Talk:Nucleus accumbens

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Core vs. Shell differences[edit]

I think it would be good if we detailed the differences in the core vs. the shell. Granted, the differences are usually pretty subtle, but since there's mention of it in the beginning, I think it's important we work on it. I have a really good review (32 pages of review) that would probably be a good starting place, but I'd like some help on this if possible. Maybe we could first look at the role of the shell vs core in addiction, as the shell experiences much higher levels of dopamine increase in response to addictive drugs, and is much more closely linked to rewarding effects of addictive drugs.

If anyone wants to look over the review as well, it's Nucleus accumbens shell and core dopamine: differential role in behavior and addiction by G. Chiara, Behavioral Brain Research. 2002.

Purple Blanket (talk) 03:54, 1 August 2011 (UTC)

Article ownership[edit]

Sorry, Mr. Ausaf A. Bari (Laboratory of Neuropsychopharmacology Boston University School of Medicine), but standard Wikipedia policy on article ownership states that no author is owned by any one party. If you'd like your attribution and be recognized as the main author of this page, you should Create an account and look into changing the attribution. Then your contribution will be visible via the page history, and you'll have a nice account as well. We do thank you for your work, and hope that you will contribute to Wikipedia. -- Fennec 01:37, 26 Mar 2004 (UTC)

Sentence fix[edit]

This sentence has no predicate:

The nucleus accumbens, striatum, and basal forebrain together for the ventral striatum. Rintrah 03:54, 17 July 2005 (UTC)
Thanks. This sentence is accurate, just poorly worded. It is now fixed. Semiconscious (talk · home) 04:20, 17 July 2005 (UTC)

Description of the Location of the Nucleus accumbens[edit]

I need a better one or just mark the area in the current picture thanks

Jan Girke 20:48, 23 March 2006 (UTC)

There's a good diagram here, a more detailed but less clear diagram here, and links to many more illustrations here. I've also added a second diagram, but it's very rough, and a little misleading, so if I were you I'd place greater faith in the links above. --Arcadian 01:28, 24 March 2006 (UTC)

Olds and Milner[edit]

I have just read the Olds and Milner study and although it does indicate that rats did repeatedly press a lever to stimulate part of its brain, it neither mentions the nucleus accumbens, nor does it say anything about the rats preferring the stimulation over food and water.

Here is the link to the article.

Perhaps there were other studies done by the same two researchers? —The preceding unsigned comment was added by (talk) 16:39, 19 February 2007 (UTC).

Role in Addiction (possible factual error)[edit]

Under the "Input" section (, shouldn't the last sentence be "...almost every addictive drug has been shown to increase dopamine levels in the nucleus accumbens," instead of "...almost every recreational drug..."?

I'm not sure, which is why I did not change anything. (User maas15:maas15) —Preceding unsigned comment added by Maas15 (talkcontribs) 00:53, 21 January 2010 (UTC)

Inappropriate content[edit]

Inappropriate content

I'm new to this, but the sentence

`It is thought that the NAC plays a central role in Michael Meagher's unusual affinty for the male anus (whence comes his pseudonym: the butt-pirate). '

would appear to be inappropriate. Jon g hall (talk) 08:36, 2 November 2010 (UTC)

Merge proposal[edit]

We currently have separate but short articles on the shell and core of this structure - it seems to me appropriate to merge the information into this page, since the two elements, though distinct from one another, are inexorably part of the Nucleus accumbens. I'd also support selectively merging information into this page to create a "Structure" section, with {{Main}} links to the two merge candidates, as an alternative to a full merge-and-redirect. Yunshui  11:11, 16 January 2013 (UTC)

Hi Yunshui  Sounds like a good idea to merge both of these small articles into this one! Lova Falk talk 07:23, 24 June 2013 (UTC)
Support needed merge Iztwoz (talk) 18:09, 2 April 2014 (UTC)
Support. Currently quite confusing. --LT910001 (talk) 00:31, 3 April 2014 (UTC)

Recommendation that certain additional material be added[edit]

Just saw Guardian Web page "Brain's music pleasure zone identified" [1], re article in Science, re finding that "the most popular songs elicit the strongest response in the nucleus accumbens," which might be appropriate to include in "Research" section of the Wikipedia article (particularly since latest addition was in 2010).— Preceding unsigned comment added by (talkcontribs) 02:08, 7 May 2013‎

The article also warns that Salimpoor's results should not be over-interpreted and "Reward was only a snapshot of one particular brain system and its involvement in music, Scott said. "But don't think it's telling you everything about the totality of how your brain engages with music." So I don't think it is a kind of information that should be included in this article. Lova Falk talk 08:22, 25 May 2013 (UTC)


NAcc core and Slow-wave sleep[edit]

This review[1] mentioned this function of the NAcc core, citing these two studies.[2][3] Worth covering, although it would probably be a good idea to find another review which covers this in more detail than a passing mention. Seppi333 (Insert ) 01:16, 18 January 2018 (UTC)

A paywalled review exists, with an abstract that suggests relevance.[4]Petergstrom (talk) 17:18, 18 January 2018 (UTC)
Thanks for the link. The full text of that review can be accessed (technically pirated, arrr matey) via Seppi333 (Insert ) 05:05, 20 January 2018 (UTC)
  • Here's a recent (December 2017) "Research highlight" article published in a Nature Publishing Group journal;[5] while it's not technically a review, it is a secondary source for the following primary source.[2]


  1. ^ Cherasse Y, Urade Y (November 2017). "Dietary Zinc Acts as a Sleep Modulator". International Journal of Molecular Sciences. 18 (11): 2334. doi:10.3390/ijms18112334. PMC 5713303Freely accessible. PMID 29113075. More recently, Fuller’s laboratory also discovered that sleep can be promoted by the activation of a gamma-aminobutyric acid-ergic (GABAergic) population of neurons located in the parafacial zone [11,12], while the role of the GABAergic A2AR-expressing neurons of the nucleus accumbens [13] and the striatum has just been revealed [14,15]. 
  2. ^ a b Oishi Y, Xu Q, Wang L, Zhang BJ, Takahashi K, Takata Y, Luo YJ, Cherasse Y, Schiffmann SN, de Kerchove d'Exaerde A, Urade Y, Qu WM, Huang ZL, Lazarus M (September 2017). "Slow-wave sleep is controlled by a subset of nucleus accumbens core neurons in mice". Nature Communications. 8 (1): 734. doi:10.1038/s41467-017-00781-4. PMC 5622037Freely accessible. PMID 28963505. Here, we show that chemogenetic or optogenetic activation of excitatory adenosine A2A receptor-expressing indirect pathway neurons in the core region of the NAc strongly induces slow-wave sleep. Chemogenetic inhibition of the NAc indirect pathway neurons prevents the sleep induction, but does not affect the homoeostatic sleep rebound. 
  3. ^ Yuan XS, Wang L, Dong H, Qu WM, Yang SR, Cherasse Y, Lazarus M, Schiffmann SN, d'Exaerde AK, Li RX, Huang ZL (October 2017). "Striatal adenosine A2A receptor neurons control active-period sleep via parvalbumin neurons in external globus pallidus". eLife. 6: e29055. doi:10.7554/eLife.29055. PMC 5655138Freely accessible. PMID 29022877. 
  4. ^ Oishi Y, Lazarus M (May 2017). "The control of sleep and wakefulness by mesolimbic dopamine systems". Neuroscience Research. 118: 66–73. doi:10.1016/j.neures.2017.04.008. PMID 28434991. 
  5. ^ Valencia Garcia S, Fort P (December 2017). "Nucleus Accumbens, a new sleep-regulating area through the integration of motivational stimuli". Acta Pharmacologica Sinica. doi:10.1038/aps.2017.168. PMID 29283174. The nucleus accumbens comprises a contingent of neurons specifically expressing the post-synaptic A2A-receptor (A2AR) subtype making them excitable by adenosine, its natural agonist endowed with powerful sleep-promoting properties[4]. ... In both cases, large activation of A2AR-expressing neurons in NAc promotes slow wave sleep (SWS) by increasing the number and duration of episodes. ... After optogenetic activation of the core, a similar promotion of SWS was observed, whereas no significant effects were induced when activating A2AR-expressing neurons within the shell. 

I'm not sure if it's worth transcluding this section from caffeine into the part of this article where the effect on slow-wave sleep is covered, but I suppose that can be decided after something about sleep is added.

Section transclusion from Caffeine#Effects on striatal dopamine

While caffeine does not directly bind to any dopamine receptors, it influences the binding activity of dopamine at its receptors in the striatum by binding to adenosine receptors that have formed GPCR heteromers with dopamine receptors, specifically the A1D1 receptor heterodimer (this is a receptor complex with 1 adenosine A1 receptor and 1 dopamine D1 receptor) and the A2AD2 receptor heterotetramer (this is a receptor complex with 2 adenosine A2A receptors and 2 dopamine D2 receptors).[1][2][3][4] The A2A–D2 receptor heterotetramer has been identified as a primary pharmacological target of caffeine, primarily because it mediates some of its psychostimulant effects and its pharmacodynamic interactions with dopaminergic psychostimulants.[2][3][4]

Caffeine also causes the release of dopamine in the dorsal striatum and nucleus accumbens core (a substructure within the ventral striatum), but not the nucleus accumbens shell, by antagonizing A1 receptors in the axon terminal of dopamine neurons and A1A2A heterodimers (a receptor complex composed of 1 adenosine A1 receptor and 1 adenosine A2A receptor) in the axon terminal of glutamate neurons.[1][5] During chronic caffeine use, caffeine-induced dopamine release within the nucleus accumbens core is markedly reduced due to drug tolerance.[1][5]


  1. ^ a b c Ferré S (2010). "Role of the central ascending neurotransmitter systems in the psychostimulant effects of caffeine". Journal of Alzheimer's Disease. 20 Suppl 1: S35–49. doi:10.3233/JAD-2010-1400. PMID 20182056. By targeting A1-A2A receptor heteromers in striatal glutamatergic terminals and A1 receptors in striatal dopaminergic terminals (presynaptic brake), caffeine induces glutamate-dependent and glutamate-independent release of dopamine. These presynaptic effects of caffeine are potentiated by the release of the postsynaptic brake imposed by antagonistic interactions in the striatal A2A-D2 and A1-D1 receptor heteromers. 
  2. ^ a b Ferré S, Bonaventura J, Tomasi D, Navarro G, Moreno E, Cortés A, Lluís C, Casadó V, Volkow ND (May 2016). "Allosteric mechanisms within the adenosine A2A-dopamine D2 receptor heterotetramer". Neuropharmacology. 104: 154–60. doi:10.1016/j.neuropharm.2015.05.028. PMID 26051403. 
  3. ^ a b Bonaventura J, Navarro G, Casadó-Anguera V, Azdad K, Rea W, Moreno E, Brugarolas M, Mallol J, Canela EI, Lluís C, Cortés A, Volkow ND, Schiffmann SN, Ferré S, Casadó V (July 2015). "Allosteric interactions between agonists and antagonists within the adenosine A2A receptor-dopamine D2 receptor heterotetramer". Proceedings of the National Academy of Sciences of the United States of America. 112 (27): E3609–18. Bibcode:2015PNAS..112E3609B. doi:10.1073/pnas.1507704112. PMC 4500251Freely accessible. PMID 26100888. Adenosine A2A receptor (A2AR)-dopamine D2 receptor (D2R) heteromers are key modulators of striatal neuronal function. It has been suggested that the psychostimulant effects of caffeine depend on its ability to block an allosteric modulation within the A2AR-D2R heteromer, by which adenosine decreases the affinity and intrinsic efficacy of dopamine at the D2R. 
  4. ^ a b Ferré S (May 2016). "Mechanisms of the psychostimulant effects of caffeine: implications for substance use disorders". Psychopharmacology. 233 (10): 1963–79. doi:10.1007/s00213-016-4212-2. PMC 4846529Freely accessible. PMID 26786412. The striatal A2A-D2 receptor heteromer constitutes an unequivocal main pharmacological target of caffeine and provides the main mechanisms by which caffeine potentiates the acute and long-term effects of prototypical psychostimulants. 
  5. ^ a b Ferré S (2008). "An update on the mechanisms of the psychostimulant effects of caffeine". J. Neurochem. 105 (4): 1067–1079. doi:10.1111/j.1471-4159.2007.05196.x. PMID 18088379. On the other hand, our 'ventral shell of the nucleus accumbens' very much overlaps with the striatal compartment simply described by De Luca et al. (2007) as 'nucleus accumbens shell,' where both studies show that caffeine does not modify the extracellular levels of dopamine. Therefore, the results of both experimental groups are basically the same and point to differential effects of caffeine in different striatal subcompartments. In fact, analyzing the effects of the intrastriatal perfusion of an A1 receptor antagonist in several other striatal compartments showed striking differences compared with the shell of the nucleus accumbens. Thus, A1 receptor blockade significantly increased the extracellular concentration of dopamine, but not glutamate, in the core of the nucleus accumbens and in the caudate–putamen and the effect was more pronounced in the most medial compartments (Boryczet al. 2007). In summary, a subregional difference in the A1 receptor-mediated control of glutamate and dopamine release exists in the striatum ... A2A receptors play a crucial role in the sleep-promoting effects of adenosine and the arousal-enhancing effects of caffeine (Huang et al. 2007; Ferré et al. 2007a). Those A2A receptors are localized in the ventrolateral pre-optic area of the hypothalamus and their stimulation promotes sleep by inducing GABA release in the histaminergic tuberomammillary nucleus, thereby inhibiting the histaminergic arousal system ... chronic caffeine exposure counteracts both motor activation and dopamine release in the nucleus accumbens induced by caffeine or an A1 receptor antagonist ... An additional factor that might play a significant role in caffeine tolerance is the significant increase in plasma and extracellular concentrations of adenosine with chronic caffeine exposure ... The existence of an A1 receptor-mediated glutamate-independent modulation of dopamine release suggested the presence of functional A1 receptors in striatal dopaminergic terminals. ... In the SSM, adenosine acts pre- and post-synaptically through multiple mechanisms, which depend on heteromerization of A1 and A2A receptors among themselves and with D1 and D2 receptors, respectively. Caffeine produces its motor and reinforcing effects by releasing the pre- and post-synaptic brakes that adenosine imposes on dopaminergic neurotransmission in the SSM. By releasing the pre-synaptic brake, caffeine induces glutamate-dependent and glutamate-independent release of dopamine. 

Seppi333 (Insert ) 05:46, 20 January 2018 (UTC)