Evidence map›Paper›PMID 27255453›Full record

ArticleMedical & biological engineering & computing2017

Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.

Pınar Kanlikilicer, Die Zhang, Andrei Dragomir, Yasemin M Akay, Metin Akay

Abstract read
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In one paragraph

Article in Medical & biological engineering & computing, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022
    Review
  4. Sex-specific nicotine sensitization and imprinting of self-administration in rats inform GWAS findings on human addiction phenotypes.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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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.

Pınar KanlikilicerDepartment of Biomedical Engineering, University of Houston, SERC Building, 3605 Cullen Blvd, Houston, TX, 77204, USA.
Die ZhangDepartment of Biomedical Engineering, University of Houston, SERC Building, 3605 Cullen Blvd, Houston, TX, 77204, USA.
Andrei DragomirDepartment of Biomedical Engineering, University of Houston, SERC Building, 3605 Cullen Blvd, Houston, TX, 77204, USA.
Yasemin M AkayDepartment of Biomedical Engineering, University of Houston, SERC Building, 3605 Cullen Blvd, Houston, TX, 77204, USA.
Metin AkayDepartment of Biomedical Engineering, University of Houston, SERC Building, 3605 Cullen Blvd, Houston, TX, 77204, USA. makay@uh.edu.
University of Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal smoking during pregnancy is associated with low birth weight, increased risk of stillbirth, conduct disorder, attention-deficit/hyperactivity disorder and neurocognitive deficits. Ventral tegmental area dopamine (DA) neurons in the mesocorticolimbic pathway were suggested to play a critical role in these pathological mechanisms induced by nicotine. Nicotine-mediated changes in genetic expression during pregnancy are of great interest for current researchers. We used patch clamp methods to identify and harvest DA and non-DA neurons separately and assayed them using oligonucleotide arrays to elucidate the alterations in gene expressions in these cells upon gestational nicotine exposure. Microarray analysis identified a set of 135 genes as significantly differentially expressed between DA and non-DA neurons. Some of the genes were found to be related to neurological disease pathways, such as Alzheimer's disease, Parkinson's disease and Huntington's disease. Significantly up-/down-regulated genes found in DA neurons were mostly related to G-protein-coupled protein receptor signaling and developmental processes. These alterations in gene expressions may explain, partially at least, the possible pathological mechanisms for the diseases induced by maternal smoking.

Indexed as

Gene Expression ProfilingAction PotentialsAnimalsCluster AnalysisDopaminergic NeuronsDown-RegulationFemaleGene OntologyMesencephalonMolecular Sequence AnnotationNicotineOligonucleotide Array Sequence AnalysisPregnancyRats, Sprague-DawleyReal-Time Polymerase Chain ReactionReproducibility of ResultsNicotineRNA, MessengerDopamineGestational nicotineMicroarrayNeurological diseasesVTA

Identifiers

PMID27255453
OpenAlexW2461651347

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.