID 40419727 · DOI · PMC12708781
- Salamone JD, Correa M. The mysterious motivational functions of mesolimbic dopamine. Neuron. 2012. PMID 23141060 · DOI · PMC4450094
- Floresco SB. The nucleus accumbens: an interface between cognition, emotion, and action. Annu Rev Psychol. 2015. PMID 25251489 · DOI
- Di Chiara G. Nucleus accumbens shell and core dopamine: differential role in behavior and addiction. Behav Brain Res. 2002. PMID 12445717 · DOI
- Salamone JD, Correa M, Farrar A, Mingote SM. Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits. Psychopharmacology (Berl). 2007. PMID 17225164 · DOI
- Horvitz JC. Mesolimbocortical and nigrostriatal dopamine responses to salient non-reward events. Neuroscience. 2000. PMID 10727783 · DOI
- Di Chiara G, Bassareo V, Fenu S, De Luca MA, Spina L, Cadoni C, et al.. Dopamine and drug addiction: the nucleus accumbens shell connection. Neuropharmacology. 2004. PMID 15464140 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.