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Nucleus accumbens shell

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The nucleus accumbens shell is a structure that, together with the nucleus accumbens core, makes up the entire nucleus accumbens (NAc), an important area of the brain related to motor function, reward, and emotionality.

Location: The shell of the nucleus accumbens is located in the rostral pole of extended amygdala.

Cell types: Neurons in the nucleus accumbens are mostly medium spiny neurons. The neurons in the shell, as compared to the core, have a lower density of dendritic spines, less terminal segments, and less branch segments than those in the core. The shell neurons project to the subcommissural part of the ventral pallidum as well as the ventral tegmental area and to extensive areas in the hypothalamus and extended amygdala.[1][2][3]

Function: The shell of the nucleus accumbens plays a role in regulating motivation, reward, and psychiatric disorders related to improper regulation of these qualities. Particularly important are the effects of drug and food stimuli on the NAc shell because these effects are related to addiction and behavioral inhibition.

HormonesEdit

Dopamine: Dopamine is related to drugs of abuse like amphetamines, cocaine, and morphine, which increase extracellular levels of dopamine in both the NAc shell and the NAc core, but the effect of these increases is more pronounced in the shell. Only amphetamine at high levels increased extracellular levels of dopamine to similar levels in both the shell and the core. All of this points to a 'functional heterogeneity' in the nucleus accumbens between the shell region and the core region.[4] Similarly to drug rewards, non-drug rewards also increase levels of extracellular dopamine in the NAc shell, but drug induced DA increase is more resilient to habituation when exposed repeatedly to drug-stimuli, unlike non-drug rewarding stimuli induced dopamine increases, which do succumb to habituation. RecentTemplate:When studies have shown that the repeated influence of drug-inducing DA projection has an abnormal strengthening effect on stimulus-drug associations and increases the drug-reward stimuli’s resistance to extinction. This may be a contributing factor to addiction. This effect was more pronounced in the NAc shell than in the NAc core.[5][6](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475798/)

Glucocorticoids and dopamine: Glucocorticoid receptors are the only corticosteroid receptors in the nucleus accumbens shell. L-DOPA, steroids, and specifically glucocorticoids are currently known to be the only known endogenous compounds that can induce psychotic problems, so understanding the hormonal control over dopaminergic projections with regards to glucocorticoid receptors could lead to new treatments for psychotic symptoms. A recent study demonstrated that suppression of the glucocorticoid receptors led to a decrease in the release of dopamine, which may lead to future research involving anti-glucocorticoid drugs to potentially relieve psychotic symptoms.[7]

GABA: A recent study on rats that used GABA agonists and antagonists indicated that GABAA receptors in the NAc shell have inhibitory control on turning behavior influenced by dopamine, and GABAB receptors in the have inhibitory control over turning behavior mediated by acetylcholine.[8][9]

Serotonin (5-HT): Overall, 5-HT synapses are more abundant and have a greater number of synaptic contacts in the NAc shell than in the core. They are also larger and thicker, and contain more large dense core vesicles than their counterparts in the core.

References Edit

  1. Shirayama, Yukihiko, and Shigeyuki Chaki. "Neurochemistry of the Nucleus Accumbens and Its Relevance to Depression and Antidepressant Action in Rodents." Current Neuropharmocology 4.4 (2006): 277-91. Bentham Science Publishers Ltd. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475798/>.
  2. Meredith, G. E., R. Agolia, M. P. Arts, H. J. Groenewegen, and D. S. Zahm. "Morphological Differences between Projection Neurons of the Core and Shell in the Nucleus Accumbens of the Rat." Neuroscience 50.1 (1992): 149-62. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/1383869>.
  3. Meredith, G. E., C. M. Pennartz, and H. J. Groenewegen. "The Cellular Framework for Chemical Signalling in the Nucleus Accumbens." Progress in Brain Research 99 (1993): 3-24. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/7906426>.
  4. Pontieri, F. E., G. Tanda, and G. Di Chiara. "Intravenous Cocaine, Morphine, and Amphetamine Preferentially Increase Extracellular Dopamine in the "shell" as Compared with the "core" of the Rat Nucleus Accumbens." Proc. Natl. Acad. Sci. USA 92 (1995): 12304-2308. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC40345/pdf/pnas01504-0367.pdf>.
  5. Chiara, G. Di. "Nucleus Accumbens Shell and Core Dopamine: Differential Role in Behavior and Addiction." Behav Brain Res. 137.1-2 (2002): 75-114. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/12445717>.
  6. Shirayama, Yukihiko, and Shigeyuki Chaki. "Neurochemistry of the Nucleus Accumbens and Its Relevance to Depression and Antidepressant Action in Rodents." Current Neuropharmocology 4.4 (2006): 277-91. Bentham Science Publishers Ltd. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475798/>.
  7. Barrot, Michel, Michela Marinelli, Djoher N. Abrous, Francoise Rouge-pont, Michel Le Moal, and Pier V. Piazza. "The Dopaminergic Hyper-responsiveness of the Shell of the Nucleus Accumbens Is Hormone Dependent." European Journal of Neuroscience 12 (2000): 973-79. Web. 16 Nov. 2011. <http://rosalindfranklin.edu/dnn/portals/24/documents/pharmacology/Marinelli/Barrot2000.pdf>.
  8. Akiyama, G., H. Ikeda, S. Matsuzaki, M. Sato, S. Moribe, N. Koshikawa, and A. R. Cools. "GABAA and GABAB Receptors in the Nucleus Accumbens Shell Differentially Modulate Dopamine and Acetylcholine Receptor-mediated Turning Behaviour." Neuropharmacology 46.8 (2004): 1082-088. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/15111014>.
  9. Shirayama, Yukihiko, and Shigeyuki Chaki. "Neurochemistry of the Nucleus Accumbens and Its Relevance to Depression and Antidepressant Action in Rodents." Current Neuropharmocology 4.4 (2006): 277-91. Bentham Science Publishers Ltd. Web. 16 Nov. 2011. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475798/>.
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