Evidence map›Paper›PMID 24904281›Full record

ArticleFrontiers in cellular neuroscience2014

Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressure-a suggested HPNS partial mechanism.

Ben Aviner, Gideon Gradwohl, Merav Mor Aviner, Shiri Levy, Yoram Grossman

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Exocytosis from chromaffin cells: hydrostatic pressure slows vesicle fusion.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    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

5 authors at 2 institutions in 1 country.

Ben AvinerDepartment of Physiology and Neurobiology, Ben Gurion University of the Negev Beer Sheva, Israel.
Gideon GradwohlDepartment of Physics, Jerusalem College of Technology Jerusalem, Israel.
Merav Mor AvinerDepartment of Physiology and Neurobiology, Ben Gurion University of the Negev Beer Sheva, Israel.
Shiri LevyDepartment of Physiology and Neurobiology, Ben Gurion University of the Negev Beer Sheva, Israel.
Yoram GrossmanDepartment of Physiology and Neurobiology, Ben Gurion University of the Negev Beer Sheva, Israel.
Ben-Gurion University of the Negev · ILJerusalem College of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Professional deep sea divers experience motor and cognitive impairment, known as High Pressure Neurological Syndrome (HPNS), when exposed to pressures of 100 msw (1.1 MPa) and above, considered to be the result of synaptic transmission alteration. Previous studies have indicated modulation of presynaptic Ca(2+) currents at high pressure. We directly measured for the first time pressure effects on the currents of voltage dependent Ca(2+) channels (VDCCs) expressed in Xenopus oocytes. Pressure selectivity augmented the current in CaV1.2 and depressed it in CaV3.2 channels. Pressure application also affected the channels' kinetics, such as ƮRise, ƮDecay. Pressure modulation of VDCCs seems to play an important role in generation of HPNS signs and symptoms.

Indexed as

conformational changehigh pressurehigh pressure neurological syndromehyperbaric helium pressuresynaptic transmissionvoltage dependencyvoltage dependent calcium channels

Identifiers

PMID24904281
PMCPMC4034351
OpenAlexW2171145904

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.