Evidence map›Paper›PMID 12456832›Full record

ArticleThe Journal of physiology2002

Flufenamic acid blocks depolarizing afterpotentials and phasic firing in rat supraoptic neurones.

Masoud Ghamari-Langroudi, Charles W Bourque

Open access · greenAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.7field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Phasic spiking in vasopressin neurons: How and Why.Journal of neuroendocrinology · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  9. Article
  10. Calcium-activated sustained firing responses distinguish accessory from main olfactory bulb mitral cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Glutamatergic inputs contribute to phasic activity in vasopressin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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 2 institutions in 1 country.

Masoud Ghamari-LangroudiCentre for Research in Neuroscience, Montreal General Hospital & McGill University, 1650 Cedar Avenue, Montreal, QC, Canada H3G 1A4.
Charles W Bourque
McGill University · CAMontreal General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depolarizing afterpotentials (DAPs) that follow action potentials in magnocellular neurosecretory cells (MNCs) are thought to underlie the generation of phasic firing, a pattern that optimizes vasopressin release from the neurohypophysis. Previous work has suggested that the DAP may result from the Ca(2+)-dependent reduction of a resting K(+) conductance. Here we examined the effects of flufenamic acid (FFA), a blocker of Ca(2+)-dependent non-selective cation (CAN) channels, on DAPs and phasic firing using intracellular recordings from supraoptic MNCs in superfused explants of rat hypothalamus. Application of FFA, but not solvent (0.1 % DMSO), reversibly inhibited (IC(50) = 13.8 microM; R = 0.97) DAPs and phasic firing with a similar time course, but had no significant effects (P > 0.05) on membrane potential, spike threshold and input resistance, nor on the frequency and amplitude of spontaneous synaptic potentials. Moreover, FFA did not affect (P > 0.05) the amplitude, duration, undershoot, or frequency-dependent broadening of action potentials elicited during the spike trains used to evoke DAPs. These findings suggest that FFA inhibits the DAP by directly blocking the channels responsible for its production, rather than by interfering with Ca(2+) influx. They also support a role for DAPs in the generation of phasic firing in MNCs. Finally, the absence of a depolarization and increased membrane resistance upon application of FFA suggests that the DAP in MNCs may not be due to the inhibition of resting K(+) current, but to the activation of CAN channels.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCalciumElectric StimulationElectrophysiologyFlufenamic AcidIn Vitro TechniquesIon ChannelsMaleMembrane PotentialsMicroelectrodesNeuronsPatch-Clamp TechniquesPituitary Gland, PosteriorRatsRats, Long-EvansAnti-Inflammatory Agents, Non-SteroidalCalciumFlufenamic AcidIon Channels

Identifiers

PMID12456832
PMCPMC2290680
OpenAlexW2050680264

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.