Evidence map›Paper›PMID 19748836›Full record

ReviewAutonomic neuroscience : basic & clinical2009

Neurotrophins and target interactions in the development and regulation of sympathetic neuron electrical and synaptic properties.

Jason A Luther, Susan J Birren

Abstract readReview
In one paragraph

Review in Autonomic neuroscience : basic & clinical, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Brain-derived neurotrophic factor in cigarette smoke-induced airway hyperreactivity.American journal of respiratory cell and molecular biology · 2013
    Trial
  2. Review
  3. Article
  4. Article
  5. Observational
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  7. Review
  8. Review
  9. Article
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  11. Review
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  13. Review
  14. Article
  15. Merkel Cell-Driven BDNF Signaling Specifies SAI Neuron Molecular and Electrophysiological Phenotypes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Article
  17. Article
  18. An NT4/TrkB-dependent increase in innervation links early-life allergen exposure to persistent airway hyperreactivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Jason A LutherDepartment of Biology, National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA. jluther@brandeis.edu
Susan J Birren
Brandeis University · US

Funding

Divergence and maturation of autonomic lineagesR01HD042716 · NICHD · BRANDEIS UNIVERSITY · PI BIRREN, SUSAN J · 2004 to 2009
$1.7M
DEVELOPMENT AND MODULATION OF AUTONOMIC SYNAPSESR01NS040168 · NINDS · BRANDEIS UNIVERSITY · PI BIRREN, SUSAN J · 2000 to 2004
$1.3M
NICHD NIH HHS R01 HD042716NINDS NIH HHS R01 NS040168
6 · The paper itself

Abstract

The electrical and synaptic properties of neurons are essential for determining the function of the nervous system. Thus, understanding the mechanisms that control the appropriate developmental acquisition and maintenance of these properties is a critical problem in neuroscience. A great deal of our understanding of these developmental mechanisms comes from studies of soluble growth factor signaling between cells in the peripheral nervous system. The sympathetic nervous system has provided a model for studying the role of these factors both in early development and in the establishment of mature properties. In particular, neurotrophins produced by the targets of sympathetic innervation regulate the synaptic and electrophysiological properties of postnatal sympathetic neurons. In this review we examine the role of neurotrophin signaling in the regulation of synaptic strength, neurotransmitter phenotype, voltage-gated currents and repetitive firing properties of sympathetic neurons. Together, these properties determine the level of sympathetic drive to target organs such as the heart. Changes in this sympathetic drive, which may be linked to dysfunctions in neurotrophin signaling, are associated with devastating diseases such as high blood pressure, arrhythmias and heart attack. Neurotrophins appear to play similar roles in modulating the synaptic and electrical properties of other peripheral and central neuronal systems, suggesting that information provided from studies in the sympathetic nervous system will be widely applicable for understanding the neurotrophic regulation of neuronal function in other systems.

Indexed as

Action PotentialsAdrenergic FibersAnimalsAutonomic Nervous System DiseasesCholinergic FibersGanglia, SympatheticHumansIon Channel GatingNerve Growth FactorsNerve Tissue ProteinsNeuronal PlasticityNeuronsPhosphorylationPotassiumPotassium ChannelsProtein Processing, Post-TranslationalNerve Growth FactorsNerve Tissue ProteinsPotassiumPotassium ChannelsReceptor, Nerve Growth FactorReceptor, trkA

Identifiers

PMID19748836
PMCPMC2765534
OpenAlexW2018288912

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.