ArticleFrontiers in cellular neuroscience2015
Rapid modulation of synaptogenesis and spinogenesis by 17β-estradiol in primary cortical neurons.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 87 citations in OpenAlex.
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- Mechanisms Underlying Treatment-Resistant Depression: Exploring Sex-Based Biological Differences.Journal of neurochemistry · 2025Review
- Aspartate in the Brain: A Review.Neurochemical research · 2025Review
- The Placental Steroid Hypothesis of Human Brain Evolution.Evolutionary anthropology · 2025Review
- The absence of Neuroligin-1 shapes wake/sleep architecture, rhythmic and arrhythmic activities of the electrocorticogram in female mice.Molecular brain · 2025Article
- Article
- Role of estrogen in sex differences in memory, emotion and neuropsychiatric disorders.Molecular biology reports · 2024Review
- H7N7 viral infection elicits pronounced, sex-specific neuroinflammatory responsesFrontiers in cellular neuroscience · 2024Article
- Social memory in female mice is rapidly modulated by 17β-estradiol through ERK and Akt modulation of synapse formation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neonatal Exposure to Valproate Induces Long-Term Alterations in Steroid Hormone Levels in the Brain Cortex of Prepubertal Rats.International journal of molecular sciences · 2023Article
- Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions.Biomedicines · 2022Review
- Sex steroid hormone function in the brain niche: Implications for brain metastatic colonization and progression.Cancer reports (Hoboken, N.J.) · 2022Review
- Targeting 17β-estradiol biosynthesis in neural stem cells improves stroke outcome.Frontiers in cellular neuroscience · 2022Article
- Ovariectomy-induced hormone deprivation aggravates AβFrontiers in endocrinology · 2022Article
- Neonatal Oxidative Stress Impairs Cortical Synapse Formation and GABA Homeostasis in Parvalbumin-Expressing Interneurons.Oxidative medicine and cellular longevity · 2022Article
- Estrogenic hormones receptors in Alzheimer's disease.Molecular biology reports · 2021Review
- Sex differences in recovery of motor function in a rhesus monkey model of cortical injury.Biology of sex differences · 2021Article
- Estrogen Receptor β Contributes to Both Hypertension and Hypothalamic Plasticity in a Mouse Model of Peri-Menopause.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- A Putative Role for Ubiquitin-Proteasome Signaling in Estrogenic Memory Regulation.Frontiers in behavioral neuroscience · 2021Article
- Sex-Specific Effect of Serum Lipids and Body Mass Index on Psychotic Symptoms, a Cross-Sectional Study of First-Episode Psychosis Patients.Frontiers in psychiatry · 2021Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
In the mammalian forebrain, the majority of excitatory synapses occur on dendritic spines. Changes in the number of these structures is important for brain development, plasticity and the refinement of neuronal circuits. The formation of excitatory synapses involves the coordinated formation of dendritic spines and targeting of multi-protein complexes to nascent connections. Recent studies have demonstrated that the estrogen 17β-estradiol (E2) can rapidly increase the number of dendritic spines, an effect consistent with the ability of E2 to rapidly influence cognitive function. However, the molecular composition of E2-induced spines and whether these protrusions form synaptic connections has not been fully elucidated. Moreover, which estrogen receptor(s) (ER) mediate these spine-morphogenic responses are not clear. Here, we report that acute E2 treatment results in the recruitment of postsynaptic density protein 95 (PSD-95) to novel dendritic spines. In addition neuroligin 1 (Nlg-1) and the NMDA receptor subunit GluN1 are recruited to nascent synapses in cortical neurons. The presence of these synaptic proteins at nascent synapses suggests that the machinery to allow pre- and post-synapses to form connections are present in E2-induced spines. We further demonstrate that E2 treatment results in the rapid and transient activation of extracellular signal-regulated kinase 1/2 (ERK1/2), Akt and the mammalian target of rapamycin (mTOR) signaling pathways. However, only ERK1/2 and Akt are required for E2-mediated spinogenesis. Using synthetic receptor modulators, we further demonstrate that activation of the estrogen receptor beta (ERβ) but not alpha (ERα) mimics rapid E2-induced spinogenesis and synaptogenesis. Taken together these findings suggest that in primary cortical neurons, E2 signaling via ERβ, but not through ERα, is capable of remodeling neuronal circuits by increasing the number of excitatory synapses.
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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.