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Cassandra D. Gipson

Researcher at University of Kentucky

Publications -  80
Citations -  2903

Cassandra D. Gipson is an academic researcher from University of Kentucky. The author has contributed to research in topics: Nucleus accumbens & Nicotine. The author has an hindex of 25, co-authored 72 publications receiving 2321 citations. Previous affiliations of Cassandra D. Gipson include Medical University of South Carolina & Icahn School of Medicine at Mount Sinai.

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The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis.

TL;DR: A review of the literature describing how synaptic plasticity in the accumbens is altered after exposure to drugs of abuse and withdrawal and also how pharmacological manipulation of glutamate systems in the Accumbens can inhibit drug seeking in the laboratory setting is provided.
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Reinstatement of nicotine seeking is mediated by glutamatergic plasticity

TL;DR: It is suggested that targeting glutamate transmission might inhibit cue-induced nicotine seeking, and pharmacological inhibition of GluN2A with 3-Chloro-4-fluoro-N-[4-[[2-(phenylcarbonyl)hydrazino] carbonyl]benzyl]benzenesulfonamide or Glun2B with ifenprodil abolished reinstated nicotine seeking is found.
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Relapse Induced by Cues Predicting Cocaine Depends on Rapid, Transient Synaptic Potentiation

TL;DR: It is found that cocaine-associated cues initiate cocaine seeking by inducing a rapid, transient increase in dendritic spine size and synaptic strength in the nucleus accumbens, which required neural activity in the prefrontal cortex.
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Potential Role of N-Acetylcysteine in the Management of Substance Use Disorders

TL;DR: This review will focus specifically on N-acetylcysteine (NAC), a safe and well-tolerated glutamatergic agent, as a promising potential pharmacotherapy for the treatment of SUDs across several substances of abuse.
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Glutamate transporter GLT-1 mediates N-acetylcysteine inhibition of cocaine reinstatement.

TL;DR: It is hypothesized that the increased reinstatement after inhibiting NAC induction of GLT‐1 resulted from increased extracellular glutamate, and show that augmented reinstatement is prevented by blocking mGluR5.