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A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
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Accumbens nNOS Interneurons Regulate Cocaine Relapse.

Alexander C W Smith1, Michael D Scofield2, Jasper A Heinsbroek2

  • 1Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, New York 10029.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|January 27, 2017
PubMed
Summary

Drug cues trigger relapse by activating specific interneurons in the brain, leading to synaptic changes that drive cocaine seeking. Targeting these neuronal nitric oxide synthase (nNOS) interneurons may offer new addiction treatments.

Keywords:
MMPcocaineglutamatemetabotropic glutamate receptornitric oxiderelapse

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Area of Science:

  • Neuroscience
  • Addiction Research
  • Synaptic Plasticity

Background:

  • Relapse to drug use is often triggered by drug-associated cues.
  • Cue-induced relapse is linked to synaptic potentiation in the nucleus accumbens core (NAcore).

Purpose of the Study:

  • To elucidate the cellular mechanisms underlying cue-induced relapse to cocaine seeking.
  • To identify the specific neuronal populations involved in mediating synaptic potentiation during relapse.

Main Methods:

  • Rodent self-administration/reinstatement model of relapse.
  • Electrophysiology and NO-sensitive electrodes.
  • Chemogenetic and transgenic strategies targeting specific interneurons.

Main Results:

  • Cue-induced relapse and synaptic potentiation depend on glutamate spillover activating metabotropic glutamate receptor 5 (mGluR5) on nNOS interneurons.
  • Activation of mGluR5 on nNOS interneurons increases nitric oxide (NO) production, stimulating matrix metalloproteinases (MMPs).
  • Selective elimination or chemogenetic activation of nNOS interneurons directly modulated cue-induced reinstatement and synaptic potentiation.

Conclusions:

  • A sparse population of nNOS-expressing interneurons plays a critical role in processing drug-associated cues and driving cocaine seeking.
  • This nNOS interneuron pathway represents a potential therapeutic bottleneck for addiction treatment.