Evidence map›Paper›PMID 11956342›Full record

ArticleThe Journal of physiology2002

Calcium and calcium-activated currents in vagotomized rat primary vagal afferent neurons.

Eric Lancaster, Eun Joo Oh, Tony Gover, Daniel Weinreich

Abstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  3. Article
  4. NSAIDs modulate GABA-activated currents via CaExperimental and therapeutic medicine · 2016
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  13. Article
  14. Best1 is a gene regulated by nerve injury and required for Ca2+-activated Cl- current expression in axotomized sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  15. Tumor necrosis factor potentiates central vagal afferent signaling by modulating ryanodine channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  16. 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

4 authors.

Eric LancasterThe Neuroscience Program, University of Maryland, School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201-1559, USA.
Eun Joo Oh
Tony Gover
Daniel Weinreich

Funding

CHEMORECEPTION AND SIGNAL PROCESSING IN VAGAL AFFERENTSR01NS022069 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI WEINREICH, DANIEL · 1985 to 2006
$1.7M
NINDS NIH HHS R01 NS022069
6 · The paper itself

Abstract

Adult inferior vagal ganglion neurons (nodose ganglion neurons, NGNs) were acutely isolated 4-6 days after section of their peripheral axons (vagotomy) and examined with the whole-cell patch-clamp technique. A subset (approximately 25 %) of vagotomized NGNs displayed depolarizing after-potentials (DAPs), not present in control NGNs. DAPs were inhibited by niflumic acid (125 microM) or cadmium (100 microM), and had a reversal potential near E(Cl), indicating that they were due to Ca(2+)-activated chloride current (I(Cl(Ca))). N-type, L-type, T-/R- and other types of voltage-dependent Ca(2+) channels provided about 43, 2, 16 and 40 % of the trigger Ca(2+) for DAP generation, respectively. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was estimated using fura-2 fluorescence. Resting [Ca(2+)](i) and peak [Ca(2+)](i) elevation induced by activating Ca(2+)-induced Ca(2+) release (CICR) stores with 10 mM caffeine were not significantly different among control NGNs, vagotomized NGNs with DAPs and vagotomized NGNs without DAPs, averaging 54 +/- 7.9 (n = 19; P = 0.49) and 2022 +/- 1059 nM (n = 19; P = 0.44), respectively. Blocking CICR with 10 microM ryanodine reduced DAP amplitude by approximately 37 %. Ca(2+) influx induced by action potential waveforms was increased by over 250 % in vagotomized NGNs with DAPs (19.0 +/- 2.1 pC) compared to control NGNs (5.0 +/- 0.8 pC) or vagotomized NGNs without DAPs (7.0 +/- 0.8 pC). L-type, N-type, T-/R-type and other types of Ca(2+) influx were increased proportionately in vagotomized NGNs with DAPs. In conclusion, a subset of vagotomized NGNs have increased Ca(2+) currents and express I(Cl(Ca)). These NGNs respond electrically to increases in [Ca(2+)](i) during regeneration.

Indexed as

VagotomyAnimalsCalciumCalcium Channel BlockersCalcium SignalingChloride ChannelsElectric StimulationElectrophysiologyMaleMembrane PotentialsMicroelectrodesNeurons, AfferentNodose GanglionPatch-Clamp TechniquesRatsRats, Sprague-DawleyCalciumCalcium Channel BlockersChloride Channels

Identifiers

PMID11956342
PMCPMC2290244

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.