ArticleProceedings of the National Academy of Sciences of the United States of America2008
Estrogens directly potentiate neuronal L-type Ca2+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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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.
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Who cites it
68 citing papers in PubMed, 113 citations in OpenAlex.
- Synaptic Actions of Estradiol in the Brain's Reward System: Linking Mechanisms to Behavior and Disease.Biological psychiatry global open science · 2026Review
- Hypothalamic actions of estrogens in the regulation of energy and glucose homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- Uncovering the transcriptional landscape of estrogen-induced gonadal feminization in the Chinese giant salamander.BMC genomics · 2026Article
- Deletion ofFrontiers in cellular neuroscience · 2026Article
- Mitochondrial dysfunction in Alzheimer's disease and related sex differences.Frontiers in aging neuroscience · 2026Review
- Beyond Estrogen: Unraveling the Complexities of Hormonal Signaling Pathways in Alzheimer's Disease and Their Implications for Precision Therapy.Molecular neurobiology · 2025Review
- Deletion ofbioRxiv : the preprint server for biology · 2025Article
- The CaInternational journal of molecular sciences · 2025Review
- The E3 Ubiquitin Ligase PRAJA1: A Key Regulator of Synaptic Dynamics and Memory Processes with Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Identification of an ionic mechanism for ERα-mediated rapid excitation in neurons.Science advances · 2024Article
- Sex-Specific Mechanisms Underlie Long-Term Potentiation at Hippocampus→Medium Spiny Neuron Synapses in the Medial Shell of the Nucleus Accumbens.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cellular profiling of a recently-evolved social behavior in cichlid fishes.Nature communications · 2023Article
- Caldendrin represses neurite regeneration and growth in dorsal root ganglion neurons.Scientific reports · 2023Article
- Nutrients and Dementia: Prospective Study.Nutrients · 2023Article
- Temperament traits mediate the relationship between CACNA1C polymorphisms and bipolar disorder in cisgender women.European archives of psychiatry and clinical neuroscience · 2023Article
- Review
- Effects of Diastolic Blood Pressure on Brain Structures and Cognitive Functions in Middle and Old Ages: Longitudinal Analyses.Nutrients · 2022Article
- Calcium and calcium-related proteins in endometrial cancer: opportunities for pharmacological intervention.International journal of biological sciences · 2022Review
- Steroid Sulfation in Neurodegenerative Diseases.Frontiers in molecular biosciences · 2022Review
- The Aging GABAergic System and Its Nutritional Support.Journal of nutrition and metabolism · 2021Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
L-type voltage-gated Ca(2+)channels (VGCC) play an important role in dendritic development, neuronal survival, and synaptic plasticity. Recent studies have demonstrated that the gonadal steroid estrogen rapidly induces Ca(2+) influx in hippocampal neurons, which is required for neuroprotection and potentiation of LTP. The mechanism by which estrogen rapidly induces this Ca(2+) influx is not clearly understood. We show by electrophysiological studies that extremely low concentrations of estrogens acutely potentiate VGCC in hippocampal neurons, hippocampal slices, and HEK-293 cells transfected with neuronal L-type VGCC, in a manner that was estrogen receptor (ER)-independent. Equilibrium, competitive, and whole-cell binding assays indicate that estrogen directly interacts with the VGCC. Furthermore, a L-type VGCC antagonist to the dihydropyridine site displaced estrogen binding to neuronal membranes, and the effects of estrogen were markedly attenuated in a mutant, dihydropyridine-insensitive L-type VGCC, demonstrating a direct interaction of estrogens with L-type VGCC. Thus, estrogen-induced potentiation of calcium influx via L-type VGCC may link electrical events with rapid intracellular signaling seen with estrogen exposure leading to modulation of synaptic plasticity, neuroprotection, and memory formation.
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Registered trials
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.