ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Post-traumatic hyperexcitability is not caused by impaired buffering of extracellular potassium.
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 22 papers.
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Who cites it
22 citing papers in PubMed.
- Article
- Innovative drug discovery strategies in epilepsy: integrating next-generation syndrome-specific mouse models to address pharmacoresistance and epileptogenesis.Expert opinion on drug discovery · 2024Review
- Effects of isoflurane and urethane anesthetics on glutamate neurotransmission in rat brain using in vivo amperometry.BMC neuroscience · 2023Article
- Single Neuron Modeling Identifies Potassium Channel Modulation as Potential Target for Repetitive Head Impacts.Neuroinformatics · 2023Article
- Early Appearance and Spread of Fast Ripples in the Hippocampus in a Model of Cortical Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Acute treatment with doxorubicin affects glutamate neurotransmission in the mouse frontal cortex and hippocampus.Brain research · 2017Article
- Toll-like receptor 4 enhancement of non-NMDA synaptic currents increases dentate excitability after brain injury.Neurobiology of disease · 2015Article
- Distinct effect of impact rise times on immediate and early neuropathology after brain injury in juvenile rats.Journal of neuroscience research · 2014Article
- Divide and conquer: functional segregation of synaptic inputs by astrocytic microdomains could alleviate paroxysmal activity following brain trauma.PLoS computational biology · 2013Article
- Decrease in tonic inhibition contributes to increase in dentate semilunar granule cell excitability after brain injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Hypersensitive glutamate signaling correlates with the development of late-onset behavioral morbidity in diffuse brain-injured circuitry.Journal of neurotrauma · 2012Article
- Alterations of A-type potassium channels in hippocampal neurons after traumatic brain injury.Journal of neurotrauma · 2012Article
- The impact of the glial spatial buffering on the K(+) Nernst potential.Cognitive neurodynamics · 2011Article
- GABAA receptor-mediated modulation of neuronal activity propagation upon tetanic stimulation in rat hippocampal slices.Pflugers Archiv : European journal of physiology · 2010Article
- Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury.Nature reviews. Neurology · 2010Review
- Monitoring hippocampus electrical activity in vitro on an elastically deformable microelectrode array.Journal of neurotrauma · 2009Article
- A novel apparatus for lateral fluid percussion injury in the rat.Journal of neuroscience methods · 2009Article
- Potassium dynamics in the epileptic cortex: new insights on an old topic.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2008Review
- Homeostatic plasticity studied using in vivo hippocampal activity-blockade: synaptic scaling, intrinsic plasticity and age-dependence.PloS one · 2007Article
- The impact of astrocytic gap junctional coupling on potassium buffering in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
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Authors and funding
4 authors.
Funding
Abstract
Impaired extracellular potassium buffering has been proposed as one of the major mechanisms underlying the increased risk for temporal lobe epilepsy after brain injury (D'Ambrosio et al., 1999). The present study systematically tested this hypothesis by measuring the resting [K+]o and recovery of the stimulation-evoked [K+]o increases in the dentate gyrus after experimental head trauma, using a combination of whole-cell recordings and ion-selective microelectrode recordings in rat hippocampal slices. Despite the presence of hyperexcitability, the resting [K+]o was not increased after injury. The faster rate of increase and larger amplitude of the orthodromically evoked [K+]o elevation after head trauma occurred in association with a greater population spike with shorter response latency. Contrary to the assumption in previous studies that the evoked activity in control and injured neuronal circuits is the same during antidromic activation, stimulation of granule cell axons in glutamate receptor antagonists evoked a greater [K+]o increase and a larger population spike. Although perforant path stimulation resulted in a larger [K+]o elevation after injury, the rate of clearance of the [K+]o transients evoked either by neuronal activity or by external application of potassium was not compromised. The [K+]o increase evoked by activation of the presynaptic afferents in isolation was not increased. In addition, the postsynaptic neuronal depolarization and firing evoked by exogenous potassium application was decreased after trauma. These results show that the regulation of [K+]o is not impaired after injury and indicate that the larger [K+]o increase evoked by neuronal activity is a consequence, rather than the primary mechanism underlying post-traumatic hyperexcitability.
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12843291PMC6741221What OpenQuestion holds
Registered trials
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