ArticleEpilepsy research2011
Persistent ictal-like activity in rat entorhinal/perirhinal cortex following washout of 4-aminopyridine.
Article in Epilepsy research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Rapid volume pulsation of the extracellular space coincides with epileptiform activity in mice and depends on the NBCe1 transporter.The Journal of physiology · 2021Article
- Brain extracellular space, hyaluronan, and the prevention of epileptic seizures.Reviews in the neurosciences · 2017Review
- Beneficial Effects of Selective Orexin-A Receptor Antagonist in 4-aminopyridine-induced Seizures in Male Rats.Advanced biomedical research · 2017Article
- Compromising KCC2 transporter activity enhances the development of continuous seizure activity.Neuropharmacology · 2016Article
- The piriform, perirhinal, and entorhinal cortex in seizure generation.Frontiers in neural circuits · 2015Review
- Tools, methods, and applications for optophysiology in neuroscience.Frontiers in molecular neuroscience · 2013Article
- Targeted deletion of Kcne2 impairs HCN channel function in mouse thalamocortical circuits.PloS one · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Application of 4-aminopyridine (4-AP, 100μM) in a solution containing 0.6mM Mg(2+) and 1.2mM Ca(2+) to hippocampal-entorhinal-perirhinal slices of adult rat brain induced ictal-like epileptiform activity in entorhinal and perirhinal cortices as revealed by electrophysiological field potential recordings. The ictal-like activity persisted after washing out the 4-AP. This persistence indicated that a change had occurred in the slice so that it was now "epileptic" in the absence of the convulsant 4-AP. Induction of persistent ictal-like activity was dependent upon the concentration of divalent cations during 4-AP exposure; that is, although 4-AP caused ictal-like activity in approximately half the slices in solution containing 1.6mM Mg(2+) and 2.0mM Ca(2+), this ictal-like activity did not persist upon washout of the 4-AP. Expression of the persistent ictal-like epileptiform activity required ionotropic glutamate-mediated synaptic transmission: application of the AMPA/kainate receptor antagonist NBQX after 4-AP washout reduced persistent ictal-like activity, and the combined application of NBQX and the NMDA receptor antagonist d-AP5 completely blocked it. In order to investigate the mechanism of induction of persistent ictal-like activity, several agents were applied before the introduction of 4-AP. Application of d-AP5 did not block the onset of ictal-like activity upon introduction of 4-AP but did prevent the persistence of the ictal-like activity upon washout of the 4-AP. In contrast, induction of persistent ictal-like activity was not prevented by simultaneous application of the group I metabotropic glutamate receptor (mGluR) antagonists LY 367385 and MPEP or by application of the protein synthesis inhibitor cycloheximide. In conclusion, we have characterized a new in vitro model of epileptogenesis in which induction of ictal-like activity is dependent upon NMDA receptor activation but not upon group I mGluR activation or protein synthesis.
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