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(The FASEB Journal. 2008;22:2113)
© 2008 FASEB
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Regarding "Dynorphin is a downstream effector of striatal BDNF regulation of ethanol intake"

Brendan M. Walker*,1 and George F. Koob{dagger},1

* Molecular and Integrative Neurosciences Department, and

{dagger} Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California, USA

1Correspondence: Molecular and Integrative Neurosciences Department The Scripps Research Institute, 10550 North Torrey Pines Rd., Mail code: SP30-1501, La Jolla, California 92037, USA. E-mail: bwalker@scripps.edu; Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, 10550 North Torrey Pines Rd., Mail code: SP30-2400, La Jolla, California 92037, USA. E-mail: gkoob{at}scripps.edu

Upon reading the interesting article by M. Logrip, P. Janak, and D. Ron that was published online on February 29th, 2008, in [and appears in this issue of] The FASEB Journal, it was noticed that a section of that manuscript’s discussion section referenced our work focusing on the role of {kappa}-opioid receptors and dynorphin systems in ethanol dependence and withdrawal (1) . Unfortunately, both the results of our study and the hypothesis that guided the research appear to have been misunderstood within the discussion section of the Logrip et al. manuscript (2) .

We would like to clarify that the behavioral observations from our experiments indicated that blockade of {kappa}-opioid receptors with nor-binaltorphimine (nor-BNI) selectively decreased ethanol self-administration in ethanol-dependent animals; leaving self-administration behavior of ethanol in nondependent animals intact (the Logrip et al. manuscript stated we observed increases in ethanol self-administration by blocking dynorphin systems). Additionally, we proposed in that manuscript that the dynorphin system has increased activity in ethanol dependent states. It is hypothesized that when ethanol-dependent animals are in withdrawal, the increased activity of the dynorphin system produces a negative affective/dysphoric state that ethanol self-administration relieves via a negative reinforcement mechanism. By blocking this putatively up-regulated dynorphin state during ethanol withdrawal with nor-BNI, the negative emotional state produced by an overactive dynorphin system is removed temporarily and the need to continue self-administering ethanol is lowered.

We hope that this letter helps to clarify the effect of {kappa}-opioid receptor antagonism in ethanol-dependent animals that was observed in our laboratory. Numerous lines of research focusing on the role of endogenous dynorphin within motivationally relevant systems are beginning to converge and it has recently been shown that the dynorphin system can be driven through multiple mechanisms [e.g., CREB-induced, CRF-induced, etc. (3 , 4) ] to impact emotional behavior.

FOOTNOTES

The opinions expressed in editorials, essays, letters to the editor, and other articles comprising the Up Front section are those of the authors and do not necessarily reflect the opinions of FASEB or its constituent societies. The FASEB Journal welcomes all points of view and many voices. We look forward to hearing these in the form of op-ed pieces and/or letters from its readers addressed to journals{at}faseb.org

REFERENCES

  1. Walker, B. M., Koob, G. F. (2008) Pharmacological evidence for a motivational role of kappa-opioid systems in ethanol dependence. Neuropsychopharmacology 33,643-652[CrossRef][Medline]
  2. Logrip, M. L., Janak, P. H., Ron, D. (2008) Dynorphin is a downstream effector of striatal BDNF regulation of ethanol intake. FASEB J. E-pub ahead of print
  3. Carlezon, W. A., Jr, Duman, R. S., Nestler, E. J. (2005) The many faces of CREB. Trends Neurosci. 28,436-445[CrossRef][Medline]
  4. Land, B. B., Bruchas, M. R., Lemos, J. C., Xu, M., Melief, E. J., Chavkin, C. (2008) The dysphoric component of stress is encoded by activation of the dynorphin kappa-opioid system. J. Neurosci. 28,407-414[Abstract/Free Full Text]




This Article
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Right arrow Articles by Koob, G. F.

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