ArticleCNS neuroscience & therapeutics2015
Traumatic brain injury induces rapid enhancement of cortical excitability in juvenile rats.
Article in CNS neuroscience & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Bursts of brain erosion: seizures and age-dependent neurological vulnerability.Trends in molecular medicine · 2025Review
- Efficacy of repetitive transcranial magnetic stimulation for consciousness recovery in children with disorders of consciousness following traumatic brain injury.Frontiers in neurology · 2025Article
- Endocannabinoid-mediated rescue of somatosensory cortex activity, plasticity and related behaviors following an early in life concussion.bioRxiv : the preprint server for biology · 2024Article
- Flexibility ofFrontiers in cellular neuroscience · 2022Article
- High-frequency head impact causes chronic synaptic adaptation and long-term cognitive impairment in mice.Nature communications · 2021Article
- Progesterone treatment following traumatic brain injury in the 11-day-old rat attenuates cognitive deficits and neuronal hyperexcitability in adolescence.Experimental neurology · 2020Article
- Selective vulnerability of hippocampal interneurons to graded traumatic brain injury.Neurobiology of disease · 2019Review
- Modelling traumatic brain injury and posttraumatic epilepsy in rodents.Neurobiology of disease · 2019Review
- In search of antiepileptogenic treatments for post-traumatic epilepsy.Neurobiology of disease · 2019Review
- Homeostatic activity regulation as a mechanism underlying the effect of brain stimulation.Bioelectronic medicine · 2019Review
- Parvalbumin fast-spiking interneurons are selectively altered by paediatric traumatic brain injury.The Journal of physiology · 2018Article
- Altered Sodium and Potassium, but not Calcium Currents in Cerebellar Granule Cells in an In Vitro Model of Neuronal Injury.Cellular and molecular neurobiology · 2017Article
- Brain Region-Specific Histopathological Effects of Varying Trajectories of Controlled Cortical Impact Injury Model of Traumatic Brain Injury.CNS neuroscience & therapeutics · 2016Article
- Review
- Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats.Journal of neurophysiology · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
aimsFollowing a traumatic brain injury (TBI), 5-50% of patients will develop posttraumatic epilepsy (PTE) with children being particularly susceptible. Currently, PTE cannot be prevented and there is limited understanding of the underlying epileptogenic mechanisms. We hypothesize that early after TBI the brain undergoes distinct cellular and synaptic reorganization that facilitates cortical excitability and promotes the development of epilepsy.
methodsTo examine the effect of pediatric TBI on cortical excitability, we performed controlled cortical impact (CCI) on juvenile rats (postnatal day 17). Following CCI, animals were monitored for the presence of epileptiform activity by continuous in vivo electroencephalography (EEG) and/or sacrificed for in vitro whole-cell patch-clamp recordings.
resultsFollowing a short latent period, all animals subjected to CCI developed spontaneous recurrent epileptiform activity within 14 days. Whole-cell patch-clamp recordings of layer V pyramidal neurons showed no changes in intrinsic excitability or spontaneous excitatory postsynaptic currents (sEPSCs) properties. However, the decay of spontaneous inhibitory postsynaptic currents (sIPSCs) was significantly increased. In addition, CCI induced over a 300% increase in excitatory and inhibitory synaptic bursting. Synaptic bursting was prevented by blockade of Na(+)-dependent action potentials or select antagonism of glutamate or GABA-A receptors, respectively.
conclusionOur results demonstrate that CCI in juvenile rats rapidly induces epileptiform activity and enhanced cortical synaptic bursting. Detection of epileptiform activity early after injury suggests it may be an important pathophysiological component and potential indicator of developing PTE.
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