Evidence map›Paper›PMID 23844726›Full record

ArticleAddiction biology2014

Ectopic hippocampal neurogenesis in adolescent male rats following alcohol dependence.

Justin A McClain, Stephanie A Morris, S Alexander Marshall, Kimberly Nixon

Abstract read
In one paragraph

Article in Addiction biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Liability of Youthful Alcohol Misuse.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2018
    Article
  18. Article
  19. Bone Marrow Derived Mesenchymal Stem Cells in Addiction Related Hippocampal Damages.International journal of molecular and cellular medicine · 2018
    Review
  20. [Research progress of neurobiological function of 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2017
    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

4 authors at 1 institution in 1 country.

Justin A McClainDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY, USA.
Stephanie A Morris
S Alexander Marshall
Kimberly Nixon
University of Kentucky · US

Funding

Ethanol Alteration of the Neurogenic NicheR01AA016959 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI NIXON, KIMBERLY · 2007 to 2022
$4.8M
Training in Drug Abuse Related Research.T32DA016176 · NIDA · UNIVERSITY OF KENTUCKY · PI DWOSKIN, LINDA P · 2004 to 2020
$4.0M
Neurogenesis and neurodegeneration in adolescent binge alcohol exposureR21AA016307 · NIAAA · UNIVERSITY OF KENTUCKY · PI NIXON, KIMBERLY · 2008 to 2009
$372k
NIAAA NIH HHS R01 AA016959NIAAA NIH HHS R21 AA016307NIDA NIH HHS T32 DA016176
6 · The paper itself

Abstract

The adolescent hippocampus is highly vulnerable to alcohol-induced damage, which could contribute to their increased susceptibility to alcohol use disorder. Altered adult hippocampal neurogenesis represents one potential mechanism by which alcohol (ethanol) affects hippocampal function. Based on the vulnerability of the adolescent hippocampus to alcohol-induced damage, and prior reports of long-term alcohol-induced effects on adult neurogenesis, we predicted adverse effects on adult neurogenesis in the adolescent brain following abstinence from alcohol dependence. Thus, we examined neurogenesis in adolescent male rats during abstinence following a 4-day binge model of alcohol dependence. Bromodeoxyuridine and Ki67 immunohistochemistry revealed a 2.2-fold increase in subgranular zone cell proliferation after 7 days of abstinence. Increased proliferation was followed by a 75% increase in doublecortin expression and a 56% increase in surviving bromodeoxyuridine-labeled cells 14 and 35 days post-ethanol exposure, respectively. The majority of newborn cells in ethanol and control groups co-localized with NeuN, indicating a neuronal phenotype and therefore a 1.6-fold increase in hippocampal neurogenesis during abstinence. Although these results mirror the magnitude of reactive neurogenesis described in adult rat studies, ectopic bromodeoxyuridine and doublecortin positive cells were detected in the molecular layer and hilus of adolescent rats displaying severe withdrawal symptoms, an effect that has not been described in adults. The presence of ectopic neuroblasts suggests that a potential defect exists in the functional incorporation of new neurons into the existing hippocampal circuitry for a subset of rats. Age-related differences in functional incorporation could contribute to the increased vulnerability of the adolescent hippocampus to ethanol.

Indexed as

AlcoholismAnimalsCentral Nervous System DepressantsDisease Models, AnimalDoublecortin ProteinEnzyme-Linked Immunosorbent AssayEthanolHippocampusHumansMaleNeurogenesisRatsRats, Sprague-DawleySubstance Withdrawal SyndromeCentral Nervous System DepressantsDcx protein, ratDoublecortin ProteinEthanolAlcoholismethanolwithdrawal

Identifiers

PMID23844726
PMCPMC3844012
OpenAlexW1569718348

What OpenQuestion holds

Textmetadata
LicenceTDM
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.