ArticleThe Journal of biological chemistry2014
The nuclear calcium signaling target, activating transcription factor 3 (ATF3), protects against dendrotoxicity and facilitates the recovery of synaptic transmission after an excitotoxic insult.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 61 citations in OpenAlex.
- Article
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- Hybrid Amyloid Quantum Dot Nano-Bio Assemblies to Probe Neuroinflammatory Damage.ACS chemical neuroscience · 2024Article
- A human in vitro neuronal model for studying homeostatic plasticity at the network level.Stem cell reports · 2023Article
- Quantum Dot Biomimetic for SARS-CoV-2 to Interrogate Blood-Brain Barrier Damage Relevant to NeuroCOVID Brain Inflammation.ACS applied nano materials · 2023Article
- Reactivation of corticogenesis-related transcriptional factors BCL11B and SATB2 after ischemic lesion of the adult mouse brain.Scientific reports · 2023Article
- Activating Transcription Factor 3 Diminishes Ischemic Cerebral Infarct and Behavioral Deficit by Downregulating Carboxyl-Terminal Modulator Protein.International journal of molecular sciences · 2023Article
- Neuronal nuclear calcium signaling suppression of microglial reactivity is mediated by osteoprotegerin after traumatic brain injury.Journal of neuroinflammation · 2022Article
- Protective role of activating transcription factor 3 against neuronal damage in rats with cerebral ischemia.Brain and behavior · 2022Article
- The bitter end: T2R bitter receptor agonists elevate nuclear calcium and induce apoptosis in non-ciliated airway epithelial cells.Cell calcium · 2022Article
- 1,5-Anhydro-D-fructose Protects against Rotenone-Induced Neuronal Damage In Vitro through Mitochondrial Biogenesis.International journal of molecular sciences · 2021Article
- Role ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- A microscopy-based small molecule screen in primary neurons reveals neuroprotective properties of the FDA-approved anti-viral drug Elvitegravir.Molecular brain · 2020Article
- VEGFD Protects Retinal Ganglion Cells and, consequently, Capillaries against Excitotoxic Injury.Molecular therapy. Methods & clinical development · 2020Article
- Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush.Investigative ophthalmology & visual science · 2020Article
- Post-injury Nose-to-Brain Delivery of Activin A and SerpinB2 Reduces Brain Damage in a Mouse Stroke Model.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- The Activating Transcription Factor 3 (Frontiers in molecular neuroscience · 2018Article
- Bioinformatics analysis of gene expression profiling for identification of potential key genes among ischemic stroke.Medicine · 2017Observational
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The focal swellings of dendrites ("dendritic beading") are an early morphological hallmark of neuronal injury and dendrotoxicity. They are associated with a variety of pathological conditions, including brain ischemia, and cause an acute disruption of synaptic transmission and neuronal network function, which contribute to subsequent neuronal death. Here, we show that increased synaptic activity prior to excitotoxic injury protects, in a transcription-dependent manner, against dendritic beading. Expression of activating transcription factor 3 (ATF3), a nuclear calcium-regulated gene and member of the core gene program for acquired neuroprotection, can protect against dendritic beading. Conversely, knockdown of ATF3 exacerbates dendritic beading. Assessment of neuronal network functions using microelectrode array recordings revealed that hippocampal neurons expressing ATF3 were able to regain their ability for functional synaptic transmission and to participate in coherent neuronal network activity within 48 h after exposure to toxic concentrations of NMDA. Thus, in addition to attenuating cell death, synaptic activity and expression of ATF3 render hippocampal neurons more resistant to acute dendrotoxicity and loss of synapses. Dendroprotection can enhance recovery of neuronal network functions after excitotoxic insults.
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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.