Evidence map›Paper›PMID 27193318›Full record

ArticleJournal of neurophysiology2016

Spontaneously active NaV1.5 sodium channels may underlie odor sensitivity.

Vincent E Dionne

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

1 author at 1 institution in 1 country.

Vincent E DionneDepartment of Biology, Boston University, Boston, Massachusetts vdionne@bu.edu.ORCID 0000-0002-5805-0807
Boston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The olfactory system is remarkably sensitive to airborne odor molecules, but precisely how very low odor concentrations bordering on just a few molecules per olfactory sensory neuron can trigger graded changes in firing is not clear. This report reexamines signaling in olfactory sensory neurons in light of the recent account of NaV1.5 sodium channel-mediated spontaneous firing. Using a model of spontaneous channel activity, the study shows how even submillivolt changes in membrane potential elicited by odor are expected to cause meaningful changes in NaV1.5-dependent firing. The results suggest that the random window currents of NaV1.5 channels may underpin not only spontaneous firing in olfactory sensory neurons but the cellular response to odor as well, thereby ensuring the robustness and sensitivity of signaling that is especially important for low odor concentrations.

Indexed as

Models, NeurologicalOdorantsAction PotentialsAnimalsComputer SimulationElectric StimulationHumansNAV1.5 Voltage-Gated Sodium ChannelNAV1.7 Voltage-Gated Sodium ChannelOlfactory BulbOlfactory Receptor NeuronsNAV1.5 Voltage-Gated Sodium ChannelNAV1.7 Voltage-Gated Sodium ChannelNaV1.5 sodium channelodor signalingolfactionspontaneous channel activitywindow current

Identifiers

PMID27193318
PMCPMC4992733
OpenAlexW2398170522

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.