ArticleNeuropsychiatric disease and treatment2014
Acute lipopolysaccharide exposure facilitates epileptiform activity via enhanced excitatory synaptic transmission and neuronal excitability in vitro.
Article in Neuropsychiatric disease and treatment, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 37 citations in OpenAlex.
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- Microglia-triggered hypoexcitability plasticity of pyramidal neurons in the rat medial prefrontal cortex.Current research in neurobiology · 2022Article
- Immune-Triggered Forms of Plasticity Across Brain Regions.Frontiers in cellular neuroscience · 2022Review
- Gut Microbes Regulate Innate Immunity and Epilepsy.Frontiers in neuroscience · 2022Review
- A Proinflammatory Stimulus Disrupts Hippocampal Plasticity and Learning via Microglial Activation and 25-Hydroxycholesterol.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Lipopolysaccharide-induced neuroinflammation disrupts functional connectivity and community structure in primary cortical microtissues.Scientific reports · 2021Article
- A Destruction Model of the Vascular and Lymphatic Systems in the Emergence of Psychiatric Symptoms.Biology · 2021Review
- Resveratrol inhibits LPS-induced apoptosis in VSC4.1 motoneurons through enhancing SIRT1-mediated autophagy.Iranian journal of basic medical sciences · 2021Article
- Serial Systemic Injections of Endotoxin (LPS) Elicit Neuroprotective Spinal Cord Microglia through IL-1-Dependent Cross Talk with Endothelial Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Metformin Ameliorates Lipopolysaccharide-Induced Depressive-Like Behaviors and Abnormal Glutamatergic Transmission.Biology · 2020Article
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- Immune Challenges and Seizures: How Do Early Life Insults Influence Epileptogenesis?Frontiers in pharmacology · 2020Review
- Cytokine inflammatory threat, but not LPS one, shortens GABAergic synaptic currents in the mouse spinal cord organotypic cultures.Journal of neuroinflammation · 2019Article
- Reversal of a Treatment-Resistant, Depression-Related Brain State with the Kv7 Channel Opener Retigabine.Neuroscience · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence indicates brain inflammation has been involved in the genesis of seizures. However, the direct effect of acute inflammation on neuronal circuits is not well known. Lipopolysaccharide (LPS) has been used extensively to stimulate brain inflammatory responses both in vivo and in vitro. Here, we observed the contribution of inflammation induced by 10 μg/mL LPS to the excitability of neuronal circuits in acute hippocampal slices. When slices were incubated with LPS for 30 minutes, significant increased concentration of tumor necrosis factor α and interleukin 1β were detected by enzyme-linked immunosorbent assay. In electrophysiological recordings, we found that frequency of epileptiform discharges and spikes per burst increased 30 minutes after LPS application. LPS enhanced evoked excitatory postsynaptic currents but did not modify evoked inhibitory postsynaptic currents. In addition, exposure to LPS enhanced the excitability of CA1 pyramidal neurons, as demonstrated by a decrease in rheobase and an increase in action potential frequency elicited by depolarizing current injection. Our observations suggest that acute inflammation induced by LPS facilitates epileptiform activity in vitro and that enhancement of excitatory synaptic transmission and neuronal excitability may contribute to this facilitation. These results may provide new clues for treating seizures associated with brain inflammatory disease.
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