Evidence map›Paper›PMID 14602831›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Capsazepine protects against neuronal injury caused by oxygen glucose deprivation by inhibiting I(h).

Alison M Ray, Ceri D Benham, Jenny C Roberts, Catherine H Gill, Christophe Lanneau, Danniel P Gitterman, Mark Harries, John B Davis, Christopher H Davies

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Inhibition of transient receptor potential vanilloid type 1 through αThe Journal of veterinary medical science · 2021
    Article
  3. Article
  4. Suppression of Presynaptic Glutamate Release by Postsynaptic Metabotropic NMDA Receptor Signalling to Pannexin-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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  18. Transient receptor potential vanilloid subtype 1 mediates cell death of mesencephalic dopaminergic neurons in vivo and in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  19. 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

9 authors at 1 institution in 1 country.

Alison M RayNeurology Centre of Excellence for Drug Discovery, GlaxoSmithKline, Harlow, Essex, CM19 5AW, United Kingdom. alison_m_ray@gsk.com
Ceri D Benham
Jenny C Roberts
Catherine H Gill
Christophe Lanneau
Danniel P Gitterman
Mark Harries
John B Davis
Christopher H Davies
GlaxoSmithKline (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell death mechanisms frequently involve the influx of extracellular calcium through voltage- and ligand-gated ion channels, e.g., the NMDA receptor (Greene, 1999). The vanilloid receptor (VR1) is present in regions of the brain (Mezey et al., 2000) that are highly susceptible to neurodegenerative insults, suggesting that this ion channel might contribute to the cellular processes involved in neuronal death. We tested the effects of VR1 ligands in the oxygen glucose deprivation (OGD) model of cell death in organotypic hippocampal slice cultures. The VR1 agonist capsaicin at concentrations that are selective for VR1 did not affect cell viability per se or the extent of neurodegeneration induced by the OGD insult. In contrast, the VR1 antagonist capsazepine (0.1-10 microm) significantly reduced the amount of OGD-induced cell death. However, capsazepine was still neuroprotective in slices prepared from VR1 knock-out mice, which exhibited the same degree of neurodegeneration to that observed in slices prepared from wild-type mice, excluding the possibility that it afforded neuroprotection through inhibition of VR1. Instead, capsazepine inhibited the hyperpolarization-activated nonspecific cation channel generated current I(h) in a concentration range similar to that which was neuroprotective. Furthermore, the specific I(h) blocker ZD-7288 was also neuroprotective, mirroring the effects of capsazepine, in that it was effective at preventing cell death when applied either during or after the OGD insult. These results demonstrate that capsazepine affords neuroprotection through inhibition of I(h) rather than inhibition of VR1.

Indexed as

Nerve Tissue ProteinsAnimalsCapsaicinCell DeathCell HypoxiaCells, CulturedCyclic Nucleotide-Gated Cation ChannelsCytoprotectionDose-Response Relationship, DrugGlucoseHippocampusHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIn Vitro TechniquesIon ChannelsMiceMice, KnockoutCapsaicincapsazepineCyclic Nucleotide-Gated Cation ChannelsGlucoseHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsNerve Tissue ProteinsNeuroprotective AgentsPotassium ChannelsReceptors, Drug

Identifiers

PMID14602831
PMCPMC6740864
OpenAlexW2118839775

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.