Role of conditioned reinforcers in the initiation, maintenance and extinction of drug-seeking behavior

1976 ◽  
Vol 11 (4) ◽  
pp. 222-236
Author(s):  
W. Marvin Davis ◽  
Stanley G. Smith
2020 ◽  
Vol 237 (11) ◽  
pp. 3505-3506
Author(s):  
Bo Ram Cho ◽  
Jennifer Gerena ◽  
Doris I. Olekanma ◽  
Aneesh Bal ◽  
André N. Herrera Charpentier ◽  
...  

2020 ◽  
Vol 237 (9) ◽  
pp. 2823-2833
Author(s):  
Bo Ram Cho ◽  
Jennifer Gerena ◽  
Doris I. Olekanma ◽  
Aneesh Bal ◽  
André N. Herrera Charpentier ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yusuf S. Althobaiti ◽  
Atiah Almalki ◽  
Hashem Alsaab ◽  
Walaa Alsanie ◽  
Ahmed Gaber ◽  
...  

Abstract Drug addiction remains a prevalent and fatal disease worldwide that carries significant social and economic impacts. Recent reports suggest illicit pregabalin (Lyrica) use may be increasing among youth, however the addictive potential of pregabalin has not been well established. Drug seeking behavior and chronic drug use are associated with deficits in glutamate clearance and activation of postsynaptic glutamatergic receptors. In the current study, we investigated the abuse potential of pregabalin using conditioned place preference (CPP) paradigm. Different doses of pregabalin (30, 60, 90, and 120 mg/kg) were used to assess the seeking behavior in mice. Glutamate homeostasis is maintained by glutamate transporter type-1 (GLT-1), which plays a vital role in clearing the released glutamate from synapses and drug seeking behavior. Therefore, we investigated the role of glutamate in pregabalin-seeking behavior with ceftriaxone (CEF), a potent GLT-1 upregulator. Mice treated with pregabalin 60 and 90 mg/kg doses demonstrated drug seeking-like behavior, which was significantly blocked by CEF pretreatment. These results suggest that pregabalin-induced CPP was successfully modulated by CEF which could serve as a lead compound for developing treatment for pregabalin abuse.


Synapse ◽  
2005 ◽  
Vol 57 (1) ◽  
pp. 17-28 ◽  
Author(s):  
Jeremy G. Gilbert ◽  
Amy Hauck Newman ◽  
Eliot L. Gardner ◽  
Charles R. Ashby ◽  
Christian A. Heidbreder ◽  
...  

2010 ◽  
Vol 35 (2) ◽  
pp. 303-314 ◽  
Author(s):  
Gal Yadid ◽  
Einav Sudai ◽  
Rachel Maayan ◽  
Iris Gispan ◽  
Abraham Weizman

Author(s):  
Irena Smaga ◽  
Małgorzata Frankowska ◽  
Małgorzata Filip

AbstractSubstance use disorder (SUD) is a chronic brain condition, with compulsive and uncontrollable drug-seeking that leads to long-lasting and harmful consequences. The factors contributing to the development of SUD, as well as its treatment settings, are not fully understood. Alterations in brain glutamate homeostasis in humans and animals implicate a key role of this neurotransmitter in SUD, while the modulation of glutamate transporters has been pointed as a new strategy to diminish the excitatory glutamatergic transmission observed after drugs of abuse. N-acetylcysteine (NAC), known as a safe mucolytic agent, is involved in the regulation of this system and may be taken into account as a novel pharmacotherapy for SUD. In this paper, we summarize the current knowledge on the ability of NAC to reduce drug-seeking behavior induced by psychostimulants, opioids, cannabinoids, nicotine, and alcohol in animals and humans. Preclinical studies showed a beneficial effect in animal models of SUD, while the clinical efficacy of NAC has not been fully established. In summary, NAC will be a small add-on to usual treatment and/or psychotherapy for SUD, however, further studies are required.


2020 ◽  
Vol 20 (17) ◽  
pp. 1696-1708 ◽  
Author(s):  
Athirah Hanim ◽  
Isa Naina Mohamed ◽  
Rashidi M. Pakri Mohamed ◽  
Srijit Das ◽  
Norefrina Shafinaz Md Nor ◽  
...  

Alcohol use disorder (AUD) is characterized by compulsive binge alcohol intake, leading to various health and social harms. Protein Kinase C epsilon (PKCε), a specific family of PKC isoenzyme, regulates binge alcohol intake, and potentiates alcohol-related cues. Alcohol via upstream kinases like the mammalian target to rapamycin complex 1 (mTORC1) or 2 (mTORC2), may affect the activities of PKCε or vice versa in AUD. mTORC2 phosphorylates PKCε at hydrophobic and turn motif, and was recently reported to be associated with alcohol-seeking behavior, suggesting the potential role of mTORC2-PKCε interactions in the pathophysiology of AUD. mTORC1 regulates translation of synaptic proteins involved in alcohol-induced plasticity. Hence, in this article, we aimed to review the molecular composition of mTORC1 and mTORC2, drugs targeting PKCε, mTORC1, and mTORC2 in AUD, upstream regulation of mTORC1 and mTORC2 in AUD and downstream cellular mechanisms of mTORCs in the pathogenesis of AUD.


2015 ◽  
Vol 33 (12) ◽  
pp. 1799-1801 ◽  
Author(s):  
Frederick Fiesseler ◽  
Renee Riggs ◽  
David Salo ◽  
Richard Klemm ◽  
Ashley Flannery ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document