Evidence map›Paper›PMID 15056713›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Differential distribution and function of hyperpolarization-activated channels in sensory neurons and mechanosensitive fibers.

Thanh N Doan, Kevin Stephans, Angelina N Ramirez, Patricia A Glazebrook, Michael C Andresen, Diana L Kunze

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

57 citing papers in PubMed, 120 citations in OpenAlex.

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  8. Vascular mechanotransduction.Physiological reviews · 2023
    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

6 authors at 3 institutions in 1 country.

Thanh N DoanRammelkamp Center for Education and Research, MetroHealth Medical Center, and Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44109-1998, USA.
Kevin Stephans
Angelina N Ramirez
Patricia A Glazebrook
Michael C Andresen
Diana L Kunze
Case Western Reserve University · USMetroHealth Medical Center · USOregon Health & Science University · US

Funding

ION CHANNELS IN MECHANOSENSITIVE NEURONSR01HL061436 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KUNZE, DIANA L · 1999 to 2007
$2.1M
NHLBI NIH HHS HL061436NHLBI NIH HHS R01 HL061436
6 · The paper itself

Abstract

Sensory neurons express hyperpolarization-activated currents (I(H)) that differ in magnitude and kinetics within the populations. We investigated the structural basis for these differences and explored the functional role of the I(H) channels in sensory neurons isolated from rat nodose ganglia. Immunohistochemical studies demonstrated a differential distribution of hyperpolarization-activated cyclic nucleotide-gated (HCN) protein (HCN1, HCN2, HCN4) in sensory neurons and peripheral terminals. HCN2 and HCN4 immunoreactivity was present in all nodose neurons. In contrast, only 20% of the total population expressed HCN1 immunoreactivity. HCN1 did not colocalize with IB4 (a marker for C-type neurons), and only 15% of HCN1-positive neurons colocalized with immunoreactivity for the vanilloid receptor VR1, another protein associated primarily with C-type neurons. Therefore, most HCN1-containing neurons were A-type neurons. In further support, HCN1 was present in the mechanosensitive terminals of myelinated but not unmyelinated sensory fibers, whereas HCN2 and HCN4 were present in receptor terminals of both myelinated and unmyelinated fibers. In voltage-clamp studies, cell permeant cAMP analogs shifted the activation curve for I(H) to depolarized potentials in C-type neurons but not A-type neurons. In current-clamp recording, CsCl, which inhibits only I(H) in nodose neurons, hyperpolarized the resting membrane potential from -63 +/- 1 to -73 +/- 2 mV and nearly doubled the input resistance from 1.3 to 2.2 GOmega. In addition, action potentials were initiated at lower depolarizing current injections in the presence of CsCl. At the sensory receptor terminal, CsCl decreased the threshold pressure for initiation of mechanoreceptor discharge. Therefore, elimination of the I(H) increases excitability of both the soma and the peripheral sensory terminals.

Indexed as

AnimalsAorta, ThoracicCells, CulturedCesiumChloridesCyclic Nucleotide-Gated Cation ChannelsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsImmunohistochemistryIon ChannelsMaleMechanoreceptorsNeurons, AfferentNodose GanglionPatch-Clamp TechniquesPotassium ChannelsPressoreceptorsCesiumcesium chlorideChloridesCyclic Nucleotide-Gated Cation ChannelsHcn1 protein, ratHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsPotassium Channels

Identifiers

PMID15056713
PMCPMC6730026
OpenAlexW2147765376

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.