ArticleJournal of neurotrauma2016
Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo.
Article in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed.
- Peripheral B cell populations tune spontaneous neuronal activity in the uninjured hippocampus after stroke.bioRxiv : the preprint server for biology · 2026Article
- Imaging the large-scale and cellular response to focal traumatic brain injury in mouse neocortex.Experimental physiology · 2025Article
- Oligodendrocyte precursor cells facilitate neuronal lysosome release.Nature communications · 2025Article
- Imaging the large-scale and cellular response to focal traumatic brain injury in mouse neocortex.bioRxiv : the preprint server for biology · 2024Article
- Article
- Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- Article
- Electrical stimulation methods and protocols for the treatment of traumatic brain injury: a critical review of preclinical research.Journal of neuroengineering and rehabilitation · 2023Review
- GABAkines - Advances in the discovery, development, and commercialization of positive allosteric modulators of GABAPharmacology & therapeutics · 2022Review
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
- Input rate encoding and gain control in dendrites of neocortical pyramidal neurons.Cell reports · 2022Article
- Novel Approaches to Prevent Epileptogenesis After Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Article
- Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function.Frontiers in cellular neuroscience · 2021Article
- Cortical Electrical Stimulation Ameliorates Traumatic Brain Injury-Induced Sensorimotor and Cognitive Deficits in Rats.Frontiers in neural circuits · 2021Article
- Compensatory functional connectome changes in a rat model of traumatic brain injury.Brain communications · 2021Article
- The Positive Allosteric Modulator ofThe Journal of pharmacology and experimental therapeutics · 2020Article
- Neurotransmitter changes after traumatic brain injury: an update for new treatment strategies.Molecular psychiatry · 2019Review
- Homeostatic activity regulation as a mechanism underlying the effect of brain stimulation.Bioelectronic medicine · 2019Review
- What goes up must come down: homeostatic synaptic plasticity strategies in neurological disease.Future neurology · 2018Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Traumatic brain injury (TBI) often results in structural damage and a loss of neurons that is commonly accompanied by early changes in neuronal electrical activity. Loss of neuronal activity has been hypothesized to contribute to post-traumatic epileptogenesis through the regulation of homeostatic plasticity. The existence of activity loss in cortical neurons after TBI and its subsequent transition into hyperactivity over time is not well characterized, however, particularly in models of TBI in vivo. In the current study, changes in neuronal activity in the primary motor cortex after moderate controlled cortical impact (CCI) in mice were studied using a single-unit recording technique in vivo. Recordings were made at different time points after CCI from cortical layer V pyramidal neurons that were within 1-2 mm from the anterior edge of the injured foci. Within 1-4 h after CCI, the frequency of spontaneous single-unit activity depressed significantly, with the mean firing frequency decreasing from 2.59 ± 0.18 Hz in the sham group to 1.05 ± 0.20 Hz of the injured group. The firing frequencies recovered to the normal level at 1 day and 7 days post-CCI, but became significantly higher at 3 days and 14 days post-CCI. The results suggest that TBI caused initial loss of activity in neurons of the perilesional cortical region, which was followed by compensatory recovery and enhancement of activity. These time-dependent changes in neuronal activity may contribute to the development of hyperexcitability through homeostatic activity regulation.
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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.