Evidence map›Paper›PMID 15152042›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Burst initiation and termination in phasic vasopressin cells of the rat supraoptic nucleus: a combined mathematical, electrical, and calcium fluorescence study.

Peter Roper, Joseph Callaway, William Armstrong

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.9field-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

28 citing papers in PubMed, 84 citations in OpenAlex.

  1. Phasic spiking in vasopressin neurons: How and Why.Journal of neuroendocrinology · 2021
    Review
  2. Article
  3. Review
  4. Article
  5. Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of physiology · 2017
    Article
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  7. Article
  8. Review
  9. Article
  10. Review
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  12. Article
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  18. Review
  19. Article
  20. Glutamatergic inputs contribute to phasic activity in vasopressin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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

3 authors at 2 institutions in 1 country.

Peter RoperLaboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. pete.roper@nih.gov
Joseph Callaway
William Armstrong
University of Tennessee Health Science Center · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Electrophysiological Correlates of Vasopressin SecretionR01NS023941 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ARMSTRONG, WILLIAM E · 1986 to 2009
$1.8M
Dendritic Role in Dopamine Neuron FiringR01NS042276 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CALLAWAY, JOSEPH CHARLES · 2002 to 2004
$632k
Electrophysiological Correlates of Vasopressin ReleaseR56NS023941 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ARMSTRONG, WILLIAM E · 2011 to 2011
$354k
NINDS NIH HHS NS23941NINDS NIH HHS NS42276NINDS NIH HHS R01 NS023941NINDS NIH HHS R01 NS042276NINDS NIH HHS R56 NS023941
6 · The paper itself

Abstract

Vasopressin secreting neurons of the rat hypothalamus discharge lengthy, repeating bursts of action potentials in response to physiological stress. Although many electrical currents and calcium-dependent processes have been isolated and analyzed in these cells, their interactions are less well fathomed. In particular, the mechanism of how each burst is triggered, sustained, and terminated is poorly understood. We present a mathematical model for the bursting mechanism, and we support our model with new simultaneous electrical recording and calcium imaging data. We show that bursts can be initiated by spike-dependent calcium influx, and we propose that the resulting elevation of bulk calcium inhibits a persistent potassium current. This inhibition depolarizes the cell above threshold and so triggers regenerative spiking and further calcium influx. We present imaging data to show that bulk calcium reaches a plateau within the first few seconds of the burst, and our model indicates that this plateau occurs when calcium influx is balanced by efflux and uptake into stores. We conjecture that the burst is terminated by a slow, progressive desensitization to calcium of the potassium leak current. Finally, we propose that the opioid dynorphin, which is known to be secreted from the somatodendritic region and has been shown previously to regulate burst length and phasic activity in these cells, is the autocrine messenger for this desensitization.

Indexed as

Models, NeurologicalAction PotentialsAnimalsArginine VasopressinAutocrine CommunicationCalciumDynorphinsFemaleIn Vitro TechniquesModels, TheoreticalNeuronsPatch-Clamp TechniquesPotassiumPotassium ChannelsRatsSecretory VesiclesArginine VasopressinCalciumDynorphinsPotassiumPotassium Channels

Identifiers

PMID15152042
PMCPMC6729454
OpenAlexW2085334031

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.