Evidence map›Paper›PMID 19244351›Full record

ArticleJournal of neurophysiology2009

Dopamine inhibits N-type channels in visceral afferents to reduce synaptic transmitter release under normoxic and chronic intermittent hypoxic conditions.

David D Kline, Gabriel Hendricks, Gerlinda Hermann, Richard C Rogers, Diana L Kunze

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Hypoxia augments TRPM3-mediated calcium influx in vagal sensory neurons.Autonomic neuroscience : basic & clinical · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. HAmerican journal of physiology. Cell physiology · 2017
    Article
  10. Review
  11. Article
  12. Article
  13. Spinal metaplasticity in respiratory motor control.Frontiers in neural circuits · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

5 authors at 5 institutions in 1 country.

David D KlineDepartment of Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA. klinedd@missouri.edu
Gabriel Hendricks
Gerlinda Hermann
Richard C Rogers
Diana L Kunze
Case Western Reserve University · USMetroHealth Medical Center · USNeurosciences Institute · USPennington Biomedical Research Center · USUniversity of Pennsylvania · US

Funding

VENTROLATERAL PONS SHAPES THE RESPONSE TO HYPOXIAP01HL025830 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KUMAR, GANESH K · 1985 to 2006
$11.1M
Adaptation of Brainstem Circuits to Chronic HypoxiaR01HL085108 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KLINE, DAVID DOUGLAS · 2008 to 2012
$1.9M
NHLBI NIH HHS HL-085108NHLBI NIH HHS HL-25830NHLBI NIH HHS R01 HL085108NINDS NIH HHS NS-52142
6 · The paper itself

Abstract

Glutamatergic synaptic currents elicited in second-order neurons in the nucleus of the solitary tract (nTS) by activation of chemosensory and other visceral afferent fibers are severely reduced following 10 days of chronic intermittent hypoxia (CIH). The mechanism by which this occurs is unknown. A strong candidate for producing the inhibition is dopamine, which is also released from the presynaptic terminals and which we have shown exerts a tonic presynaptic inhibition on glutamate release. We postulated that tonic activation of the D2 receptors inhibits presynaptic calcium currents to reduce transmitter release and that in CIH this occurs in conjunction with an increase in the dopamine inhibitory response due to the increase in presynaptic D2 receptors or an increase in dopamine release further suppressing the evoked excitatory postsynaptic current (eEPSC). Thus we predicted that blockade of the D2 receptors would return the EPSC to values of animals maintained under normoxic conditions. We found that dopamine and quinpirole, the selective D2-like agonist, inhibit calcium currents via the D2 receptors by acting on the N-type calcium channel in presynaptic neurons and their nTS central terminals. However, in brain slice studies from CIH animals, although the D2 antagonist sulpiride increased the CIH-reduced amplitude of synaptic currents, EPSCs were not restored to normal levels. This indicates that while the dopamine inhibitory effect remains intact in CIH, most of the reduction in the eEPSC amplitude occurs via alternative mechanisms.

Indexed as

AnimalsBiophysicsCalciumCalcium Channel BlockersCalcium Channels, N-TypeCells, CulturedDopamineDopamine AgonistsDrug InteractionsElectric StimulationExcitatory Postsynaptic PotentialsFemaleGlutamic AcidHypoxiaIn Vitro TechniquesMale4-(4-dihexadecylaminostyryl)-N-methylpyridiumCalciumCalcium Channel BlockersCalcium Channels, N-TypeDopamineDopamine AgonistsGlutamic AcidPyridinium CompoundsQuinpirole

Identifiers

PMID19244351
PMCPMC2681443
OpenAlexW2060614335

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.