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The Brain Immune Axis and Substance Abuse pp 73–83Cite as

Relevance of Opioid Bimodality to Tolerance/Dependence Formation

From Transmitter Release to Second Messenger Formation

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 373))

Abstract

It is very well established - indeed dogma - that the predominant effect of opioids in the central nervous system is to depress neuronal function and inhibit the release of neurotransmitters (see[1]). When excitatory opioid actions are observed, they are usually attributed to disinhibition[2], i.e., opioids are known to inhibit inhibitory neurons and thus cause excitation.

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Author information

Authors and Affiliations

  1. Department of Biochemistry, State University of New York Health Science Center, Brooklyn, New York, USA

    Alan R. Gintzler

Authors
  1. Alan R. Gintzler
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Editor information

Editors and Affiliations

  1. Hennepin County Medical Center and University of Minnesota, Minneapolis, Minnesota, USA

    Burt M. Sharp

  2. Temple University School of Medicine, Philadelphia, Pennsylvania, USA

    Toby K. Eisenstein

  3. Emory University School of Medicine, Atlanta, Georgia, USA

    John J. Madden

  4. University of South Florida College of Medicine, Tampa, Florida, USA

    Herman Friedman

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© 1995 Springer Science+Business Media New York

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Gintzler, A.R. (1995). Relevance of Opioid Bimodality to Tolerance/Dependence Formation. In: Sharp, B.M., Eisenstein, T.K., Madden, J.J., Friedman, H. (eds) The Brain Immune Axis and Substance Abuse. Advances in Experimental Medicine and Biology, vol 373. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1951-5_11

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  • DOI: https://doi.org/10.1007/978-1-4615-1951-5_11

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5801-5

  • Online ISBN: 978-1-4615-1951-5

  • eBook Packages: Springer Book Archive

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