Evidence map›Paper›PMID 19581379›Full record

ArticleThe Journal of physiology2009

Excitability of paraventricular nucleus neurones that project to the rostral ventrolateral medulla is regulated by small-conductance Ca2+-activated K+ channels.

Qing-Hui Chen, Glenn M Toney

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Small-Conductance CaNeuroscience bulletin · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Glutamate Spillover Dynamically Strengthens Gabaergic Synaptic Inhibition of the Hypothalamic Paraventricular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Hypothalamic Ion Channels in Hypertension.Current hypertension reports · 2018
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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.

Qing-Hui ChenDepartment of Physiology-MC7756, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. chenq@uthscsa.edu
Glenn M Toney
The University of Texas Health Science Center at San Antonio · US

Funding

Long-Term Neural Determinants of Cardiovascular DiseasesR01HL076312 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI OSBORN, JOHN W · 2005 to 2009
$5.6M
Neural Mechanisms in Congestive Heart FailureR01HL071645 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI TONEY, GLENN M · 2004 to 2007
$1.3M
Synaptic Activation of Sympathetic PVN Neurons by Chronic Intermittent HypoxiaR01HL092089 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI TONEY, GLENN M · 2008 to 2008
$363k
NHLBI NIH HHS HL071645NHLBI NIH HHS HL-076312NHLBI NIH HHS R01 HL071645NHLBI NIH HHS R01 HL076312NHLBI NIH HHS R01 HL092089
6 · The paper itself

Abstract

Whole cell patch-clamp recordings were performed in brain slices to investigate mechanisms regulating the excitability of paraventricular nucleus (PVN) neurones that project directly to the rostral ventrolateral medulla (RVLM) (PVN-RVLM neurones) of rats. In voltage-clamp recordings, step depolarization elicited a calcium-dependent outward tail current that reversed near E(K). The current was nearly abolished by apamin and by UCL1684, suggesting mediation by small-conductance Ca(2+)-activated K(+) (SK) channels. In current-clamp recordings, depolarizing step current injections evoked action potentials that underwent spike-frequency adaptation (SFA). SK channel blockade with apamin or UCL1684 increased the spike frequency without changing the rate of SFA. Upon termination of step current injection, a prominent medium after-hyperpolarization potential (mAHP) was observed. SK channel blockade abolished the mAHP and revealed an after-depolarization potential (ADP). In response to ramp current injections, the rate of sub-threshold depolarization was increased during SK channel blockade, indicating that depolarizing input resistance was increased. Miniature EPSC frequency, amplitude, and decay kinetics were unaltered by bath application of apamin, suggesting that SK channel blockade likely increased excitability by a postsynaptic action. We conclude that although SK channels play little role in generating SFA in PVN-RVLM neurones, their activation nevertheless does dampen excitability. The mechanism appears to involve activation of a mAHP that opposes a prominent ADP that would otherwise facilitate firing.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsMaleMedulla OblongataModels, NeurologicalNerve NetNeural InhibitionNeural PathwaysNeuronsParaventricular Hypothalamic NucleusPotassium Channels, Calcium-ActivatedRatsRats, Sprague-DawleySympathetic Nervous SystemPotassium Channels, Calcium-Activated

Identifiers

PMID19581379
PMCPMC2754362
OpenAlexW2144957675

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.