Evidence map›Paper›PMID 22948980›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012

Glycine transporter-1 inhibition preceding extinction training inhibits reacquisition of cocaine seeking.

Cindy Achat-Mendes, Bríd Á Nic Dhonnchadha, Donna M Platt, Kathleen M Kantak, Roger D Spealman

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. GlyT1 (SLC6A9) inhibition in neurological and psychiatric disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  2. Review
  3. Article
  4. Neurobiology of Stress-Induced Nicotine Relapse.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. GlyT-1 Inhibition Attenuates Attentional But Not Learning or Motivational Deficits of the Sp4 Hypomorphic Mouse Model Relevant to Psychiatric Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  12. Article
  13. Review
  14. Recent developments in animal models of drug relapse.Current opinion in neurobiology · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Cindy Achat-MendesDivision of Neuroscience, New England Primate Research Center, Harvard Medical School, Southborough, MA, USA. cindy_achat-mendes@hms.harvard.edu
Bríd Á Nic Dhonnchadha
Donna M Platt
Kathleen M Kantak
Roger D Spealman
Boston University · USHarvard University · USNew England Biolabs (United States) · US

Funding

ZETA CHAIN OF T CELL RECEPTOR INTERACTS W/ NEF OF SIV &HIV2P51RR000168 · NCRR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WESTMORELAND, SUSAN V. · 1985 to 2011
$139.3M
New England Primate Research Center Base GrantP51OD011103 · OD · HARVARD MEDICAL SCHOOL · PI FLIER, JEFFREY S · 2012 to 2013
$24.7M
Strategies for Enhancing Extinction of Drug-Seeking BehaviorR01DA024315 · NIDA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI KANTAK, KATHLEEN M. · 2007 to 2011
$1.9M
MOUSE MODELS OF CANCER, BONE DISEASE, AND LACTATIONK26RR000168 · NCRR · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2000 to 2004
$547k
NCRR NIH HHS K26 RR000168NCRR NIH HHS P51 RR000168NCRR NIH HHS RR00168NIDA NIH HHS DA024315NIDA NIH HHS DA024315-S1NIDA NIH HHS R01 DA024315NIH HHS OD011103NIH HHS P51 OD011103
6 · The paper itself

Abstract

Cognitive enhancers that act by increasing glycine transmission might be useful adjuncts to cocaine-cue extinction training to deter relapse. The study investigated the effects of combining treatments of the glycine transporter-1 (GlyT-1) inhibitor, Org24598, with extinction training on the subsequent reacquisition of cocaine self-administration. Squirrel monkeys and rats were trained to self-administer cocaine under a second-order schedule of intravenous drug injection in which responding was maintained by cocaine injections and a cocaine-paired visual stimulus. During three weekly extinction sessions, saline was substituted for cocaine but responding still produced the cocaine-paired stimulus. Subjects were treated with Org24598 or vehicle, either before or after each extinction session. One week later, cocaine injections were restored, and reacquisition of cocaine self-administration was evaluated over 15 sessions. Compared with vehicle, administration of Org24598 (1.0 mg/kg in monkeys; 3.0 or 7.5 mg/kg in rats) before each extinction session significantly inhibited reacquisition of cocaine self-administration in each species. In contrast, administration of Org24598 (1.0 mg/kg in monkeys) following, rather than preceding, each extinction session did not affect reacquisition compared with vehicle. When extinction training was replaced by cocaine self-administration or abstinence control conditions, treatment with the same doses of Org24598 resulted in reacquisition that was significantly more rapid than the reacquisition observed when Org24598 was administered before extinction training sessions. The results support the potential clinical utility of GlyT-1 inhibitor pretreatments combined with cocaine-cue extinction training to inhibit relapse.

Indexed as

AnimalsBehavior, AddictiveCocaineExtinction, PsychologicalGlycineGlycine Plasma Membrane Transport ProteinsMaleRatsRats, WistarSaimiriSelf AdministrationCocaineGlycineGlycine Plasma Membrane Transport Proteinsorg 24598Slc6a9 protein, rat

Identifiers

PMID22948980
PMCPMC3499725
OpenAlexW2045019639

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.