Evidence map›Paper›PMID 27405470›Full record

ArticleMolecular neurobiology2017

Nicotine Significantly Improves Chronic Stress-Induced Impairments of Cognition and Synaptic Plasticity in Mice.

Xueliang Shang, Yingchun Shang, Jingxuan Fu, Tao Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 67 citations in OpenAlex.

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  18. Independent and Combined Effects of Nicotine or Chronic Tobacco Smoking and HIV on the Brain: A Review of Preclinical and Clinical Studies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  19. Review
  20. Neurotoxicity of e-cigarettes.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    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 2 institutions in 1 country.

Xueliang ShangCollege of Life Sciences and State Key Laboratory of Medicinal Chemical Biology, Nankai University, 300071, Tianjin, People's Republic of China.
Yingchun ShangCollege of Life Sciences and State Key Laboratory of Medicinal Chemical Biology, Nankai University, 300071, Tianjin, People's Republic of China.
Jingxuan FuCollege of Life Sciences and State Key Laboratory of Medicinal Chemical Biology, Nankai University, 300071, Tianjin, People's Republic of China.
Tao ZhangCollege of Life Sciences and State Key Laboratory of Medicinal Chemical Biology, Nankai University, 300071, Tianjin, People's Republic of China. zhangtao@nankai.edu.cn.
Nankai University · CNState Key Laboratory of Medicinal Chemical Biology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to examine if nicotine was able to improve cognition deficits in a mouse model of chronic mild stress. Twenty-four male C57BL/6 mice were divided into three groups: control, stress, and stress with nicotine treatment. The animal model was established by combining chronic unpredictable mild stress (CUMS) and isolated feeding. Mice were exposed to CUMS continued for 28 days, while nicotine (0.2 mg/kg) was also administrated for 28 days. Weight and sucrose consumption were measured during model establishing period. The anxiety and behavioral despair were analyzed using the forced swim test (FST) and open-field test (OFT). Spatial cognition was evaluated using Morris water maze (MWM) test. Following behavioral assessment, both long-term potentiation (LTP) and depotentiation (DEP) were recorded in the hippocampal dentate gyrus (DG) region. Both synaptic and Notch1 proteins were measured by Western. Nicotine increased stressed mouse's sucrose consumption. The MWM test showed that spatial learning and reversal learning in stressed animals were remarkably affected relative to controls, whereas nicotine partially rescued cognitive functions. Additionally, nicotine considerably alleviated the level of anxiety and the degree of behavioral despair in stressed mice. It effectively mitigated the depression-induced impairment of hippocampal synaptic plasticity, in which both the LTP and DEP were significantly inhibited in stressed mice. Moreover, nicotine enhanced the expression of synaptic and Notch1 proteins in stressed animals. The results suggest that nicotine ameliorates the depression-like symptoms and improves the hippocampal synaptic plasticity closely associated with activating transmembrane ion channel receptors and Notch signaling components. Graphical Abstract ᅟ.

Indexed as

Neuronal PlasticityAnimalsBody WeightChoice BehaviorChronic DiseaseCognition DisordersGene Expression RegulationGlutamate DecarboxylaseHippocampusLong-Term PotentiationMaleMaze LearningMice, Inbred C57BLNicotineReceptors, N-Methyl-D-AspartateStress, PsychologicalGlutamate Decarboxylaseglutamate decarboxylase 1NicotineNR2A NMDA receptorNR2B NMDA receptorReceptors, N-Methyl-D-AspartateSucroseC57 miceChronic unpredictable mild stressNicotineNotch1 signalingSynaptic plasticity

Identifiers

PMID27405470
OpenAlexW2469550585

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.