Evidence map›Paper›PMID 18483150›Full record

ArticleEndocrinology2008

Kisspeptin excites gonadotropin-releasing hormone neurons through a phospholipase C/calcium-dependent pathway regulating multiple ion channels.

Xinhuai Liu, Kiho Lee, Allan E Herbison

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 2 pooled it
23.2field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 2 syntheses or guidelines pooled it, 266 citations in OpenAlex.

  1. Pooled it
  2. Kisspeptins in human reproduction-future therapeutic potential.Journal of assisted reproduction and genetics · 2012
    Pooled it
  3. Trial
  4. Article
  5. Knockout of PI4-Kinase A in GnRH Neurons Causes their Prepubertal Death.bioRxiv : the preprint server for biology · 2026
    Article
  6. Exploring the Role of Kisspeptin in Polycystic Ovary Syndrome and Its Associated Pregnancy Complications.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Modelling KNDy neurons and gonadotropin-releasing hormone pulse generation.Current opinion in endocrine and metabolic research · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

55 more citing papers are in PubMed but not listed here.

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.

Xinhuai LiuCentre for Neuroendocrinology, Department of Physiology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New Zealand.
Kiho Lee
Allan E Herbison
University of Otago · NZ

Funding

Wellcome Trust 063216
6 · The paper itself

Abstract

The present study used perforated-patch electrophysiology and calcium imaging in GnRH transgenic mouse lines to determine the mechanisms underlying the potent excitatory effects of kisspeptin upon GnRH neurons in the acute brain slice preparation. Kisspeptin (100 nm) depolarized (6 +/- 1 mV) and/or evoked an 87 +/- 4% increase in firing rate of 75% of adult GnRH neurons (n = 51). No sex differences were found. Analyses of input resistance and current-voltage curves indicated that a heterogeneous closure of potassium channels and opening of nonselective cation (NSC) channels was involved in kisspeptin's depolarizing response. Pharmacological pretreatment with either barium, a potassium channel blocker, or flufenamic acid, an NSC channel antagonist, reduced the percentage of responding GnRH neurons from 75 to 40% (P < 0.05). Pretreatment with both barium and flufenamic acid reduced the response rate to 17% (P < 0.05). To examine the intracellular signaling cascade involved, GnRH neurons were treated with antagonists of phospholipase C (PLC), inositol-trisphosphate receptors (IP3R), and ERK1/2 before kisspeptin exposure. PLC and IP3R antagonism reduced the percentage of responding GnRH neurons from 80 to 15 and 7%, respectively (P < 0.001). Real-time calcium imaging showed that kisspeptin evoked an approximately 10% increase in intracellular calcium levels in GnRH neurons that was followed by a decrease and return to pretest calcium levels. Additional experiments indicated that mechanisms intrinsic to the GnRH neuron are responsible for their prolonged depolarizing response to kisspeptin. These studies indicate that kisspeptin activates G protein-coupled receptor 54 (GPR54) to initiate a PLC-IP3R-calcium cascade that modulates both potassium and NSC channels to initiate depolarization in GnRH neurons.

Indexed as

AnimalsCalcium SignalingFemaleGonadotropin-Releasing HormoneInositol 1,4,5-Trisphosphate ReceptorsIon ChannelsKisspeptinsMaleMiceMice, TransgenicModels, BiologicalNeuronsPatch-Clamp TechniquesPotassium ChannelsReceptors, G-Protein-CoupledReceptors, Kisspeptin-1Gonadotropin-Releasing HormoneInositol 1,4,5-Trisphosphate ReceptorsIon ChannelsKiss1 protein, mouseKiss1r protein, mouseKisspeptinsPotassium ChannelsReceptors, G-Protein-CoupledReceptors, Kisspeptin-1Tumor Suppressor ProteinsType C Phospholipases

Identifiers

PMID18483150
PMCPMC6116891
OpenAlexW1991847642

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.