Evidence map›Paper›PMID 22434221›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012

Chronic adolescent exposure to delta-9-tetrahydrocannabinol in COMT mutant mice: impact on indices of dopaminergic, endocannabinoid and GABAergic pathways.

Aine T Behan, Magdalena Hryniewiecka, Colm M P O'Tuathaigh, Anthony Kinsella, Mary Cannon, Maria Karayiorgou, Joseph A Gogos, John L Waddington, David R Cotter

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 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
8.4field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Adolescent ΔBiological psychiatry · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. The effects of ΔNature · 2016
    Review
  16. The Role of Pharmacotherapy in the Treatment of Adolescent Substance Use Disorders.Child and adolescent psychiatric clinics of North America · 2016
    Review
  17. Review
  18. Review
  19. Review
  20. Cannabis, the pregnant woman and her child: weeding out the myths.Journal of perinatology : official journal of the California Perinatal Association · 2014
    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

9 authors at 3 institutions in 2 countries.

Aine T BehanDepartment of Psychiatry, Royal College of Surgeons in Ireland, Dublin, Ireland. abehan@rcsi.ie
Magdalena Hryniewiecka
Colm M P O'Tuathaigh
Anthony Kinsella
Mary Cannon
Maria Karayiorgou
Joseph A Gogos
John L Waddington
David R Cotter
Royal College of Surgeons in Ireland · IEColumbia University · USUniversity College Cork · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cannabis use confers a two-fold increase in risk for psychosis, with adolescent use conferring an even greater risk. A high-low activity polymorphism in catechol-O-methyltransferase (COMT), a gene encoding the COMT enzyme involved in dopamine clearance in the brain, may interact with adolescent cannabis exposure to increase risk for schizophrenia. The impact of such an interaction on central neurotransmitter pathways implicated in schizophrenia is unknown. Male mice with knockout of the COMT gene were treated chronically with delta-9-tetrahydrocannabinol (THC) during adolescence (postnatal day 32-52). We measured the size and density of GABAergic cells and the protein expression of cannabinoid receptor 1 (CB1R) in the prefrontal cortex (PFC) and hippocampus (HPC) in knockout mice relative to heterozygous mutants and wild-type controls. Size and density of dopaminergic neurons was also assessed in the ventral tegmental area (VTA) across the genotypes. COMT genotype × THC treatment interactions were observed for: (1) dopaminergic cell size in the VTA, (2) CB1R protein expression in the HPC, and (3) parvalbumin (PV) cell size in the PFC. No effects of adolescent THC treatment were observed for PV and dopaminergic cell density across the COMT genotypes. COMT genotype modulates the effects of chronic THC administration during adolescence on indices of neurotransmitter function in the brain. These findings illuminate how COMT deletion and adolescent cannabis use can interact to modulate the function of neurotransmitters systems implicated in schizophrenia.

Indexed as

EndocannabinoidsAnimalsBrainCannabinoid Receptor ModulatorsCatechol O-MethyltransferaseCell CountDopamineDopaminergic NeuronsDronabinolGABAergic Neuronsgamma-Aminobutyric AcidMaleMiceMice, KnockoutTyrosine 3-MonooxygenaseCannabinoid Receptor ModulatorsCatechol O-MethyltransferaseDopamineDronabinolEndocannabinoidsgamma-Aminobutyric AcidTyrosine 3-Monooxygenase

Identifiers

PMID22434221
PMCPMC3358747
OpenAlexW1989764163

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.