Evidence map›Paper›PMID 26387685›Full record

ArticleCNS neuroscience & therapeutics2016

Na(+) -Ca(2+) Exchanger, Leak K(+) Channel and Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Comediate the Histamine-Induced Excitation on Rat Inferior Vestibular Nucleus Neurons.

Lei Yu, Xiao-Yang Zhang, Shu-Liang Cao, Shi-Yu Peng, Deng-Yu Ji, Jing-Ning Zhu, Jian-Jun Wang

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. The intestinalMicrobiology spectrum · 2026
    Article
  2. [Research advances in the mechanism of vestibular compensation and treatment].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024
    Article
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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

7 authors at 1 institution in 1 country.

Lei YuState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Xiao-Yang ZhangState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Shu-Liang CaoState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Shi-Yu PengState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Deng-Yu JiState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Jing-Ning ZhuState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Jian-Jun WangState Key Laboratory of Pharmaceutical Biotechnology, Department of Biological Science and Technology, School of Life Sciences, Nanjing University, Nanjing, China.
Nanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAntihistaminergic drugs have traditionally been used to treat vestibular disorders in the clinic. As a potential central target for antihistaminergic drugs, the inferior vestibular nucleus (IVN) is the largest subnucleus of the central vestibular nuclear complex and is considered responsible for vestibular-autonomic responses and integration of vestibular, cerebellar, and multisensory signals. However, the role of histamine on the IVN, particularly the underlying mechanisms, is still not clear.

methodsUsing whole-cell patch-clamp recordings on rat brain slices, histamine-induced effect on IVN neurons and the underlying receptor and ionic mechanisms were investigated.

resultsWe found that histamine remarkably depolarized both spontaneous firing neurons and silent neurons in IVN via both histamine H1 and histamine H2 receptors. Furthermore, Na(+) -Ca(2+) exchangers (NCXs) and background leak K(+) channels linked to H1 receptors and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels coupled to H2 receptors comediate the histamine-induced depolarization on IVN neurons.

conclusionThese results demonstrate the multiple ionic mechanisms underlying the excitatory modulation of histamine/central histaminergic system on IVN neurons and the related vestibular reflexes and functions. The findings also suggest potential targets for the treatment of vestibular disorders in the clinic, at the level of ionic channels in central vestibular nuclei.

Indexed as

AnimalsAnimals, NewbornBenzyl CompoundsCesiumChloridesCyclic Nucleotide-Gated Cation ChannelsDose-Response Relationship, DrugHistamineHistamine AgentsIn Vitro TechniquesMembrane PotentialsNeuronsPatch-Clamp TechniquesPotassium Channel BlockersPotassium ChannelsPyrimidines2-(4-(4-nitrobenzyloxy)benzyl)thiazolidine-4-carboxylic acid ethyl esterBenzyl CompoundsCesiumcesium chlorideChloridesCNGA1 protein, ratCyclic Nucleotide-Gated Cation ChannelsHistamineHistamine AgentsICI D2788Potassium Channel BlockersPotassium ChannelsPyrimidinesSodium-Calcium ExchangerSodium Channel BlockersTetrodotoxinThiazolidinesH1 receptorsH2 receptorsHistamineInferior vestibular nucleusIonic mechanisms

Identifiers

PMID26387685
PMCPMC6492809
OpenAlexW1931778381

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Registered trials

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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.