Evidence map›Paper›PMID 29285614›Full record

ArticleNeurotoxicity research2018

The Effects of Quinine on Neurophysiological Properties of Dopaminergic Neurons.

Li Zou, Yingchao Xue, Michael Jones, Thomas Heinbockel, Mingyao Ying, Xiping Zhan

Abstract read
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In one paragraph

Article in Neurotoxicity research, 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
1.1field-weighted citation impact, top 26% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Inhibition of connexin hemichannels alleviates neuroinflammation and hyperexcitability in temporal lobe epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Will Tonic Water Stop My Eyelid Twitching?Clinical ophthalmology (Auckland, N.Z.) · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. 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

6 authors at 2 institutions in 1 country.

Li ZouDepartment of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA.
Yingchao XueDepartment of Neurology, Hugo W. Moser Research Institute at Kennedy Krieger, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michael JonesDepartment of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA.
Thomas HeinbockelDepartment of Anatomy, Howard University College of Medicine, Washington, DC, USA.
Mingyao YingDepartment of Neurology, Hugo W. Moser Research Institute at Kennedy Krieger, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Xiping ZhanDepartment of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA. xipingzhan@hotmail.com.ORCID 0000-0003-2008-6326
Howard University · USKennedy Krieger Institute · US

Funding

Hearing Health Foundation 14-02613
6 · The paper itself

Abstract

Quinine is an antimalarial drug that is toxic to the auditory system by commonly inducing hearing loss and tinnitus, presumably due to its ototoxic effects on disruption of cochlear hair cells and blockade of ion channels of neurons in the auditory system. To a lesser extent, quinine also causes ataxia, tremor, and dystonic reactions. As dopaminergic neurons are implicated to play a role in all of these diseases, we tested the toxicity of quinine on induced dopaminergic (iDA) neurons derived from human pluripotent stem cells (iPSCs) and primary dopaminergic (DA) neurons of substantia nigra from mice brain slices. Patch clamp recordings and combined drug treatments were performed to examine key physiological properties of the DA neurons. We found that quinine (12.5-200 μM) depolarized the resting membrane potential and attenuated the amplitudes of rebound spikes induced by hyperpolarization. Action potentials were also broadened in spontaneously spiking neurons. In addition to quinine attenuating hyperpolarization-dependent conductance, the tail currents following withdrawal of hyperpolarizing currents were also attenuated. Taken together, we found that iPSC-derived DA neurons recapitulated all the tested physiological properties of human DA neurons, and quinine had distinct effects on the physiology of both iDA and primary DA neurons. This toxicity of quinine may be the underlying mechanism for the movement disorders of cinchonism or quinism and may play a role in tinnitus modulation.

Indexed as

Action PotentialsAnalgesics, Non-NarcoticAnimalsAutistic DisorderBiotinCardiovascular AgentsDopaminergic NeuronsDose-Response Relationship, DrugFemaleHumansIn Vitro TechniquesMaleMiceMice, Inbred C57BLPatch-Clamp TechniquesPiperidines4-aminopiperidineAnalgesics, Non-NarcoticBiotinCardiovascular AgentsICI D2788neurobiotinPiperidinesPotassium Channel BlockersPyrimidinesQuinineSodium Channel BlockersTetrodotoxinTyrosine 3-MonooxygenaseDopaminergic neuronHyperpolarizationiPS cellQuinine

Identifiers

PMID29285614
OpenAlexW2777894334

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.