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A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
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Behavioral and morphological responses to cocaine require kalirin7.

Drew D Kiraly1, Xin-Ming Ma, Christopher M Mazzone

  • 1Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut, USA.

Biological Psychiatry
|May 11, 2010
PubMed
Summary

Kalirin7 is crucial for cocaine-induced dendritic spine changes in the nucleus accumbens. Its absence enhances locomotor sensitization but reduces cocaine preference.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Chronic cocaine use causes lasting changes in the nucleus accumbens, including dendritic spine density and gene expression.
  • The precise molecular mechanisms underlying these cocaine-induced neuroadaptations remain largely unknown.

Purpose of the Study:

  • To investigate the role of Kalirin7 (Kal7), a guanine nucleotide exchange factor, in mediating the effects of chronic cocaine exposure.
  • To determine Kal7's involvement in cocaine-induced changes in dendritic spine morphology and behavioral responses.

Main Methods:

  • Utilized Kalirin7 knockout (Kal7(KO)) and wild-type (Wt) mice, administering high-dose cocaine for 4 or 8 days.
  • Assessed locomotor sensitization and conditioned place preference.
  • Quantified dendritic spine density and morphology in the nucleus accumbens core using confocal microscopy.

Main Results:

  • Cocaine increased Kalirin7 expression in wild-type mice.
  • Kal7(KO) mice exhibited enhanced locomotor sensitization and reduced place preference for cocaine compared to Wt mice.
  • Dendritic spine density and size increases following cocaine treatment were abolished in Kal7(KO) mice.

Conclusions:

  • Kalirin7 is essential for the development of dendritic spine plasticity in response to chronic cocaine.
  • The absence of Kalirin7 leads to altered behavioral responses to cocaine, specifically increased locomotor activity and decreased reward-seeking behavior.