Nucleus Accumbens

Anatomy

• At the ventral junction of the caudate head and putamen, lateral to the septum; the main component of the ventral striatum.
• Core and shell regions.
• Input: VTA (mesolimbic dopamine), vmPFC/OFC, amygdala, hippocampus. Output: ventral pallidum.
• Blood supply: lenticulostriate arteries, recurrent artery of Heubner.

Functions

• Reward anticipation and motivation (“wanting”, incentive salience).
• Reinforcement learning through reward prediction error (the VTA dopamine signal).
• Translating limbic information into motor action (the “limbic–motor interface”).
• Hedonic pleasure (opioidergic “hot spots” in the shell), social reward, placebo response.

Connections and chemistry

• VTA (mesolimbic dopamine pathway)
• vmPFC and OFC
• Amygdala and hippocampus
• Ventral pallidum → mediodorsal thalamus
• Dopamine, endogenous opioids, glutamate

Development

Developmental course through childhood and adolescence.

• In adolescence the accumbens response to reward is higher than in children and adults, while the OFC is still at a child-like level. Maturation of the reward circuit ahead of the control circuit may explain novelty seeking and risk taking (Galván et al., 2006; ages 7–29). B
• In the presence of peers, adolescents’ risk taking and ventral striatal activity increase (Chein et al., 2011).
• Pubertal hormones affect reward sensitivity.

Clinical

• Substance use disorders: adolescence is a particularly vulnerable period.
• ADHD: ventral striatal hypoactivation during reward anticipation (Plichta and Scheres, 2014), delay aversion. In adult ADHD, accumbens D2/3 levels relate to inattention and motivation (Volkow et al., 2009). B
• Depression and anhedonia: in 1,576 adolescents (IMAGEN), ventral striatal activity during reward anticipation was lower in depression. In healthy adolescents, low activity predicted transition to subthreshold or clinical depression within 2 years. The finding relates more to anhedonia than to low mood (Stringaris et al., 2015). A group-level marker, not an individual diagnostic tool. A
• Behavioral addictions (gaming disorder), conduct disorder.

Treatment

This region from the perspective of medication, psychotherapy and neuromodulation. Letter badges are evidence levels.

• Behavioral activation: systematically increases rewarding activities in anhedonia; a psychotherapy that works through the reward circuit.
• Stimulants and addiction risk: oral methylphenidate at therapeutic doses produces a slow dopamine rise, unlike the rapid rise that drives addiction.
• Deep brain stimulation (accumbens): in refractory OCD, Y-BOCS fell by 46% at 8 months in 16 adults, with 9 responders; a 25% difference vs sham stimulation (Denys et al., 2010). Adults only, a late-line option. C

Assessment

Neuropsychological tasks and measures that probe this region's function.

• Monetary Incentive Delay task (MID, fMRI)
• Effort–reward task (EEfRT), delay discounting
• Balloon Analogue Risk Task (BART)

Lesions and damage

Clinical findings expected with damage or dysfunction.

• Anhedonia, apathy, loss of motivation.
• A DBS target in adult refractory OCD and depression.

In the model

How this structure is defined in the 3D model, and the data source.

CerebrA accumbens area label.

References

Full citations for the card; links go to the paper (DOI) or a PubMed search.

1. Galván A et al. Earlier development of the accumbens relative to orbitofrontal cortex might underlie risk-taking behavior in adolescents. J Neurosci 2006;26(25):6885–6892. Search PubMed
2. Stringaris A et al. The brain's response to reward anticipation and depression in adolescence. Am J Psychiatry 2015;172(12):1215–1223. Search PubMed
3. Volkow ND et al. JAMA 2009. Search PubMed
4. Denys D et al. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder. Arch Gen Psychiatry 2010;67(10):1061–1068. Search PubMed