Evidence map›Paper›PMID 11179392›Full record

ArticleThe Journal of physiology2001

Neuropeptide Y receptors differentially modulate G-protein-activated inwardly rectifying K+ channels and high-voltage-activated Ca2+ channels in rat thalamic neurons.

Q Q Sun, J R Huguenard, D A Prince

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Neuropeptide Y Signaling Regulates Recurrent Excitation in the Auditory Midbrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Role of Neuropeptides in Pathogenesis of Dry Dye.Journal of clinical medicine · 2021
    Review
  11. The Role of Neuropeptide Y in the Nucleus Accumbens.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Neuropeptide Y Expression Defines a Novel Class of GABAergic Projection Neuron in the Inferior Colliculus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. LMO4 is essential for paraventricular hypothalamic neuronal activity and calcium channel expression to prevent hyperphagia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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 1 institution in 1 country.

Q Q SunDepartment of Neurology and Neurological Science, Stanford University School of Medicine, CA 94305, USA.
J R Huguenard
D A Prince
Stanford University · US

Funding

REGULATION OF NEURONAL EXCITABILITY IN CHRONIC EPILEPTOGENESISP50NS012151 · NINDS · STANFORD UNIVERSITY · PI BUCKMASTER, PAUL S. · 1985 to 2007
$9.1M
Epilepsy Research ProgramP01NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 2008 to 2011
$4.4M
NINDS NIH HHS NS12151NINDS NIH HHS P01 NS012151NINDS NIH HHS P50 NS012151
6 · The paper itself

Abstract

1. Using whole-cell patch-clamp recordings, infrared videomicroscopy and fast focal solution exchange methods, the actions of neuropeptide Y (NPY) were examined in thalamic slices of postnatal (10-16 days) rats. 2. NPY activated a K+-selective current in neurons of the thalamic reticular nucleus (RT; 20/29 neurons) and ventral basal complex (VB; 19/25 neurons). The currents in both nuclei had activation and deactivation kinetics that were very similar to those of GABAB receptor-induced currents, were totally blocked by 0.1 mM Ba2+ and showed voltage-dependent relaxation. These properties indicate that the NPY-sensitive K+ current is mediated by G-protein-activated, inwardly rectifying K+ (GIRK) channels. 3. In RT neurons, NPY application reversibly reduced high-voltage-activated (HVA) currents to 33 +/- 5 % (n = 40) of the control level but did not affect the T-type currents. Inhibition of Ca2+ currents was voltage independent and was largely mediated by effects on N- and P/Q-type channels. 4. NPY activation of GIRK channels was mediated via NPY1 receptors, whereas inhibition of N- and P/Q-type Ca2+ channels was mediated by NPY2 receptors. 5. These results show that neuropeptide Y activates K+ channels and simultaneously inhibits HVA Ca2+ channels via different receptor subtypes.

Indexed as

Potassium Channels, Inwardly RectifyingAnimalsBariumCalcium Channel BlockersCalcium ChannelsElectrophysiologyG Protein-Coupled Inwardly-Rectifying Potassium ChannelsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)Membrane PotentialsNeuronsPatch-Clamp TechniquesPotassium ChannelsRatsRats, Sprague-DawleyReceptors, Neuropeptide YBariumCalcium Channel BlockersCalcium ChannelsG Protein-Coupled Inwardly-Rectifying Potassium ChannelsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)Potassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, Neuropeptide Y

Identifiers

PMID11179392
PMCPMC2278450
OpenAlexW2110585018

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.