Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Brief Communication
  • Published:

Cocaine-induced decision-making deficits are mediated by miscoding in basolateral amygdala

Nature Neuroscience volume 10, pages 949–951 (2007)Cite this article

Abstract

Addicts and drug-experienced animals have decision-making deficits in reversal-learning tasks and more complex 'gambling' variants. Here we show evidence that these deficits are mediated by persistent encoding of outdated associative information in the basolateral amygdala. Cue-selective neurons in the basolateral amygdala, recorded in cocaine-treated rats, failed to change cue preference during reversal learning. Further, the presence of these neurons was critical to the expression of the reversal-learning deficit in the cocaine-treated rats.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Experimental design and effect of cocaine exposure on reversal learning during recording.
Figure 2: Cocaine-induced decision-making deficits are mediated by miscoding in basolateral amygdala.

Similar content being viewed by others

References

  1. Schoenbaum, G., Saddoris, M.P., Ramus, S.J., Shaham, Y. & Setlow, B. Eur. J. Neurosci. 19, 1997–2002 (2004).

    Article  Google Scholar 

  2. Jentsch, J.D., Olausson, P., De La Garza, R. & Taylor, J.R. Neuropsychopharmacology 26, 183–190 (2002).

    Article  CAS  Google Scholar 

  3. Calu, D.J. et al. Learn. Mem. 14, 325–328 (2007).

    Article  Google Scholar 

  4. Bechara, A. et al. Neuropsychologia 39, 376–389 (2001).

    Article  CAS  Google Scholar 

  5. Stalnaker, T.A., Franz, T.M., Singh, T. & Schoenbaum, G. Neuron 54, 51–58 (2007).

    Article  CAS  Google Scholar 

  6. Saddoris, M.P., Gallagher, M. & Schoenbaum, G. Neuron 46, 321–331 (2005).

    Article  CAS  Google Scholar 

  7. Schoenbaum, G., Chiba, A.A. & Gallagher, M. J. Neurosci. 19, 1876–1884 (1999).

    Article  CAS  Google Scholar 

  8. Paton, J.J., Belova, M.A., Morrison, S.E. & Salzman, C.D. Nature 439, 865–870 (2006).

    Article  CAS  Google Scholar 

  9. Schoenbaum, G., Setlow, B., Nugent, S.L., Saddoris, M.P. & Gallagher, M. Learn. Mem. 10, 129–140 (2003).

    Article  Google Scholar 

  10. Izquierdo, A. & Murray, E.A. J. Neurosci. 27, 1054–1062 (2007).

    Article  CAS  Google Scholar 

  11. Carelli, R.M., Williams, J.G. & Hollander, J.A. J. Neurosci. 23, 8204–8211 (2003).

    Article  CAS  Google Scholar 

  12. Fuchs, R.A., Feltenstein, M.W. & See, R.E. Eur. J. Neurosci. 23, 2809–2813 (2006).

    Article  Google Scholar 

  13. See, R.E., McLaughlin, J. & Fuchs, R.A. Neuroscience 117, 477–483 (2003).

    Article  CAS  Google Scholar 

  14. Lee, J.L., Di Ciano, P., Thomas, K.L. & Everitt, B.J. Neuron 47, 795–801 (2005).

    Article  CAS  Google Scholar 

  15. Milad, M.R. & Quirk, G.J. Nature 420, 70–74 (2002).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

We are grateful to S. Warrenburg at International Flavors and Fragrances for his assistance in obtaining odor compounds. This work was supported by grants from the National Institute on Drug Abuse (DA015718, G.S.), the National Institute of Neurological Diseases and Stroke (T32-NS07375, M.R.R.) and the National Institute on Deafness and other Communication Disorders (T32-DC00054, T.S.).

Author information

Authors and Affiliations

  1. Department of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., HSF-2 S251, Baltimore, 21201, Maryland, USA

    Thomas A Stalnaker, Matthew R Roesch, Theresa M Franz & Geoffrey Schoenbaum

  2. Program in Neuroscience, University of Maryland School of Medicine, 20 Penn St., HSF-2 S251, Baltimore, 21201, Maryland, USA

    Donna J Calu & Teghpal Singh

  3. Department of Psychiatry, University of Maryland School of Medicine, 20 Penn St., HSF-2 S251, Baltimore, 21201, Maryland, USA

    Geoffrey Schoenbaum

  4. Department of Psychology, University of Maryland, Baltimore County, 1000 Hilltop Circle, Baltimore, 21250, Maryland, USA

    Geoffrey Schoenbaum

Authors
  1. Thomas A Stalnaker
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Matthew R Roesch
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Theresa M Franz
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Donna J Calu
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Teghpal Singh
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Geoffrey Schoenbaum
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

T.A.S. and G.S. conceived the experiments; T.A.S., M.R.R. and D.J.C. carried out the recording work; T.A.S. and T.S. carried out the lesion work; and T.M.F. assisted with electrode construction, surgeries and histology. The data were analyzed by T.A.S. and G.S., who also cowrote the manuscript with assistance from each of the other team members.

Corresponding author

Correspondence to Thomas A Stalnaker.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Supplementary information

Supplementary Fig. 1

Effect of cocaine on locomotor activity. (PDF 46 kb)

Supplementary Fig. 2

Average baseline firing rate and distribution of firing rates for neurons recorded in saline- and cocaine-treated rats. (PDF 15 kb)

Supplementary Fig. 3

Behavioral performance in saline- and cocaine-treated rats during recording sessions. (PDF 26 kb)

Supplementary Fig. 4

Effect of cocaine treatment on the percentage of cue-selective ABL neurons that normally reverse cue-preference during reversal learning. (PDF 34 kb)

Supplementary Fig. 5

Effect of cocaine and ABL lesions on locomotor activity. (PDF 49 kb)

Supplementary Discussion (PDF 48 kb)

Supplementary Methods (PDF 31 kb)

Supplementary Results (PDF 59 kb)

Rights and permissions

Reprints and permissions

About this article

Cite this article

Stalnaker, T., Roesch, M., Franz, T. et al. Cocaine-induced decision-making deficits are mediated by miscoding in basolateral amygdala. Nat Neurosci 10, 949–951 (2007). https://doi.org/10.1038/nn1931

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nn1931

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing