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Updated: Apr 21, 2026

Using Optogenetics to Reverse Neuroplasticity and Inhibit Cocaine Seeking in Rats
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ADAR2-dependent GluA2 editing regulates cocaine seeking.

H D Schmidt1, K N McFarland2, S B Darnell3

  • 1Center for Neurobiology and Behavior, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Molecular Psychiatry
|October 29, 2014
PubMed
Summary
This summary is machine-generated.

Reduced editing of GluA2 subunits in the nucleus accumbens shell impairs cocaine seeking. Overexpressing ADAR2b in this region promotes editing and reduces relapse behaviors, suggesting a new therapeutic target for cocaine addiction.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Activation of AMPA receptors (AMPARs) in the nucleus accumbens is crucial for cocaine-seeking behavior.
  • Calcium-permeable AMPARs (CP-AMPARs), formed by unedited GluA2(Q) subunits, are implicated in cocaine relapse.
  • The role of GluA2 Q/R site editing and ADAR2 in cocaine seeking remains unclear.

Purpose of the Study:

  • To investigate the impact of cocaine abstinence on GluA2 Q/R site editing and ADAR2 expression in the rat nucleus accumbens.
  • To determine the functional significance of ADAR2 and GluA2 Q/R site editing in cocaine seeking.

Main Methods:

  • Assessed GluA2 Q/R site editing and ADAR2 expression in cocaine-experienced rats after forced abstinence.
  • Utilized viral-mediated gene delivery to overexpress ADAR2b in the nucleus accumbens shell.
  • Measured cocaine priming-induced reinstatement of drug seeking.

Main Results:

  • Cocaine abstinence decreased GluA2 Q/R site editing and ADAR2 expression in the accumbens shell.
  • Overexpression of ADAR2b in the accumbens shell attenuated cocaine-seeking behavior.
  • Increased ADAR2b expression led to enhanced GluA2 Q/R site editing and surface expression of GluA2-containing AMPARs.

Conclusions:

  • Reduced GluA2 Q/R site editing and ADAR2 expression in the accumbens shell are associated with cocaine seeking.
  • CP-AMPARs containing unedited GluA2(Q) subunits in the accumbens shell promote cocaine seeking.
  • Targeting CP-AMPARs represents a novel therapeutic strategy for cocaine addiction.