ArticleJournal of neurotrauma2012
Alterations of A-type potassium channels in hippocampal neurons after traumatic brain injury.
Article in Journal of neurotrauma, 2012. 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, 45 citations in OpenAlex.
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- Sex differences in the effects of chronic stress and oxycodone associative learning on glial markers in rat hippocampus.Neuroscience · 2026Article
- Article
- Single Neuron Modeling Identifies Potassium Channel Modulation as Potential Target for Repetitive Head Impacts.Neuroinformatics · 2023Article
- Silencing TLR4 using an ultrasound-targeted microbubble destruction-based shRNA system reduces ischemia-induced seizures in hyperglycemic rats.Open life sciences · 2022Article
- The potassium channel Kv4.2 regulates dendritic spine morphology, electroencephalographic characteristics and seizure susceptibility in mice.Experimental neurology · 2020Article
- Identification of MicroRNA-Potassium Channel Messenger RNA Interactions in the Brain of Rats With Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2020Article
- Increased Sestrin3 Contributes to Post-ischemic Seizures in the Diabetic Condition.Frontiers in neuroscience · 2020Article
- α-Helical protein absorption at post-traumatic epileptic foci monitored by Fourier transform infrared mapping.Journal of biosciences · 2020Article
- MicroRNA inhibition upregulates hippocampal A-type potassium current and reduces seizure frequency in a mouse model of epilepsy.Neurobiology of disease · 2019Article
- The physiological variability of channel density in hippocampal CA1 pyramidal cells and interneurons explored using a unified data-driven modeling workflow.PLoS computational biology · 2018Article
- Multi-scale, multi-modal analysis uncovers complex relationship at the brain tissue-implant neural interface: new emphasis on the biological interface.Journal of neural engineering · 2018Article
- The Segregated Expression of Voltage-Gated Potassium and Sodium Channels in Neuronal Membranes: Functional Implications and Regulatory Mechanisms.Frontiers in cellular neuroscience · 2017Article
- MicroRNA-Mediated Downregulation of the Potassium Channel Kv4.2 Contributes to Seizure Onset.Cell reports · 2016Article
- Reduced expression of IA channels is associated with post-ischemic seizures.Epilepsy research · 2016Article
- Potassium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Animal Models of Posttraumatic Seizures and Epilepsy.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Knockout of Cyclophilin-D Provides Partial Amelioration of Intrinsic and Synaptic Properties Altered by Mild Traumatic Brain Injury.Frontiers in systems neuroscience · 2016Article
- Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury.Neural plasticity · 2016Article
- Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is associated with cognitive deficits, memory impairment, and epilepsy. Previous studies have reported neuronal loss and neuronal hyperexcitability in the post-traumatic hippocampus. A-type K+ currents (I(A)) play a critical role in modulating the intrinsic membrane excitability of hippocampal neurons. The disruption of I(A) is reportedly linked to hippocampal dysfunction. The present study investigates the changes of I(A) in the hippocampus after TBI. TBI in rats was induced by controlled cortical impact. The impact induced a reproducible lesion in the cortex and an obvious neuronal death in the ipsilateral hippocampus CA3 region. At one week after TBI, immunohistochemical staining and Western blotting showed that the expression of I(A) channel subunit Kv4.2 was markedly decreased in the ipsilateral hippocampus, but remained unchanged in the contralateral hippocampus. Meanwhile, electrophysiological recording showed that I(A) currents in ipsilateral CA1 pyramidal neurons were significantly reduced, which was associated with an increased neuronal excitability. Furthermore, there was an increased sensitivity to bicuculline-induced seizures in TBI rats. At 8 weeks after TBI, immunohistochemical staining and electrophysiological recording indicated that I(A) returned to control levels. These findings suggest that TBI causes a transient downregulation of I(A) in hippocampal CA1 neurons, which might be associated with the hyperexcitability in the post-traumatic hippocampus, and in turn leads to seizures and epilepsy.
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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.