ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Electrophysiological abnormalities in both axotomized and nonaxotomized pyramidal neurons following mild traumatic brain injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude.Journal of neuroscience research · 2026Article
- Simultaneous Reactive Change in Unmyelinated and Myelinated Axon Segments Following Experimental Diffuse Traumatic Brain Injury.Journal of neurotrauma · 2026Article
- Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell.The Journal of physiology · 2025Article
- A cellulosic fibre foam as a bicycle helmet impact liner for brain injury mitigation in oblique impacts.Heliyon · 2025Article
- Concussive Head Trauma Deranges Axon Initial Segment Function in Axotomized and Intact Layer 5 Pyramidal Neurons.Journal of neurotrauma · 2024Article
- Somatostatin interneurons exhibit enhanced functional output and resilience to axotomy after mild traumatic brain injury.Neurobiology of disease · 2022Article
- Imaging the stability of chronic electrical microstimulation using electrodes coated with PEDOT/CNT and iridium oxide.iScience · 2022Article
- Brain Injury Effects on Neuronal Activation and Synaptic Transmission in the Basolateral Amygdala of Adult Male and Female Wistar Rats.Journal of neurotrauma · 2022Article
- SARM1 signaling mechanisms in the injured nervous system.Current opinion in neurobiology · 2021Review
- High-frequency head impact causes chronic synaptic adaptation and long-term cognitive impairment in mice.Nature communications · 2021Article
- Article
- Paths to Successful Translation of New Therapies for Severe Traumatic Brain Injury in the Golden Age of Traumatic Brain Injury Research: A Pittsburgh Vision.Journal of neurotrauma · 2020Review
- Preventing neuronal edema increases network excitability after traumatic brain injury.The Journal of clinical investigation · 2020Article
- Endocannabinoid degradation inhibitors ameliorate neuronal and synaptic alterations following traumatic brain injury.Journal of neurophysiology · 2020Article
- Microglial process convergence on axonal segments in health and disease.Neuroimmunology and neuroinflammation · 2020Article
- Simultaneous electrophysiological and morphological assessment of functional damage to neural networks in vitro after 30-300 g impacts.Scientific reports · 2019Article
- Layer-By-Layer: The Case for 3D Bioprinting Neurons to Create Patient-Specific Epilepsy Models.Materials (Basel, Switzerland) · 2019Review
- Mechanical characterization of squid giant axon membrane sheath and influence of the collagenous endoneurium on its properties.Scientific reports · 2019Article
- Rapid Changes in Synaptic Strength After Mild Traumatic Brain Injury.Frontiers in cellular neuroscience · 2019Article
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3 authors.
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Abstract
Mild traumatic brain injury (mTBI) often produces lasting detrimental effects on cognitive processes. The mechanisms underlying neurological abnormalities have not been fully identified, in part due to the diffuse pathology underlying mTBI. Here we employ a mouse model of mTBI that allows for identification of both axotomized and intact neurons in the living cortical slice via neuronal expression of yellow fluorescent protein. Both axotomized and intact neurons recorded within injured cortex are healthy with a normal resting membrane potential, time constant (τ), and input resistance (R(in)). In control cortex, 25% of cells show an intrinsically bursting action potential (AP) firing pattern, and the rest respond to injected depolarizing current with a regular-spiking pattern. At 2 d postinjury, intrinsic bursting activity is lost within the intact population. The AP amplitude is increased and afterhyperpolarization duration decreased in axotomized neurons at 1 and 2 d postinjury. In contrast, intact neurons also show these changes at 1 d, but recover by 2 d postinjury. Two measures suggest an initial decrease in excitability in axotomized neurons followed by an increase in excitability within intact neurons. The rheobase is significantly increased in axotomized neurons at 1 d postinjury. The slope of the plot of AP frequency versus injected current is larger for intact neurons at 2 d postinjury. Together, these results demonstrate that intact and axotomized neurons are both affected by mTBI, resulting in different changes in neuronal excitability that may contribute to network dysfunction following TBI.
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