ArticleThe Journal of membrane biology2014
Effects of estradiol on voltage-gated potassium channels in mouse dorsal root ganglion neurons.
Article in The Journal of membrane biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Smart biomaterials for skeletal aging repair and regeneration.Bone research · 2026Review
- Development and prenatal exposure to androgens alter potassium currents in gonadotropin-releasing hormone neurons from female mice.Journal of neuroendocrinology · 2024Article
- Cerebral arteriolar and neurovascular dysfunction after chemically induced menopause in mice.American journal of physiology. Heart and circulatory physiology · 2022Article
- Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions.Biomedicines · 2022Review
- (-)-Naringenin 4',7-dimethyl Ether Isolated fromMolecules (Basel, Switzerland) · 2022Article
- The Mechanism of Bone Remodeling After Bone Aging.Clinical interventions in aging · 2022Review
- Estrogen augmented visceral pain and colonic neuron modulation in a double-hit model of prenatal and adult stress.World journal of gastroenterology · 2021Article
- Enhanced excitability and suppression of A-type K(+) currents in joint sensory neurons in a murine model of antigen-induced arthritis.Scientific reports · 2016Article
- The estrous cycle modulates voltage-gated ion channels in trigeminal ganglion neurons.The journal of physiological sciences : JPS · 2015Article
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Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated potassium channels are regulators of membrane potentials, action potential shape, firing adaptation, and neuronal excitability in excitable tissues including in the primary sensory neurons of dorsal root ganglion (DRG). In this study, using the whole-cell patch-clamp technique, the effect of estradiol (E2) on voltage-gated total outward potassium currents, the component currents transient "A-type" current (I A) currents, and "delayed rectifier type" (I KDR) currents in isolated mouse DRG neurons was examined. We found that the extracellularly applied 17β-E2 inhibited voltage-gated total outward potassium currents; the effects were rapid, reversible, and concentration-dependent. Moreover, the membrane impermeable E2-BSA was as efficacious as 17β-E2, whereas 17α-E2 had no effect. 17β-E2-stimulated decrease in the potassium current was unaffected by treatment with ICI 182780 (classic estrogen receptor antagonist), actinomycin D (RNA synthesis inhibitor), or cycloheximide (protein synthesis inhibitor). We also found that I A and I KDR were decreased after 17β-E2 application. 17β-E2 significantly shifted the activation curve for I A and I KDR channels in the hyperpolarizing direction. In conclusion, our results demonstrate that E2 inhibited voltage-gated K(+) channels in mouse DRG neurons through a membrane ER-activated non-genomic pathway.
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Registered trials
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