ArticleEpilepsia2011
Homeostatic increase in excitability in area CA1 after Schaffer collateral transection in vivo.
Article in Epilepsia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Mapping global brain reconfigurations following local targeted manipulations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.Frontiers in molecular neuroscience · 2023Article
- Modularity and neuronal heterogeneity: Two properties that influenceFrontiers in cellular neuroscience · 2023Article
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- Cortical stimulation for treatment of neurological disorders of hyperexcitability: a role of homeostatic plasticity.Neural regeneration research · 2019Review
- Homeostatic activity regulation as a mechanism underlying the effect of brain stimulation.Bioelectronic medicine · 2019Review
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- Removal of area CA3 from hippocampal slices induces postsynaptic plasticity at Schaffer collateral synapses that normalizes CA1 pyramidal cell discharge.Neuroscience letters · 2018Article
- Concussion Induces Hippocampal Circuitry Disruption in Swine.Journal of neurotrauma · 2017Article
- Transition from Initial Hypoactivity to Hyperactivity in Cortical Layer V Pyramidal Neurons after Traumatic Brain Injury In Vivo.Journal of neurotrauma · 2016Article
- Making Waves in the Brain: What Are Oscillations, and Why Modulating Them Makes Sense for Brain Injury.Frontiers in systems neuroscience · 2016Review
- Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury.Neural regeneration research · 2014Article
- Critical role of trkB receptors in reactive axonal sprouting and hyperexcitability after axonal injury.Journal of neurophysiology · 2013Article
- The temporoammonic input to the hippocampal CA1 region displays distinctly different synaptic plasticity compared to the Schaffer collateral input in vivo: significance for synaptic information processing.Frontiers in synaptic neuroscience · 2013Article
- Repetitive magnetic stimulation induces functional and structural plasticity of excitatory postsynapses in mouse organotypic hippocampal slice cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposeEpilepsy is a significant long-term consequence of traumatic brain injury (TBI) and is likely to result from multiple mechanisms. One feature that is common to many forms of TBI is denervation. We asked whether chronic partial denervation in vivo would lead to a homeostatic increase in the excitability of a denervated cell population.
methodsTo answer this question, we took advantage of the unique anatomy of the hippocampus where the input to the CA1 neurons, the Schaffer collaterals, could be transected in vivo with preservation of their outputs and only minor cell death. KEY
findingsWe observed a delayed increase in neuronal excitability, as apparent in extracellular recordings from hippocampal brain slices prepared 14 days (but not 3 days) post lesion. Although population spikes in slices from control and lesioned animals were comparable under resting conditions, application of solutions that were mildly proconvulsive (high K(+) , low Mg(2+) , low concentrations of bicuculline) produced increases in the number of population spikes in slices from lesioned rats, but not in slices from unlesioned sham controls. Denervation did not produce changes in several markers of γ-aminobutyric acid (GABA)ergic synaptic inhibition, including the number of GABAergic neurons, α1 GABA(A) receptor subunits, the vesicular GABA transporter, or miniature inhibitory postsynaptic currents. SIGNIFICANCE: We conclude that chronic partial denervation does lead to a delayed homeostatic increase in neuronal excitability, and may, therefore, contribute to the long-term neurologic consequences of TBI.
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