Cell Type–Specific Loss of BDNF Signaling Mimics Optogenetic Control of Cocaine Reward

  • Mary Kay Lobo
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Herbert E. Covington
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Dipesh Chaudhury
    Pharmacology and System Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Allyson K. Friedman
    Pharmacology and System Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • HaoSheng Sun
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Diane Damez-Werno
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • David M. Dietz
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Samir Zaman
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Ja Wook Koo
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Pamela J. Kennedy
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Ezekiell Mouzon
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Murtaza Mogri
    Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.
  • Rachael L. Neve
    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Karl Deisseroth
    Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.
  • Ming-Hu Han
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.
  • Eric J. Nestler
    Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.

Description

<jats:title>BDNF, Dopamine, and Cocaine Reward</jats:title> <jats:p> The nucleus accumbens plays a crucial role in mediating the rewarding effects of drugs of abuse. Different subpopulations of nucleus accumbens projection neurons exhibit balanced but antagonistic influences on their downstream outputs and behaviors. However, their roles in regulating reward behaviors remains unclear. <jats:bold> Lobo <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="385" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1188472">385</jats:related-article> ) evaluated the roles of the two subtypes of nucleus accumbens projection neurons, those expressing dopamine D1 versus D2 receptors, in cocaine reward. Deleting TrkB, the receptor for brain-derived neurotrophic factor, selectively in each cell type, and selectively controlling the firing of each cell type using optogenetic techniques allowed for confirmation that D1- and D2-containing neurons produced opposite effects on cocaine reward. </jats:p>

Journal

  • Science

    Science 330 (6002), 385-390, 2010-10-15

    American Association for the Advancement of Science (AAAS)

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