ArticleNeural networks : the official journal of the International Neural Network Society2011
Chemical synaptic and gap junctional interactions between principal neurons: partners in epileptogenesis.
Article in Neural networks : the official journal of the International Neural Network Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Dichotomy between extracellular signatures of active dendritic chemical synapses and gap junctions.eLife · 2026Article
- Infantile epileptic spasms syndrome: Mechanisms and therapeutic approaches.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Hippocampal Expression of Connexin36 and Connexin43 during Epileptogenesis in Pilocarpine Model of Epilepsy.Iranian biomedical journal · 2017Article
- Facilitation of Hippocampal Kindling and Exacerbation of Kindled Seizures by Intra-CA1 Injection of Quinine: A Possible Role of Cx36 Gap Junctions.Iranian biomedical journal · 2016Article
- High-frequency oscillations are prominent in the extended amygdala.Journal of neurophysiology · 2014Article
- Article
- Blocking of rat hippocampal Cx36 by quinine accelerates kindling epileptogenesis.EXCLI journal · 2013Article
- Shortest Loops are Pacemakers in Random Networks of Electrically Coupled Axons.Frontiers in computational neuroscience · 2012Article
- Effect of chronic intracerebroventricluar administration of lipopolysaccharide on connexin43 protein expression in rat hippocampus.Iranian biomedical journal · 2012Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Field potential signals, corresponding to electrographic seizures in cortical structures, often contain two components, which sometimes appear to be separable and other times to be superimposed. The first component consists of low-amplitude very fast oscillations (VFO, >70-80 Hz); the second component consists of larger amplitude transients, lasting tens to hundreds of ms, and variously called population spikes, EEG spikes, or bursts--terms chosen in part because of the cellular correlates of the field events. To first approximation, the two components arise because of distinctive types of cellular interactions: gap junctions for VFO (a model of which is reviewed in the following), and recurrent synaptic excitation and/or inhibition for the transients. With in vitro studies of epileptic human neocortical tissue, it is possible to elicit VFO alone, or VFO superimposed on a large transient, but not a large transient without the VFO. If such observations prove to be general, they would imply that gap junction-mediated interactions are the primary factor in epileptogenesis. It appears to be the case then, that in the setting of seizure initiation (but not necessarily under physiological conditions), the gain of gap junction-mediated circuits can actually be larger than the gain in excitatory synaptic circuits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.