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Stereotaxic Microinjection of Viral Vectors Expressing Cre Recombinase to Study the Role of Target Genes in Cocaine Conditioned Place Preference
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c-Fos is an intracellular regulator of cocaine-induced long-term changes

Ming Xu1

  • 1Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois, USA. mxu@dacc.uchicago.edu

Annals of the New York Academy of Sciences
|November 11, 2008
PubMed

Insights

The immediate early gene Fos, crucial for cocaine addiction neuroadaptation, plays a key role in D1 receptor-bearing neurons. Fos deficiency in mice reduces cocaine-induced behavioral changes and dendritic reorganization.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Addiction Research

Background:

  • Drug addiction involves long-lasting neurobiological changes.
  • Dopamine D1 receptors mediate cocaine-induced neuroadaptation, but intracellular mechanisms are unclear.

Purpose of the Study:

  • To investigate the role of the immediate early gene Fos in mediating cocaine-induced persistent neurobiological changes.
  • To examine Fos's function in D1 receptor-bearing neurons during cocaine exposure.

Main Methods:

  • Utilized genetically modified mice with Fos mutation in D1 receptor-bearing neurons.
  • Analyzed changes in AP-1 transcription complexes, transcription factors, receptors, and signaling molecules after repeated cocaine administration.
  • Assessed dendritic reorganization of medium spiny neurons and behavioral sensitization in mutant mice.

Main Results:

  • Fos-deficient brains showed altered AP-1 complex composition and expression levels of related molecules after cocaine exposure.
  • Repeated cocaine administration induced attenuated dendritic reorganization of medium spiny neurons in mutant mice.
  • Mutant mice exhibited reduced behavioral sensitization to cocaine.

Conclusions:

  • c-Fos expressed in D1 receptor-bearing neurons mediates persistent cocaine-induced neurobiological and behavioral changes.
  • Fos is a critical molecular player in cocaine addiction neuroadaptation.

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