ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Estrogen stimulates postsynaptic density-95 rapid protein synthesis via the Akt/protein kinase B pathway.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed.
- Sex differences in the effects of chronic stress and oxycodone associative learning on glial markers in rat hippocampus.Neuroscience · 2026Article
- G-protein coupled estrogen receptor 1 contributes to suppression of angiotensin II hypertension via modulation of AMPA GluA1 in the hypothalamic paraventricular nucleus in a mouse model of post-menopause.Biology of sex differences · 2026Article
- Reproductive history differentially shapes the neural response of middle-aged hAPOEɛ4 female rats to estradiol therapy after a metabolic challenge.Biology of sex differences · 2026Article
- Perinatal omega-3 sex-selectively mitigates neuropsychiatric impacts of prenatal THC in the cortico-striatal-hippocampal circuit.Molecular psychiatry · 2025Article
- Role of Cytoskeletal Elements in Regulation of Synaptic Functions: Implications Toward Alzheimer's Disease and Phytochemicals-Based Interventions.Molecular neurobiology · 2024Review
- Cardiometabolic health, menopausal estrogen therapy and the brain: How effects of estrogens diverge in healthy and unhealthy preclinical models of aging.Frontiers in neuroendocrinology · 2023Review
- Sex difference in evolution of cognitive decline: studies on mouse model and the Dominantly Inherited Alzheimer Network cohort.Translational psychiatry · 2023Article
- Estrogen Receptor-A in Medial Preoptic Area Contributes to Sex Difference of Mice in Response to Sevoflurane Anesthesia.Neuroscience bulletin · 2022Article
- Estrogen receptors and the aging brain.Essays in biochemistry · 2021Review
- Previous estradiol treatment during midlife maintains transcriptional regulation of memory-related proteins by ERα in the hippocampus in a rat model of menopause.Neurobiology of aging · 2021Article
- 17-β Estradiol Rescued Immature Rat Brain against Glutamate-Induced Oxidative Stress and Neurodegeneration via Regulating Nrf2/HO-1 and MAP-Kinase Signaling Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- IGF1R Deficiency Modulates Brain Signaling Pathways and Disturbs Mitochondria and Redox Homeostasis.Biomedicines · 2021Article
- A Putative Role for Ubiquitin-Proteasome Signaling in Estrogenic Memory Regulation.Frontiers in behavioral neuroscience · 2021Article
- Sex and chronic stress alter delta opioid receptor distribution within rat hippocampal CA1 pyramidal cells following behavioral challenges.Neurobiology of stress · 2020Article
- Oestradiol as a neuromodulator of learning and memory.Nature reviews. Neuroscience · 2020Review
- Targeted Deletion of PTEN in Kisspeptin Cells Results in Brain Region- and Sex-Specific Effects on Kisspeptin Expression and Gonadotropin Release.International journal of molecular sciences · 2020Article
- IGF1R regulates retrograde axonal transport of signalling endosomes in motor neurons.EMBO reports · 2020Article
- Complexes formed with integrin-α5 and KCNB1 potassium channel wild type or epilepsy-susceptibility variants modulate cellular plasticityFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Sex Differences in Neuroplasticity- and Stress-Related Gene Expression and Protein Levels in the Rat Hippocampus Following Oxycodone Conditioned Place Preference.Neuroscience · 2019Article
- Oxidation of KCNB1 potassium channels in the murine brain during aging is associated with cognitive impairment.Biochemical and biophysical research communications · 2019Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
Estrogens induce synaptogenesis in the CA1 region of the dorsal hippocampus during the estrous cycle of the female rat. Functional consequences of such estrogen-mediated synaptogenesis include cyclic changes in neurotransmission and memory. At the molecular level, estrogen stimulates the rapid activation of specific signal transduction pathways, and of particular interest is the activation of Akt (protein kinase B), a key signal transduction intermediate that initiates protein translation by alleviating the downstream translational repression of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1). Using a well established in vitro model system of differentiated NG108-15 neurons to investigate such rapid signaling effects of estrogen, we show that estrogen stimulates the phosphorylation of Akt, an indication of kinase activation, as well as the phosphorylation of 4E-BP1. In turn, the activation of these signaling intermediates suggests a non-genomic mechanism by which estrogen might likewise lead to protein translation of dendrite-localized mRNA transcripts in the hippocampus in vivo. We therefore considered the translation of the dendritic spine scaffolding protein postsynaptic density-95 (PSD-95). Although estrogen does not stimulate a rapid increase in PSD-95 mRNA levels in NG108-15 neurons, we show here that estrogen does however stimulate a rapid increase in PSD-95 new protein synthesis in vitro and that this new protein synthesis is Akt dependent. These results demonstrate an essential role for Akt in estrogen-stimulated dendritic spine protein expression, describe for the first time a signal transduction pathway in PSD-95 expression, and delineate a novel, molecular mechanism by which ovarian hormones might translationally regulate synaptogenesis via activating protein synthesis for dendritic function.
Indexed as
Identifiers
12657692PMC6742036What OpenQuestion holds
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.