Evidence map›Paper›PMID 20870010›Full record

ArticleNeuroscience2010

Signaling pathways that mediate nerve growth factor-induced increase in expression and release of calcitonin gene-related peptide from sensory neurons.

K A Park, J C Fehrenbacher, E L Thompson, D B Duarte, C M Hingtgen, M R Vasko

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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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.

K A ParkDepartment of Pharmacology and Toxicology, Indiana University School of Medicine, 635 Barnhill Drive A401, Indianapolis, IN 46202, USA.
J C Fehrenbacher
E L Thompson
D B Duarte
C M Hingtgen
M R Vasko
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USYale University · US

Funding

Actions of GTPase-Activating Proteins on Sensory NeuronsR01NS051668 · NINDS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI HINGTGEN, CYNTHIA M · 2006 to 2010
$2.4M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR015481 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIFE, ROSE S · 2001 to 2001
$1.6M
Lipase Products Mediate Sensitization of Sensory NeuronsR01NS048565 · NINDS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI VASKO, MICHAEL R · 2005 to 2008
$1.4M
Effects of Ras on CGRP Release or Content in NeuronsF30NS055448 · NINDS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI PARK, KELLIE A · 2006 to 2008
$75k
NCRR NIH HHS C06 RR015481NCRR NIH HHS C06 RR015481- 01NINDS NIH HHS F30 NS055448NINDS NIH HHS NS048565NINDS NIH HHS NS051668NINDS NIH HHS NS055448NINDS NIH HHS R01 NS048565NINDS NIH HHS R01 NS051668
6 · The paper itself

Abstract

Nerve growth factor (NGF) can augment transmitter release in sensory neurons by acutely sensitizing sensory neurons and by increasing the expression of calcitonin gene-related peptide (CGRP) over time. The current study examined the intracellular signaling pathways that mediate these two temporally distinct effects of NGF to augment CGRP release from sensory neurons. Growing sensory neurons in 30 or 100 ng/mL of NGF for 7 days increases CGRP content and this increase augments the amount of CGRP that is released by high extracellular potassium. Overexpressing a dominant negative Ras, Ras(17N) or treatment with a farnesyltransferase inhibitor attenuates the NGF-induced increase in CGRP content. Conversely, overexpressing a constitutively active Ras augments the NGF-induced increase in content of CGRP. Inhibiting mitogen activated protein kinase (MEK) activity also blocks the ability of NGF to increase CGRP expression. In contrast to the ability of chronic NGF to increase peptide content, acute exposure of sensory neurons to 100 ng/mL NGF augments capsaicin-evoked release of CGRP without affecting the content of CGRP. This sensitizing action of NGF is not affected by inhibiting Ras, MEK, or PI3 kinases. In contrast, the NGF-induced increase in capsaicin-evoked release of CGRP is blocked by the protein kinase C (PKC) inhibitor, BIM and the Src family kinases inhibitor, PP2. These data demonstrate that different signaling pathways mediate the alterations in expression of CGRP by chronic NGF and the acute actions of the neurotrophin to augment capsaicin-evoked release of CGRP in the absence of a change in the content of the peptide.

Indexed as

AnimalsCalcitonin Gene-Related PeptideCells, CulturedGanglia, SpinalMaleNerve Growth FactorNociceptorsRadioimmunoassayRatsRats, Sprague-DawleySensory Receptor CellsSignal TransductionUp-RegulationCalcitonin Gene-Related PeptideNerve Growth Factor

Identifiers

PMID20870010
PMCPMC2987548
OpenAlexW2035144630

What OpenQuestion 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 OpenQuestion graph.