Evidence map›Paper›PMID 22033836›Full record

ArticleCellular and molecular life sciences : CMLS2012

Developmental nicotine exposure induced alterations in behavior and glutamate receptor function in hippocampus.

Kodeeswaran Parameshwaran, Manal A Buabeid, Senthilkumar S Karuppagounder, Subramaniam Uthayathas, Karikaran Thiruchelvam, Brian Shonesy, Alexander Dityatev, Martha C Escobar, Muralikrishnan Dhanasekaran, Vishnu Suppiramaniam

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.3field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Nicotine and the developing brain: Insights from preclinical models.Pharmacology, biochemistry, and behavior · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Bisphenol A Impairs Synaptic Plasticity by Both Pre- and Postsynaptic Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2017
    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

10 authors at 1 institution in 2 countries.

Kodeeswaran ParameshwaranDepartment of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Auburn, AL 36849, USA.
Manal A Buabeid
Senthilkumar S Karuppagounder
Subramaniam Uthayathas
Karikaran Thiruchelvam
Brian Shonesy
Alexander Dityatev
Martha C Escobar
Muralikrishnan Dhanasekaran
Vishnu Suppiramaniam
Auburn University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the developing brain, nicotinic acetylcholine receptors (nAChRs) are involved in cell survival, targeting, formation of neural and sensory circuits, and development and maturation of other neurotransmitter systems. This regulatory role is disrupted when the developing brain is exposed to nicotine, which occurs with tobacco use during pregnancy. Prenatal nicotine exposure has been shown to be a strong risk factor for memory deficits and other behavioral aberrations in the offspring. The molecular mechanisms underlying these neurobehavioral outcomes are not clearly elucidated. We used a rodent model to assess behavioral, neurophysiological, and neurochemical consequences of prenatal nicotine exposure in rat offspring with specific emphasis on the hippocampal glutamatergic system. Pregnant dams were infused with nicotine (6 mg/kg/day) subcutaneously from the third day of pregnancy until birth. Results indicate that prenatal nicotine exposure leads to increased anxiety and depressive-like effects and impaired spatial memory. Synaptic plasticity in the form of long-term potentiation (LTP), basal synaptic transmission, and AMPA receptor-mediated synaptic currents were reduced. The deficit in synaptic plasticity was paralleled by declines in protein levels of vesicular glutamate transporter 1 (VGLUT1), synaptophysin, AMPA receptor subunit GluR1, phospho(Ser845) GluR1, and postsynaptic density 95 (PSD-95). These results suggest that prenatal nicotine exposure by maternal smoking could result in alterations in the glutamatergic system in the hippocampus contributing to the abnormal neurobehavioral outcomes.

Indexed as

AnimalsBehavior, AnimalElectrophysiologyFemaleGene Expression RegulationHippocampusNicotinePregnancyPrenatal Exposure Delayed EffectsRatsRats, Sprague-DawleyReceptors, GlutamateReceptors, N-Methyl-D-AspartateNicotineReceptors, GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22033836
PMCPMC11114542
OpenAlexW2015626820

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.