ArticleNeurobiology of disease2012
Interneuronal calcium channel abnormalities in posttraumatic epileptogenic neocortex.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- N-Type Ca Channel in Epileptic Syndromes and Epilepsy: A Systematic Review of Its Genetic Variants.International journal of molecular sciences · 2023Pooled it
- Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review.Frontiers in neurology · 2023Review
- 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
- From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- 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
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3 authors.
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Abstract
Decreased release probability (Pr) and increased failure rate for monosynaptic inhibitory postsynaptic currents (IPSCs) indicate abnormalities in presynaptic inhibitory terminals on pyramidal (Pyr) neurons of the undercut (UC) model of posttraumatic epileptogenesis. These indices of inhibition are normalized in high [Ca++] ACSF, suggesting dysfunction of Ca2+ channels in GABAergic terminals. We tested this hypothesis using selective blockers of P/Q and N-type Ca2+ channels whose activation underlies transmitter release in cortical inhibitory terminals. Pharmacologically isolated monosynaptic IPSCs were evoked in layer V Pyr cells by extracellular stimuli in adult rat sensorimotor cortical slices. Local perfusion of 0.2/1 μM ω-agatoxin IVa and/or 1 μM ω-conotoxin GVIA was used to block P/Q and N-type calcium channels, respectively. In control layer V Pyr cells, peak amplitude of eIPSCs was decreased by ~50% after treatment with either 1 μM ω-conotoxin GVIA or 1 μM ω-agatoxin IVa. In contrast, there was a lack of sensitivity to 1 μM ω-conotoxin GVIA in UCs. Immunocytochemical results confirmed decreased perisomatic density of N-channels on Pyr cells in UCs. We suggest that decreased calcium influx via N-type channels in presynaptic GABAergic terminals is a mechanism contributing to decreased inhibitory input onto layer V Pyr cells in this model of cortical posttraumatic epileptogenesis.
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