ArticleJournal of neurophysiology2018
Changes in potassium channel modulation may underlie afterhyperpolarization plasticity in oxytocin neurons during late pregnancy.
Article in Journal of neurophysiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia.Frontiers in pharmacology · 2026Article
- Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Advances in the neurophysiology of magnocellular neuroendocrine cells.Journal of neuroendocrinology · 2020Review
- PIPPhysiological reports · 2019Article
- Electrophysiological properties of identified oxytocin and vasopressin neurones.Journal of neuroendocrinology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Oxytocin (OT) neurons exhibit larger afterhyperpolarizations (AHPs) following spike trains during late pregnancy and lactation, times when these neurons fire in bursts and release more OT associated with labor and lactation. Calcium-dependent AHPs mediated by SK channels show this plasticity, and are reduced when the channel complex is phosphorylated by casein kinase 2 (CK2), and increased when dephosphorylated by protein phosphatase (PP)2A, by altering Ca
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Registered trials
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