Evidence map›Paper›PMID 15107473›Full record

ArticleThe Journal of physiology2004

Autocrine feedback inhibition of plateau potentials terminates phasic bursts in magnocellular neurosecretory cells of the rat supraoptic nucleus.

Colin H Brown, Charles W Bourque

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
10.3field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Phasic spiking in vasopressin neurons: How and Why.Journal of neuroendocrinology · 2021
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Regulation of Neuronal Activity in Hypothalamic Vasopressin Neurons.Interdisciplinary information sciences · 2015
    Article
  10. Drug withdrawal conceptualized as a stressor.Behavioural pharmacology · 2014
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Kainate receptor-induced retrograde inhibition of glutamatergic transmission in vasopressin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. Review
  18. Article
  19. Dual regulation of anterograde and retrograde transmission by endocannabinoids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Colin H BrownCentre for Research in Neuroscience, Montreal General Hospital and McGill University, Quebec, Canada. colin.brown@ed.ac.uk
Charles W Bourque
Montreal General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phasic activity in magnocellular neurosecretory cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials. Dynorphin is copackaged in vasopressin neurosecretory vesicles that are exocytosed from magnocellular neurosecretory cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of plateau potentials in magnocellular neurosecretory cells recorded intracellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by alpha-latrotoxin (which depletes neurosecretory vesicles) and by nor-binaltorphimine (kappa-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a micro-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-potentials requires exocytosis of an endogenous kappa-opioid peptide. kappa-Opioid inhibition of depolarizing after-potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by kappa-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of kappa-opioid receptors with nor-binaltorphimine and by depletion of neurosecretory vesicles by alpha-latrotoxin, becoming everlasting in approximately 50% of cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as plateau potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of plateau potentials in magnocellular neurosecretory cells.

Indexed as

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAction PotentialsAnimalsAutocrine CommunicationCell SizeDendritesDynorphinsElectric StimulationElectrophysiologyFeedbackMaleMembrane PotentialsNerve RegenerationNeurosecretory SystemsPatch-Clamp TechniquesRats3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerDynorphinsReceptors, Opioid, kappa

Identifiers

PMID15107473
PMCPMC1665154
OpenAlexW2162071188

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.