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AMPAR-independent effect of striatal αCaMKII promotes the sensitization of cocaine reward

Academic Article
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Overview

authors

  • Kourrich, S.
  • Klug, J. R.
  • Mayford, Mark
  • Thomas, M. J.

publication date

  • May 2012

journal

  • Journal of Neuroscience  Journal

abstract

  • Changes in CaMKII-regulated synaptic excitability are a means through which experience may modify neuronal function and shape behavior. While behavior in rodent addiction models is linked with CaMKII activity in the nucleus accumbens (NAc) shell, the key cellular adaptations that forge this link are unclear. Using a mouse strain with striatal-specific expression of autonomously active CaMKII (T286D), we demonstrate that while persistent CaMKII activity induces behaviors comparable to those in mice repeatedly exposed to psychostimulants, it is insufficient to increase AMPAR-mediated synaptic strength in NAc shell. However, autonomous CaMKII upregulates A-type K(+) current (IA) and decreases firing in shell neurons. Importantly, inactivating the transgene with doxycycline eliminates both the IA-mediated firing decrease and the elevated behavioral response to cocaine. This study identifies CaMKII regulation of IA in NAc shell neurons as a novel cellular contributor to the sensitization of cocaine reward.

subject areas

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Cocaine
  • Conditioning (Psychology)
  • Corpus Striatum
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neuronal Plasticity
  • Organ Culture Techniques
  • Receptors, AMPA
  • Reward
  • Synapses
  • Up-Regulation
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Identity

PubMed Central ID

  • PMC3448780

International Standard Serial Number (ISSN)

  • 0270-6474

Digital Object Identifier (DOI)

  • 10.1523/jneurosci.6391-11.2012

PubMed ID

  • 22573680
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Additional Document Info

start page

  • 6578

end page

  • 6586

volume

  • 32

issue

  • 19

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