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Ventral Striatum
The olfactory tubercle and nucleus accumbens of the ventral striatum.
Details
Part ofBasal ganglia
Reward system
PartsOlfactory Tubercle
Nucleus Accumbens
Identifiers
LatinStriatum
Anatomical terms of neuroanatomy

Ventral Striatum

The ventral striatum (from Latin, 'striatus' meaning 'striped), is a subcortical brain region which regulates the limbic functions of reward expectation, motivation, and reward perception[1]. By monitoring the subjective value of stimuli, it tracks the outcomes of both reward and adverse experience predictions and tracks errors made in those predictions. Whereas the dorsal striatum mediates flexible or automated motor actions, the ventral striatum mediates motivation, learning and mood[2]. The ventral striatum is directly involved in emotional regulation, particularly when regulating responses to rewarding stimuli in addiction behaviours[3]. It plays a vital role in reinforcement learning, which is to learn associations between stimulus choices that yield rewards[4]. This role extends to making moral judgements about co-operative conspecifics[5].


Anatomy

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The ventral striatum is a conglomeration of several brain areas. It consists of the main part of the olfactory tubercle, a multi-sensory processing centre[6], and the nucleus accumbens, which is innervated with dopamine when we experience reward and reinforcement[7]. It also encompasses the continuity between the caudate nucleus and putamen, ventral to the rostral internal capsule[8]. The internal capsule, a white matter tract, is overlaid with strands of grey matter between the caudate and putamen, creating a striped appearance; hence the brain region receiving the Latin name 'striatum', meaning 'striped'.

Connections

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The ventral striatum receives afferent projections from various brain regions, including;

Efferent projections from the ventral striatum project to the lateral hypothalamus, ventral pallidum, globus pallidus and the substantia nigra[14]

Function

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The Mesolimbic Pathway

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The ventral striatum contains smaller and more densely packed dopaminergic neurons compared to its dorsal counterpart[15]. Dopamine neurons play a key role in the reward circuit, also known as the mesolimbic pathway[16]. The mesolimbic pathway is a dopaminergic projection from the ventral tegmental area to the nucleus accumbens of the ventral striatum[17]. The release of dopamine to the nucleus accumbens regulates motivational cognition, incentive salience, and reinforcement learning[18].

 
Diagram showing some of the main components of the mesolimbic ("reward") pathway. Dopaminergic projections are made to the nucleus accumbens, amygdala, hippocampus and prefrontal cortex.

Anticipation and evaluation of rewards

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The nucleus accumbens has been found to respond to the anticipation of positive gains, which is additionally correlated to self-reported predictions of financial or object gains[19]. Anticipation of loss has been found to be processed elsewhere, in the insula[20], suggesting that specifically the anticipation of positive gains is processed within the nucleus accumbens. This neural activity can also act as a predictor of an individual’s purchasing decisions; willingness to pay for a product has been found to correlate with activation in the nucleus accumbens[21].

Altruism

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Functional magnetic resonance imaging evidence suggests observed differences in neural activity in the ventral striatum between participants can be used to predict an individual’s donation behaviours in charity-giving games[22]. Participants with larger ventral striatum activation responses when giving money to charity were more likely to give larger amounts of money to charity, even at their own financial expense. Altruistic behaviour was directly correlated to high neural responses in the ventral striatum.

Co-operation and reciprocity

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In the Prisoner’s Dilemma paradigm, individuals demonstrate increased neural activation in both the orbitofrontal cortex and the anteroventral striatum when reciprocating co-operative behaviour or experiencing mutual co-operation[23]. Anteroventral striatum activity was specifically activated for conspecific interactions and did not occur in trials vs computer opponents. Neural activity was also compared to a control condition where participants received a free reward, and found the act of co-operation significantly enhanced these reward processing regions. The study suggests we feel more rewarded when obtaining rewards via mutually co-operative social interactions. More ventral striatum activity was correlated with an increased likelihood of continued co-operation, and deactivation of the anteroventral striatum occurred in both players when one of the players stopped co-operating.

The ability to determine who will reciprocate co-operation is vital in social interaction, and informs our decisions of whether to interact or avoid someone[24]. A study investigating the neural activity of this evaluation process found that activity in the amygdala, extending anteriorly into the ventral striatum (the right putamen and nucleus accumbens), is significantly increased when participants view the faces of those who had previously co-operated in social dilemma games[25].

Clinical Significance

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Addiction

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Neural alterations to ventral striatal circuitry form the basis of addictive disorders[26]. Over-expression of DeltaFosB (a splice variant of protein FosB) can be found in the D1-receptor neurons of the ventral striatum[27].

DeltaFosB is the most significant bio-molecular mechanism in addiction, as it causes alterations in gene expression in mesolimbic and mesocortical pathways. As a transcription factor, DeltaFosB transcribes genetic information in a cell from DNA into RNA, which ribosomes then translate into proteins. Over-expression of DeltaFosB in the nucleus accumbens causes over-production of GluR2 within the dopamine neuron. This temporarily stimulates the neuron and increases the sensitivity to the rewarding effects of addictive stimuli, particularly drug stimulants. GluR2 binds to AMPA receptors on the neuron, which are responsible for excitatory synaptic transmission. When AMPA receptors are blocked, it reduces calcium ion permeability and reduces the overall excitability in the D1-receptor neuron[28]. This results in the dopamine neuron eliciting reduced neuronal firing in the absence of the addictive stimuli.

Over-expression of DeltaFosB in the nucleus accumbens is responsible for the behavioural effects seen in addictive behaviours (such as administering drugs or seeking addictive stimuli)[29]. DeltaFosB is increasingly expressed in the nucleus accumbens when individuals repeatedly overdose on addictive drugs, or over-expose themselves to addictive stimuli.

Studies investigating the pre-frontal striatal pathways in nicotine addiction have demonstrated that as nicotine cravings decrease, activity in the dorso-lateral prefrontal cortex increases (which reflects control over habits and behaviour, via the deployment of cognitive strategies to regulate cravings), which in turn exerts a decrease in activity on the ventral striatum[30].

Dysfunction

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In rhesus macaques, lesions of the ventral striatum impaired learning of how to obtain rewards through selecting images[31]. However, the ability to select rewarding actions remained intact, suggesting the ventral striatum is primarily involved specifically in reinforcement learning.

Individuals with focal lesions affecting the ventral striatum demonstrated significant impairment in recognising signals of anger and aggression in others, compared to individuals with more dorsal basal ganglia lesions[32]. It is theorised that this failure to identify aggression reflects a deficiency in understanding behaviours that aim to procure, or protect, valued and/or contested resources.

Neuroimaging of individuals with obsessive-compulsive disorder found that increased connectivity of the ventral striatum, amygdala and ventromedial prefrontal cortex was correlated with aggressive symptoms, whilst increased connectivity in the ventral striatum and insula was indicative of intrusive sexual thoughts[33].

References

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  1. ^ O'Doherty, J., Dayan, P., Schultz, J., Deichmann, R., Friston, K., & Dolan, R. J. (2004). Dissociable roles of ventral and dorsal striatum in instrumental conditioning. science, 304(5669), 452-454.
  2. ^ Balleine, B. W., Delgado, M. R., & Hikosaka, O. (2007). The role of the dorsal striatum in reward and decision-making. Journal of Neuroscience, 27(31), 8161-8165.
  3. ^ Balodis, I. M., Kober, H., Worhunsky, P. D., Stevens, M. C., Pearlson, G. D., & Potenza, M. N. (2012). Diminished frontostriatal activity during processing of monetary rewards and losses in pathological gambling. Biological psychiatry, 71(8), 749-757.
  4. ^ Taswell, C. A., Costa, V. D., Murray, E. A., & Averbeck, B. B. (2018). Ventral striatum’s role in learning from gains and losses. Proceedings of the National Academy of Sciences, 115(52), E12398-E12406.
  5. ^ Fairley, K., Vyrastekova, J., Weitzel, U., & Sanfey, A. G. (2019). Subjective beliefs about trust and reciprocity activate an expected reward signal in the ventral striatum. Frontiers in Neuroscience, 13, 660.
  6. ^ Yamaguchi, M. (2017). Functional sub-circuits of the olfactory system viewed from the olfactory bulb and the olfactory tubercle. Frontiers in Neuroanatomy, 11, 33.
  7. ^ Ubeda-Bañon, I., Novejarque, A., Mohedano-Moriano, A., Pro-Sistiaga, P., de la Rosa-Prieto, C., Insausti, R., ... & Martinez-Marcos, A. (2007). Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli. BMC neuroscience, 8(1), 1-10.
  8. ^ Haber, S. N., & McFARLAND, N. R. (1999). The concept of the ventral striatum in nonhuman primates. Annals of the New York Academy of Sciences, 877(1), 33-48.
  9. ^ Haber, S. N. (2011). 11 neuroanatomy of reward: A view from the ventral striatum. Neurobiology of sensation and reward, 235.
  10. ^ Haber, S. N. (2011). 11 neuroanatomy of reward: A view from the ventral striatum. Neurobiology of sensation and reward, 235.
  11. ^ Giménez‐Amaya, J. M., McFarland, N. R., De Las Heras, S., & Haber, S. N. (1995). Organization of thalamic projections to the ventral striatum in the primate. Journal of Comparative Neurology, 354(1), 127-149.
  12. ^ Fudge, J. L., Kunishio, K., Walsh, P., Richard, C., & Haber, S. N. (2002). Amygdaloid projections to ventromedial striatal subterritories in the primate. Neuroscience, 110(2), 257-275.
  13. ^ Friedman, D. P., Aggleton, J. P., & Saunders, R. C. (2002). Comparison of hippocampal, amygdala, and perirhinal projections to the nucleus accumbens: combined anterograde and retrograde tracing study in the Macaque brain. Journal of Comparative Neurology, 450(4), 345-365.
  14. ^ Haber, S. N., & McFARLAND, N. R. (1999). The concept of the ventral striatum in nonhuman primates. Annals of the New York Academy of Sciences, 877(1), 33-48.
  15. ^ Haber, S. N. (2017). Anatomy and connectivity of the reward circuit. In Decision neuroscience (pp. 3-19). Academic Press.
  16. ^ Wise, R. A. (2002). Brain reward circuitry: insights from unsensed incentives. Neuron, 36(2), 229-240.
  17. ^ Telzer, E. H. (2016). Dopaminergic reward sensitivity can promote adolescent health: A new perspective on the mechanism of ventral striatum activation. Developmental cognitive neuroscience, 17, 57-67.
  18. ^ Hauser, T. U., Eldar, E., & Dolan, R. J. (2017). Separate mesocortical and mesolimbic pathways encode effort and reward learning signals. Proceedings of the National Academy of Sciences, 114(35), E7395-E7404.
  19. ^ Knutson, B., Fong, G. W., Bennett, S. M., Adams, C. M., & Hommer, D. (2003). A region of mesial prefrontal cortex tracks monetarily rewarding outcomes: characterization with rapid event-related fMRI. Neuroimage, 18(2), 263-272.
  20. ^ Paulus, M. P., & Stein, M. B. (2006). An insular view of anxiety. Biological psychiatry, 60(4), 383-387.
  21. ^ Knutson, B., Rick, S., Wimmer, G. E., Prelec, D., & Loewenstein, G. (2007). Neural predictors of purchases. Neuron, 53(1), 147-156.
  22. ^ Harbaugh, W. T., Mayr, U., & Burghart, D. R. (2007). Neural responses to taxation and voluntary giving reveal motives for charitable donations. Science, 316(5831), 1622-1625.
  23. ^ Rilling, J. K., Gutman, D. A., Zeh, T. R., Pagnoni, G., Berns, G. S., & Kilts, C. D. (2002). A neural basis for social cooperation. Neuron, 35(2), 395-405.
  24. ^ Cosmides, L., & Tooby, J. (2000). 87 The Cognitive Neuroscience of Social Reasoning.
  25. ^ Singer, T., Kiebel, S. J., Winston, J. S., Dolan, R. J., & Frith, C. D. (2004). Brain responses to the acquired moral status of faces. Neuron, 41(4), 653-662
  26. ^ Volkow, N. D., & Morales, M. (2015). The brain on drugs: from reward to addiction. Cell, 162(4), 712-725.
  27. ^ Robison, A. J., & Nestler, E. J. (2011). Transcriptional and epigenetic mechanisms of addiction. Nature reviews neuroscience, 12(11), 623-637.
  28. ^ Zhang, Y., Crofton, E. J., Li, D., Lobo, M. K., Fan, X., Nestler, E. J., & Green, T. A. (2014). Overexpression of DeltaFosB in nucleus accumbens mimics the protective addiction phenotype, but not the protective depression phenotype of environmental enrichment. Frontiers in behavioral neuroscience, 8, 297.
  29. ^ Robison, A. J., & Nestler, E. J. (2011). Transcriptional and epigenetic mechanisms of addiction. Nature reviews neuroscience, 12(11), 623-637.
  30. ^ Kober, H., Mende-Siedlecki, P., Kross, E. F., Weber, J., Mischel, W., Hart, C. L., & Ochsner, K. N. (2010). Prefrontal–striatal pathway underlies cognitive regulation of craving. Proceedings of the National Academy of Sciences, 107(33), 14811-14816.
  31. ^ Rothenhoefer, K. M., Costa, V. D., Bartolo, R., Vicario-Feliciano, R., Murray, E. A., & Averbeck, B. B. (2017). Effects of ventral striatum lesions on stimulus-based versus action-based reinforcement learning. Journal of Neuroscience, 37(29), 6902-6914.
  32. ^ Calder, A. J., Keane, J., Lawrence, A. D., & Manes, F. (2004). Impaired recognition of anger following damage to the ventral striatum. Brain, 127(9), 1958-1969.
  33. ^ Nakao, T., Okada, K., & Kanba, S. (2014). Neurobiological model of obsessive–compulsive disorder: Evidence from recent neuropsychological and neuroimaging findings. Psychiatry and clinical neurosciences, 68(8), 587-605.
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