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Related Experiment Video

Updated: Jul 11, 2026

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DeltaFosB induction in orbitofrontal cortex mediates tolerance to cocaine-induced cognitive dysfunction.

Catharine A Winstanley1, Quincey LaPlant, David E H Theobald

  • 1Department of Psychiatry and Basic Neuroscience, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 28, 2007
PubMed
Summary

Chronic cocaine use leads to cognitive deficits, particularly in the orbitofrontal cortex (OFC). The transcription factor deltaFosB in the OFC mediates tolerance to cocaine

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Addiction Research

Background:

  • Prolonged cocaine use leads to cognitive deficits, potentially linked to orbitofrontal cortex (OFC) dysfunction.
  • Neurobiological mechanisms underlying these cognitive impairments remain largely unknown.

Purpose of the Study:

  • To investigate the role of the transcription factor deltaFosB in the OFC in mediating cognitive alterations associated with chronic cocaine use.
  • To elucidate the molecular mechanisms underlying tolerance to cocaine's cognitive effects.

Main Methods:

  • Assessed deltaFosB expression in rat prefrontal cortex following chronic cocaine self-administration.
  • Utilized rodent behavioral tests for attention and decision-making.
  • Manipulated deltaFosB and deltaJunD expression in the OFC.
  • Performed gene microarray analysis to identify molecular targets.

Main Results:

  • Chronic cocaine self-administration increased OFC deltaFosB levels, more so than experimenter-administered cocaine.
  • Overexpression of deltaFosB in the OFC mimicked chronic cocaine effects, while its antagonist (deltaJunD) blocked tolerance.
  • Identified increased transcription of metabotropic glutamate receptor 5 and GABA(A) receptors, and substance P.

Conclusions:

  • deltaFosB in the OFC is a key mediator of tolerance to cocaine's cognitive effects.
  • This finding offers new insights into the transcriptional modifications driving addiction and cognitive impairment.