ArticleThe Journal of physiology2007
Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 92 citations in OpenAlex.
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- Theta and gamma rhythmic coding through two spike output modes in the hippocampus during spatial navigation.Cell reports · 2023Article
- Degeneracy in epilepsy: multiple routes to hyperexcitable brain circuits and their repair.Communications biology · 2023Review
- Research progress on correlations between trace element levels and epilepsy.Frontiers in cell and developmental biology · 2023Review
- Active Dendrites and Local Field Potentials: Biophysical Mechanisms and Computational Explorations.Neuroscience · 2022Review
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- Short-Term Epileptiform Activity Potentiates Excitatory Synapses but Does Not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus In Vitro.Biomedicines · 2021Article
- The Subcortical-Allocortical- NeocorticalFrontiers in synaptic neuroscience · 2021Article
- Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Altered Dynamics of Canonical Feedback Inhibition Predicts Increased Burst Transmission in Chronic Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Pathogenic Cav3.2 channel mutation in a child with primary generalized epilepsy.Molecular brain · 2019Article
- Inhibition of T-Type calcium channels in mEC layer II stellate neurons reduces neuronal hyperexcitability associated with epilepsy.Epilepsy research · 2019Article
- In search of antiepileptogenic treatments for post-traumatic epilepsy.Neurobiology of disease · 2019Review
- The Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and Beyond.International journal of molecular sciences · 2019Review
- The Alteration of Intrinsic Excitability and Synaptic Transmission in Lumbar Spinal Motor Neurons and Interneurons of Severe Spinal Muscular Atrophy Mice.Frontiers in cellular neuroscience · 2019Article
- Astroglial role in the pathophysiology of statusOncotarget · 2018Review
- Organic washes of tissue sections for comprehensive analysis of small molecule metabolites by MALDI MS imaging of rat brain following status epilepticus.Metabolomics : Official journal of the Metabolomic Society · 2018Article
- Article
- Effect of eugenol on lithium-pilocarpine model of epilepsy: behavioral, histological, and molecular changes.Iranian journal of basic medical sciences · 2017Article
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
A single episode of status epilepticus (SE) induced in rodents by the convulsant pilocarpine, produces, after a latent period of > or = 2 weeks, a chronic epileptic condition. During the latent period of epileptogenesis, most CA1 pyramidal cells that normally fire in a regular pattern, acquire low-threshold bursting behaviour, generating high-frequency clusters of 3-5 spikes as their minimal response to depolarizing stimuli. Recruitment of a Ni(2+)- and amiloride-sensitive T-type Ca(2+) current (I(CaT)), shown to be up-regulated after SE, plays a critical role in burst generation in most cases. Several lines of evidence suggest that I(CaT) driving bursting is located in the apical dendrites. Thus, bursting was suppressed by focally applying Ni(2+) to the apical dendrites, but not to the soma. It was also suppressed by applying either tetrodotoxin or the K(V)7/M-type K(+) channel agonist retigabine to the apical dendrites. Severing the distal apical dendrites approximately 150 microm from the pyramidal layer also abolished this activity. Intradendritic recordings indicated that evoked bursts are associated with local Ni(2+)-sensitive slow spikes. Blocking persistent Na(+) current did not modify bursting in most cases. We conclude that SE-induced increase in I(CaT) density in the apical dendrites facilitates their depolarization by the backpropagating somatic spike. The I(CaT)-driven dendritic depolarization, in turn, spreads towards the soma, initiating another backpropagating spike, and so forth, thereby creating a spike burst. The early appearance and predominance of I(CaT)-driven low-threshold bursting in CA1 pyramidal cells that experienced SE most probably contribute to the emergence of abnormal network discharges and may also play a role in the circuitry reorganization associated with epileptogenesis.
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