ArticleJournal of neurophysiology2010
Presynaptic inhibitory terminals are functionally abnormal in a rat model of posttraumatic epilepsy.
Article in Journal of neurophysiology, 2010. 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.
- From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology.International journal of molecular sciences · 2025Review
- Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review.Frontiers in neurology · 2023Review
- Chronic partial TrkB activation reduces seizures and mortality in a mouse model of Dravet syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Prolonged prophylactic effects of gabapentin on status epilepticus-induced neocortical injury.Neurobiology of disease · 2020Article
- Partial Activation of TrkB Receptors Corrects Interneuronal Calcium Channel Dysfunction and Reduces Epileptogenic Activity in Neocortex following Injury.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Gabapentin Prevents Progressive Increases in Excitatory Connectivity and Epileptogenesis Following Neocortical Trauma.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Structural alterations in fast-spiking GABAergic interneurons in a model of posttraumatic neocortical epileptogenesis.Neurobiology of disease · 2017Article
- Aberrant excitatory rewiring of layer V pyramidal neurons early after neocortical trauma.Neurobiology of disease · 2016Article
- More Docked Vesicles and Larger Active Zones at Basket Cell-to-Granule Cell Synapses in a Rat Model of Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Excitatory and inhibitory synaptic connectivity to layer V fast-spiking interneurons in the freeze lesion model of cortical microgyria.Journal of neurophysiology · 2014Article
- Gabapentin decreases epileptiform discharges in a chronic model of neocortical trauma.Neurobiology of disease · 2012Article
- Functional alterations in GABAergic fast-spiking interneurons in chronically injured epileptogenic neocortex.Neurobiology of disease · 2012Article
- Interneuronal calcium channel abnormalities in posttraumatic epileptogenic neocortex.Neurobiology of disease · 2012Article
- Targets for preventing epilepsy following cortical injury.Neuroscience letters · 2011Review
- Reorganization of inhibitory synaptic circuits in rodent chronically injured epileptogenic neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2011Article
- Presynaptic inhibitory terminals are functionally abnormal in a rat model of posttraumatic epilepsy.Journal of neurophysiology · 2010Article
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2 authors.
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Abstract
Partially isolated "undercut" neocortex with intact pial circulation is a well-established model of posttraumatic epileptogenesis. Results of previous experiments showed a decreased frequency of miniature inhibitory postsynaptic currents (mIPSCs) in layer V pyramidal (Pyr) neurons of undercuts. We further examined possible functional abnormalities in GABAergic inhibition in rat epileptogenic neocortical slices in vitro by recording whole cell monosynaptic IPSCs in layer V Pyr cells and fast-spiking (FS) GABAergic interneurons using a paired pulse paradigm. Compared with controls, IPSCs in Pyr neurons of injured slices showed increased threshold and decreased peak amplitude at threshold, decreased input/output slopes, increased failure rates, and a shift from paired pulse depression toward paired pulse facilitation (increased paired pulse ratio or PPR). Increasing [Ca(2+)](o) from 2 to 4 mM partially reversed these abnormalities in Pyr cells of the epileptogenic tissue. IPSCs onto FS cells also had an increased PPR and failures. Blockade of GABA(B) receptors did not affect the paired results. These findings suggest that there are functional alterations in GABAergic presynaptic terminals onto both Pyr and FS cells in this model of posttraumatic epileptogenesis.
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