Evidence map›Paper›PMID 20308329›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2010

Effects of the cognition-enhancing agent ABT-239 on fetal ethanol-induced deficits in dentate gyrus synaptic plasticity.

Rafael K Varaschin, Katherine G Akers, Martina J Rosenberg, Derek A Hamilton, Daniel D Savage

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
11.4field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  2. Animal Models of Prenatal Alcohol Exposure.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The histamine HAlcohol (Fayetteville, N.Y.) · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Chemical Probes for Histamine Receptor Subtypes.Current topics in behavioral neurosciences · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 1 institution in 1 country.

Rafael K VaraschinDepartment of Neurosciences, University of New Mexico, Albuquerque, NM 87131-0001, USA.
Katherine G Akers
Martina J Rosenberg
Derek A Hamilton
Daniel D Savage
University of New Mexico · US

Funding

Fetal ethanol-induced behavioral deficits: Mechanisms, diagnoses and interventionP20AA017068 · NIAAA · UNIVERSITY OF NEW MEXICO · PI SAVAGE, DANIEL D. · 2008 to 2012
$2.6M
Screening Putative Therapeutic Agents for Fetal Ethanol-Induced Learning DeficitsR21AA016619 · NIAAA · UNIVERSITY OF NEW MEXICO · PI SAVAGE, DANIEL D. · 2007 to 2008
$394k
NIAAA NIH HHS AA016619NIAAA NIH HHS AA017068NIAAA NIH HHS P20 AA017068NIAAA NIH HHS R21 AA016619
6 · The paper itself

Abstract

Prenatal ethanol exposure causes deficits in hippocampal synaptic plasticity and learning. At present, there are no clinically effective pharmacotherapeutic interventions for these deficits. In this study, we examined whether the cognition-enhancing agent 4-(2-{2-[(2R)-2-methylpyrrolidinyl]ethyl}-benzofuran-5-yl) benzonitrile (ABT-239), a histamine H(3) receptor antagonist, could ameliorate fetal ethanol-induced long-term potentiation (LTP) deficits. Long-Evans rat dams consumed a mean of 2.82 g/kg ethanol during a 4-h period each day. This voluntary drinking pattern produced a mean peak serum ethanol level of 84 mg/dl. Maternal weight gain, offspring litter size, and birth weights were not different between ethanol-consuming and control groups. A stimulating electrode was implanted in the entorhinal cortical perforant path, and a recording electrode was implanted in the dorsal dentate gyrus of urethane-anesthetized adult male offspring. Baseline input/output responses were not affected either by prenatal ethanol exposure or by 1 mg/kg ABT-239 administered 2 h before data collection. No differences were observed between prenatal treatment groups when a 10-tetanus train protocol was used to elicit LTP. However, LTP elicited by 3 tetanizing trains was markedly impaired by prenatal ethanol exposure compared with control. This fetal ethanol-induced LTP deficit was reversed by ABT-239. In contrast, ABT-239 did not enhance LTP in control offspring using the 3-tetanus train protocol. These results suggest that histamine H(3) receptor antagonists may have utility for treating fetal ethanol-associated synaptic plasticity and learning deficits. Furthermore, the differential effect of ABT-239 in fetal alcohol offspring compared with controls raises questions about the impact of fetal ethanol exposure on histaminergic modulation of excitatory neurotransmission in affected offspring.

Indexed as

Alcohol DrinkingAnimalsBenzofuransDentate GyrusElectrophysiological PhenomenaEthanolFemaleFetal DevelopmentHistamine H3 AntagonistsLong-Term PotentiationMaleMaternal ExposureNootropic AgentsPregnancyPrenatal Exposure Delayed EffectsPyrrolidinesBenzofuransbenzonitrile, 4-(2-(2-((2r)-2-methyl-1-pyrrolidinyl)ethyl)-5-benzofuranyl)-EthanolHistamine H3 AntagonistsNootropic AgentsPyrrolidines

Identifiers

PMID20308329
PMCPMC2912053
OpenAlexW2160692765

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.