ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Prostaglandin E2-induced synaptic plasticity in neocortical networks of organotypic slice cultures.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- From mice to clinical relevance: humanizing neuroscience with human-based model systems.Frontiers in cellular neuroscience · 2026Review
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- Hippocampal interneuronal dysfunction and hyperexcitability in a porcine model of concussion.Communications biology · 2023Article
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- Inhibition of rat locus coeruleus neurons by prostaglandin EFrontiers in pharmacology · 2023Article
- The Role of Brain Cyclooxygenase-2 (Cox-2) Beyond Neuroinflammation: Neuronal Homeostasis in Memory and Anxiety.Molecular neurobiology · 2020Review
- The Pathophysiology of Rett Syndrome With a Focus on Breathing Dysfunctions.Physiology (Bethesda, Md.) · 2020Review
- Calcium-Sensing Receptor Mediates β-Amyloid-Induced Synaptic Formation Impairment and Cognitive DeficitsFrontiers in aging neuroscience · 2020Article
- [Epileptogenesis and consequences for treatment].Der Nervenarzt · 2019Review
- In utero exposure to fine particulate matter results in an altered neuroimmune phenotype in adult mice.Environmental pollution (Barking, Essex : 1987) · 2018Article
- Taxifolin prevents β-amyloid-induced impairments of synaptic formation and deficits of memory via the inhibition of cytosolic phospholipase AMetabolic brain disease · 2018Article
- Maternal exposure to prostaglandin EBiochemistry and biophysics reports · 2018Article
- Human Cerebrospinal fluid promotes long-term neuronal viability and network function in human neocortical organotypic brain slice cultures.Scientific reports · 2017Article
- Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses.Molecular autism · 2017Review
- Spontaneous Glutamatergic Synaptic Activity Regulates Constitutive COX-2 Expression in Neurons: OPPOSING ROLES FOR THE TRANSCRIPTION FACTORS CREB (cAMP RESPONSE ELEMENT BINDING) PROTEIN AND Sp1 (STIMULATORY PROTEIN-1).The Journal of biological chemistry · 2016Article
- Organotypic Hippocampal Slices as Models for Stroke and Traumatic Brain Injury.Molecular neurobiology · 2016Review
- Organotypic brain slice cultures: A review.Neuroscience · 2015Review
- cAMP-Inhibits Cytoplasmic Phospholipase A₂ and Protects Neurons against Amyloid-β-Induced Synapse Damage.Biology · 2015Article
- Prostaglandin E2 differentially modulates the central control of eupnoea, sighs and gasping in mice.The Journal of physiology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major cause of epilepsy, yet the mechanisms underlying the progression from TBI to epilepsy are unknown. TBI induces the expression of COX-2 (cyclooxygenase-2) and increases levels of prostaglandin E2 (PGE2). Here, we demonstrate that acutely applied PGE2 (2 mum) decreases neocortical network activity by postsynaptically reducing excitatory synaptic transmission in acute and organotypic neocortical slices of mice. In contrast, long-term exposure to PGE2 (2 mum; 48 h) presynaptically increases excitatory synaptic transmission, leading to a hyperexcitable network state that is characterized by the generation of paroxysmal depolarization shifts (PDSs). PDSs were also evoked as a result of depriving organotypic slices of activity by treating them with tetrodotoxin (TTX, 1 mum; 48 h). This treatment predominantly increased postsynaptically excitatory synaptic transmission. The network and cellular effects of PGE2 and TTX treatments reversed within 1 week. Differences in the underlying mechanisms (presynaptic vs postsynaptic) as well as occlusion experiments in which slices were exposed to TTX plus PGE2 suggest that the two substances evoke distinct forms of homeostatic plasticity, both of which result in a hyperexcitable network state. PGE2 and TTX (alone or together with PGE2) also increased levels of apoptotic cell death in organotypic slices. Thus, we hypothesize that the increase in excitability and apoptosis may constitute the first steps in a cascade of events that eventually lead to epileptogenesis triggered by TBI.
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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.