Evidence map›Paper›PMID 9651211›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Vasoactive intestinal peptide enhances its own expression in sympathetic neurons after injury.

R P Mohney, R E Zigmond

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

10 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Neurotrophic regulation of calcium channels by the peptide neurotransmitter luteinizing hormone releasing hormone.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  8. Article
  9. Article
  10. A new concept in the pharmacology of neuroprotection.Journal of molecular neuroscience : MN
    Review
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.

R P MohneyDepartment of Neurosciences, Case Western Reserve University, Cleveland Ohio 44106-4975, USA.
R E Zigmond
Case Western Reserve University · US

Funding

EXPERIENCE AND THE NEUROCHEMISTRY OF THE SYNAPSER01NS012651 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZIGMOND, RICHARD E · 1985 to 2002
$1.0M
NINDS NIH HHS NS12651
6 · The paper itself

Abstract

Neurons in the adult rat superior cervical sympathetic ganglion (SCG) dramatically increase their content of vasoactive intestinal peptide (VIP) and its mRNA after axotomy in vivo and after explantation. Because the VIP gene contains a functional cAMP response element, the effects of cAMP-elevating agents on VIP expression were examined. VIP, forskolin, or isoproterenol increased cAMP accumulation in explanted ganglia. Secretin, a peptide chemically related to VIP, or forskolin increased VIP levels above those seen in ganglia cultured in control medium, whereas treatment with VIP or secretin increased the level of peptide histidine isoleucine (PHI), a peptide coded for by the same mRNA that encodes VIP. VIP or forskolin also increased VIP-PHI mRNA. In contrast, isoproterenol did not alter levels of VIP, PHI, or VIP-PHI mRNA. Although VIP or forskolin increased cAMP levels in both dissociated neurons and in non-neuronal cells, isoproterenol significantly stimulated cAMP accumulation only in the latter. VIP6-28 was an effective antagonist of the actions of exogenous VIP on cAMP and VIP-PHI mRNA in neuron-enriched cultures. When adult SCG explants were cultured in defined medium, endogenous VIP immunoreactivity was released. When VIP6-28 was added to such cultures, it significantly inhibited the increase in VIP-PHI mRNA that normally occurs. These data indicate that VIP, or a closely related molecule, produced by adult neurons after injury can enhance the expression of VIP. Such a mechanism may prolong the period during which VIP is elevated after axonal damage. The possibility is also discussed that, because VIP is present in preganglionic neurons in normal animals, its release during periods of increased sympathetic nerve activity could alter VIP expression in the SCG.

Indexed as

AnimalsAxotomyCells, CulturedColforsinCyclic AMPFeedbackIsoproterenolMaleNeuronsOrgan Culture TechniquesPeptide FragmentsRadioimmunoassayRatsRats, Sprague-DawleyRNA, MessengerStimulation, ChemicalColforsinCyclic AMPIsoproterenolPeptide FragmentsRNA, MessengerVasoactive Intestinal Peptidevasoactive intestinal peptide (6-28)

Identifiers

PMID9651211
PMCPMC6793472
OpenAlexW2153631516

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.