Evidence map›Paper›PMID 29619740›Full record

ArticleMolecular neurobiology2018

Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons.

Juan A Godoy, Angel G Valdivieso, Nibaldo C Inestrosa

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Mitochondria as a possible target for nicotine action.Journal of bioenergetics and biomembranes · 2019
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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 3 institutions in 3 countries.

Juan A GodoyCentro de Envejecimiento y Regeneración (CARE UC); Departamento de Biología Celular y Molecular; Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Angel G ValdiviesoInstitute for Biomedical Research (BIOMED), Laboratory of Cellular and Molecular Biology, School of Medical Sciences, Pontifical Catholic University of Argentina (UCA) and The National Scientific and Technical Research Council of Argentina (CONICET), Buenos Aires, Argentina.
Nibaldo C InestrosaCentro de Envejecimiento y Regeneración (CARE UC); Departamento de Biología Celular y Molecular; Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile. ninestrosa@bio.puc.cl.
Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable · ESConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad de Magallanes · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process. Mitochondrial health depends on balanced fusion-fission events, termed mitochondrial dynamics, to repair damaged organelles and/or improve the quality of mitochondrial function, ATP production, calcium homeostasis, and apoptosis, which represent some mitochondrial functions closely related to mitochondrial dynamics. Several neurodegenerative disorders, such as Alzheimer's, Parkinson's, and Huntington's diseases, have been correlated with severe mitochondrial dysfunction. In this regard, nicotine, which has been associated with relevant neuroprotective effects mainly through activation of the nicotinic acetylcholine receptor (nAChR), exerts its effects at least in part by acting directly on mitochondrial physiology and morphology. Additionally, a recent description of mitochondrial nAChR localization suggests a nicotine-dependent mitochondrial function. In the present work, we evaluated in cultured hipocampal neurons the effects of nicotine on mitochondrial dynamics by assessing mitochondrial morphology, membrane potential, as well as interactions between mitochondria, cytoskeleton and IP

Indexed as

AnimalsCells, CulturedCytoskeletonDynaminsHippocampusInositol 1,4,5-Trisphosphate ReceptorsMitochondrial DynamicsNeuronsNicotinePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphorylationRats, Sprague-DawleyDnm1l protein, ratDynaminsInositol 1,4,5-Trisphosphate ReceptorsNicotinePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratDpr1Mitochondrial dynamicsNeuronsNicotinePGC-1α

Identifiers

PMID29619740
OpenAlexW2795953932

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.