Evidence map›Paper›PMID 20926664›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Hyperpolarization-activated currents in gonadotropin-releasing hormone (GnRH) neurons contribute to intrinsic excitability and are regulated by gonadal steroid feedback.

Zhiguo Chu, Hiroshi Takagi, Suzanne M Moenter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. A unified model for two modes of bursting in GnRH neurons.Journal of computational neuroscience · 2016
    Article
  14. Article
  15. Review
  16. Pacemaking kisspeptin neurons.Experimental physiology · 2013
    Review
  17. Article
  18. Article
  19. Kisspeptin excitation of GnRH neurons.Advances in experimental medicine and biology · 2013
    Review
  20. Interactions between kisspeptins and neurokinin B.Advances in experimental medicine and biology · 2013
    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 2 countries.

Zhiguo ChuDepartment of Medicine, University of Virginia, Charlottesville, Virginia 22908, USA.
Hiroshi Takagi
Suzanne M Moenter
University of Virginia · USWaseda University · JP

Funding

Cellular and Molecular bases for rhythmic GnRH releaseR01HD034860 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MOENTER, SUZANNE M · 2002 to 2016
$4.8M
NICHD NIH HHS R01 HD034860NICHD NIH HHS R01 HD34860
6 · The paper itself

Abstract

Pulsatile release of gonadotropin-releasing hormone (GnRH) is required for fertility and is regulated by steroid feedback. Hyperpolarization-activated currents (I(h)) play a critical role in many rhythmic neurons. We examined the contribution of I(h) to the membrane and firing properties of GnRH neurons and the modulation of this current by steroid milieu. Whole-cell voltage- and current-clamp recordings were made of GFP-identified GnRH neurons in brain slices from male mice that were gonad-intact, castrated, or castrated and treated with estradiol implants. APV, CNQX, and bicuculline were included to block fast synaptic transmission. GnRH neurons (47%) expressed a hyperpolarization-activated current with pharmacological and biophysical characteristics of I(h). The I(h)-specific blocker ZD7288 reduced hyperpolarization-induced sag and rebound potential, decreased GnRH neuron excitability and action potential firing, and hyperpolarized membrane potential in some cells. ZD7288 also altered the pattern of burst firing and reduced the slope of recovery from the after-hyperpolarization potential. Activation of I(h) by hyperpolarization increased spike frequency, whereas inactivation of I(h) by depolarization reduced spike frequency. Castration increased I(h) compared with that in gonad-intact males. This effect was reversed by in vivo estradiol replacement. Together, these data indicate I(h) provides an excitatory drive in GnRH neurons that contributes to action potential burst firing and that estradiol regulates I(h) in these cells. As estradiol is the primary central negative feedback hormone on GnRH neuron firing in males, this provides insight into the mechanisms by which steroid hormones potentially alter the intrinsic properties of GnRH neurons to change their activity.

Indexed as

Action PotentialsAnimalsCardiovascular AgentsCell PolarityEstradiolExcitatory Amino Acid AntagonistsFeedback, PhysiologicalGABA AntagonistsGonadotropin-Releasing HormoneHypothalamusMaleMembrane PotentialsMiceNeuronsOrgan Culture TechniquesPatch-Clamp TechniquesCardiovascular AgentsEstradiolExcitatory Amino Acid AntagonistsGABA AntagonistsGonadotropin-Releasing HormoneICI D2788Pyrimidines

Identifiers

PMID20926664
PMCPMC2968704
OpenAlexW1964587473

What OpenQuestion holds

Textmetadata
LicenceTDM
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.