ReviewNeuroscience2013
Estrogen promotes learning-related plasticity by modifying the synaptic cytoskeleton.
Review in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- The effects of acute stress on episodic memory: A meta-analysis and integrative review.Psychological bulletin · 2017Pooled it
- Effects of estrogen on spatial navigation and memory.Psychopharmacology · 2024Trial
- Trial
- Metabolic regulation of synaptic plasticity in anorexia nervosa.Frontiers in synaptic neuroscience · 2026Review
- Frequency-Dependent Modulation of Short-Term Neuronal Dynamics in the Female and Male Dorsal and Ventral Rat Hippocampus.International journal of molecular sciences · 2025Article
- The Placental Steroid Hypothesis of Human Brain Evolution.Evolutionary anthropology · 2025Review
- Mechanism of Microwave Radiation-Induced Learning and Memory Impairment Based on Hippocampal Metabolomics.Brain sciences · 2024Article
- Estrogen dysregulation, intraocular pressure, and glaucoma risk.Experimental eye research · 2023Review
- Steroid Hormone Interaction with Dendritic Spines: Implications for Neuropsychiatric Disease.Advances in neurobiology · 2023Review
- Estrogen Receptor-A in Medial Preoptic Area Contributes to Sex Difference of Mice in Response to Sevoflurane Anesthesia.Neuroscience bulletin · 2022Article
- Extracellular matrix metalloproteinase-9 (MMP-9) is required in female mice for 17β-estradiol enhancement of hippocampal memory consolidation.Psychoneuroendocrinology · 2022Article
- Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions.Biomedicines · 2022Review
- Sex-dependent effects of multiple acute concurrent stresses on memory: a role for hippocampal estrogens.Frontiers in behavioral neuroscience · 2022Article
- Sex Hormones, Sleep, and Memory: Interrelationships Across the Adult Female Lifespan.Frontiers in aging neuroscience · 2022Review
- Brain-derived estrogen and neural function.Neuroscience and biobehavioral reviews · 2022Review
- Differential Role of Sex and Age in the Synaptic Transmission of Degus (Frontiers in integrative neuroscience · 2022Article
- Ovariectomy-induced hormone deprivation aggravates AβFrontiers in endocrinology · 2022Article
- 17β-estradiol activation of dorsal hippocampal TrkB is independent of increased mature BDNF expression and is required for enhanced memory consolidation in female mice.Psychoneuroendocrinology · 2021Article
- Unexpected Role of Physiological Estrogen in Acute Stress-Induced Memory Deficits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Oestradiol as a neuromodulator of learning and memory.Nature reviews. Neuroscience · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Estrogen's acute, facilitatory effects on glutamatergic transmission and long-term potentiation (LTP) provide a potential explanation for the steroid's considerable influence on behavior. Recent work has identified mechanisms underlying these synaptic actions. Brief infusion of 17ß-estradiol (E2) into adult male rat hippocampal slices triggers actin polymerization within dendritic spines via a signaling cascade beginning with the GTPase RhoA and ending with inactivation of the filament-severing protein cofilin. Blocking this sequence, or actin polymerization itself, eliminates E2's effects on synaptic physiology. Notably, the theta burst stimulation used to induce LTP activates the same signaling pathway as E2 plus events that stabilize the reorganization of the sub-synaptic cytoskeleton. These observations suggest that E2 elicits a partial form of LTP, resulting in an increase of fast excitatory postsynaptic potentials (EPSPs) and a reduction in the threshold for lasting synaptic changes. While E2's effects on the cytoskeleton could be direct, results described here indicate that the hormone activates synaptic tropomyosin-related kinase B (TrkB) receptors for brain-derived neurotrophic factor (BDNF), a releasable neurotrophin that stimulates the RhoA to cofilin pathway. It is therefore possible that E2 acts via transactivation of neighboring receptors to modify the composition and structure of excitatory contacts. Finally, there is the question of whether a loss of acute synaptic actions contributes to the memory problems associated with estrogen depletion. Initial tests found that ovariectomy in middle-aged rats disrupts RhoA signaling, actin polymerization, and LTP consolidation. Acute applications of E2 reversed these defects, a result consistent with the idea that disturbances to actin management are one cause of behavioral effects that emerge with reductions in steroid levels.
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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.