Evidence map›Paper›PMID 21167848›Full record

ArticleNeuropharmacology2011

Nicotine ameliorates NMDA receptor antagonist-induced deficits in contextual fear conditioning through high-affinity nicotinic acetylcholine receptors in the hippocampus.

Jessica M André, Prescott T Leach, Thomas J Gould

Abstract read
In one paragraph

Article in Neuropharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Neurotoxicity of e-cigarettes.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    Review
  5. Nicotinic Receptor Intervention in Parkinson's Disease: Future Directions.Clinical pharmacology and translational medicine · 2017
    Article
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  8. Review
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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

3 authors at 1 institution in 1 country.

Jessica M AndréDepartment of Psychology, Temple University, Philadelphia, PA 19122, USA.
Prescott T Leach
Thomas J Gould
Temple University · US

Funding

TRAINING PROGRAM: DRUGS OF ABUSE RELATED NEUROPEPTIDEST32DA007237 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI ELLEN M UNTERWALD · 1988 to 2026
$10.6M
Neuroimaging Abstinence and Medication ResponseP50CA143187 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BLENDY, JULIE A · 2009 to 2013
$8.6M
Nicotine Addiction: Learning, Neural &Genetic ProcessR01DA017949 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI GOULD, THOMAS J · 2005 to 2015
$2.7M
Genetic, Behavioral, & Neurobiological Substrates of Nicotine WithdrawalR01DA024787 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI GOULD, THOMAS J · 2008 to 2012
$1.7M
NCI NIH HHS CA143187NCI NIH HHS P50 CA143187NIDA NIH HHS DA017949NIDA NIH HHS DA024787NIDA NIH HHS R01 DA017949NIDA NIH HHS R01 DA024787NIDA NIH HHS T32 DA007237
6 · The paper itself

Abstract

NMDA glutamate receptors (NMDARs) and nicotinic acetylcholine receptors (nAChRs) are both involved in learning and synaptic plasticity. Increasing evidence suggests processes mediated by these receptors may interact to modulate learning; however, little is known about the neural substrates involved in these interactive processes. The present studies investigated the effects of nicotine on MK-801 hydrogen maleate (MK-801) and DL-2-Amino-5-phosphonovaleric acid (APV)-induced disruption of contextual fear conditioning in male C57BL/6J mice, using direct drug infusion and selective nAChR antagonists to define the brain regions and the nAChR subtypes involved. Mice treated with MK-801 showed a deficit in contextual fear conditioning that was ameliorated by nicotine. Direct drug infusion demonstrated that the NMDAR antagonists disrupted hippocampal function and that nicotine acted in the dorsal hippocampus to ameliorate the deficit in learning. The high-affinity nAChR antagonist Dihydro-β-erythroidine hydrobromide (DhβE) blocked the effects of nicotine on MK-801-induced deficits while the α7 nAChR antagonist methyllycaconitine citrate salt hydrate (MLA) did not. These results suggest that NMDARs and nAChRs may mediate similar hippocampal processes involved in contextual fear conditioning. Furthermore, these results may have implications for developing effective therapeutics for the cognitive deficits associated with schizophrenia because a large subset of patients with schizophrenia exhibit cognitive deficits that may be related to NMDAR dysfunction and smoke at much higher rates than the healthy population, which may be an attempt to ameliorate cognitive deficits.

Indexed as

Analysis of VarianceAnimalsAssociation LearningConditioning, ClassicalExcitatory Amino Acid AntagonistsFearHippocampusMaleMiceNicotineNicotinic AgonistsReceptors, NicotinicReceptors, N-Methyl-D-AspartateValine2-amino-5-phosphopentanoic acidExcitatory Amino Acid AntagonistsNicotineNicotinic AgonistsReceptors, NicotinicReceptors, N-Methyl-D-AspartateValine

Identifiers

PMID21167848
PMCPMC3031743
OpenAlexW2084643802

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.