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Molecular Pharmacology

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Research ArticleArticle

A Role for Kalirin in the Response of Rat Medium Spiny Neurons to Cocaine

Xin-Ming Ma, Jian-ping Huang, Xiaonan Xin, Yan Yan, Richard E. Mains and Betty A. Eipper
Molecular Pharmacology October 2012, 82 (4) 738-745; DOI: https://doi.org/10.1124/mol.112.080044
Xin-Ming Ma
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Jian-ping Huang
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Xiaonan Xin
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Yan Yan
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Richard E. Mains
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Betty A. Eipper
University of Connecticut Health Center, Department of Neuroscience, Farmington, Connecticut
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Abstract

Kalirin-7 (Kal7), the major kalirin isoform in adult brain, plays a key role in the formation of dendritic spines in hippocampal/cortical neurons. Its role in the GABAergic medium spiny neurons (MSNs) of the nucleus accumbens (NAc) and striatum, the areas known to play a key role in the common reward pathway, is not as well understood. Although Kal7 expression in mouse NAc increased in response to cocaine, MSN dendritic spine density did not differ from that for the wild type in Kal7-null mice. Unlike wild-type mice, Kal7-null mice did not respond to cocaine with an increase in MSN dendritic spine density. To explore further the role of Kal7 in cocaine-induced alterations in MSN morphology, we turned to the rat. Based on immunostaining, both Kal7 and Kal12 are expressed at moderate levels in the MSNs of the NAc and striatum. Expression of Kal7 and Kal12 in MSNs of both areas increases after repeated cocaine treatments. Overexpression of Kal7 in cultured MSN neurons increases dendritic spine density, as observed in rats after long-term cocaine administration. Reducing endogenous expression of all major kalirin isoforms in cultured MSN neurons causes a decrease in total dendritic length and dendritic spine density. These data suggest that kalirin is essential for maintaining spine density in NAc MSNs under normal conditions and that Kal7 is an obligatory intermediate in the response of MSNs to repeated exposure to cocaine.

Footnotes

  • ↵Embedded Image The online version of this article (available at http://molpharm.aspetjournals.org) contains supplemental material.

  • This work was supported by the National Institutes of Health National Institute on Drug Abuse [Grant DA15464].

  • Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org.

    http://dx.doi.org/10.1124/mol.112.080044.

  • ABBREVIATIONS:

    MSN
    medium spiny neuron
    NAc
    nucleus accumbens
    Kal
    kalirin
    NDMA
    N-methyl-d-aspartate
    GEF
    guanine nucleotide exchange factor
    GFP
    green fluorescent protein
    VTA
    ventral tegmental area
    KO
    knockout.

  • Received May 21, 2012.
  • Accepted July 23, 2012.
  • Copyright © 2012 The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 82 (4)
Molecular Pharmacology
Vol. 82, Issue 4
1 Oct 2012
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Research ArticleArticle

Cocaine Regulates Kalirin Expression in Rat Nucleus Accumbens

Xin-Ming Ma, Jian-ping Huang, Xiaonan Xin, Yan Yan, Richard E. Mains and Betty A. Eipper
Molecular Pharmacology October 1, 2012, 82 (4) 738-745; DOI: https://doi.org/10.1124/mol.112.080044

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Research ArticleArticle

Cocaine Regulates Kalirin Expression in Rat Nucleus Accumbens

Xin-Ming Ma, Jian-ping Huang, Xiaonan Xin, Yan Yan, Richard E. Mains and Betty A. Eipper
Molecular Pharmacology October 1, 2012, 82 (4) 738-745; DOI: https://doi.org/10.1124/mol.112.080044
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