Evidence map›Paper›PMID 18614767›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008

Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation.

Megan A Doczi, Anthony D Morielli, Deborah H Damon

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Unconventional EGF-induced ERK1/2-mediated Kv1.3 endocytosis.Cellular and molecular life sciences : CMLS · 2016
    Article
  3. Article
  4. Article
  5. Selective Kv1.3 channel blocker as therapeutic for obesity and insulin resistance.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

3 authors at 1 institution in 1 country.

Megan A DocziDepartment of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA.
Anthony D Morielli
Deborah H Damon
University of Vermont · US

Funding

Mechanisms of Kv1.2 regulation by tyrosine kinaseR01NS050623 · NINDS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MORIELLI, ANTHONY D · 2004 to 2008
$1.7M
Vascular determinants of sympathetic innervationR01HL076774 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI DAMON, DEBORAH HEINS · 2005 to 2008
$1.5M
NHLBI NIH HHS HL-076774NINDS NIH HHS NS-050623
6 · The paper itself

Abstract

Kv1.3 channels are known to modulate many aspects of neuronal function. We tested the hypothesis that Kv1.3 modulates the function of postganglionic sympathetic neurons. RT-PCR, immunoblot, and immunohistochemical analyses indicated that Kv1.3 channels were expressed in these neurons. Immunohistochemical analyses indicated that Kv1.3 protein was localized to neuronal cell bodies, processes, and nerve fibers at sympathetic neurovascular junctions. Margatoxin (MgTX), a specific inhibitor of Kv1.3, was used to assess the function of the channel. Electrophysiological analyses indicated that MgTX significantly reduced outward currents [P < 0.05; n = 18 (control) and 15 (MgTX)], depolarized resting membrane potential, and decreased the latency to action potential firing [P < 0.05; n = 11 (control) and 13 (MgTX)]. The primary physiological input to postganglionic sympathetic neurons is ACh, which activates nicotinic and muscarinic ACh receptors. MgTX modulated nicotinic ACh receptor agonist-induced norepinephrine release (P < 0.05; n >or= 6), and MgTX-sensitive current was suppressed upon activation of muscarinic ACh receptors with bethanechol (P < 0.05; n = 12). These data indicate that Kv1.3 affects the function of postganglionic sympathetic neurons, which suggests that Kv1.3 influences sympathetic control of cardiovascular function. Our data also indicate that modulation of Kv1.3 is likely to affect sympathetic control of cardiovascular function.

Indexed as

AnimalsAnimals, NewbornBlood PressureCells, CulturedFemaleGene ExpressionGreen Fluorescent ProteinsImmunohistochemistryKv1.3 Potassium ChannelMaleNeuronsPatch-Clamp TechniquesRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionScorpion VenomsGreen Fluorescent ProteinsKv1.3 Potassium ChannelmargatoxinScorpion Venoms

Identifiers

PMID18614767
PMCPMC2536860
OpenAlexW1965832750

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.