FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2562266950> ?p ?o ?g. }

• W2562266950 endingPage "4" @default.
• W2562266950 startingPage "4" @default.
• W2562266950 abstract "Video Podcast: https://youtu.be/irqLF8mtzN8 Abnormal synchronization of firing in large neuronal ensembles is considered the cardinal mechanism underlying epilepsy. It is classically ascribed to an imbalance between excitation and inhibition in the cerebral cortex due to enhanced excitatory or decreased inhibitory transmission. This perspective currently provides the main basis for pharmacological management of epilepsy, and many effective antiepileptic drugs are known to act on chemical synapses. However, many non-synaptic mechanisms are also known to be able to affect the synchronization of neuronal firing in the context of epilepsy. They include local changes in the concentration of extracellular ions (e.g. K+) and local electrical field resulting from repetitive firing, referred to as ephaptic coupling, which increase the membrane excitability of adjacent neurons. In addition, the role of non-chemical synapses (i.e. electrical synapses or gap junctions) have attracted fluctuating interest in the study of the pathophysiology of epileptic activity onset, maintenance, and termination, with a view to better treatments. There is still some debate about the exact distribution of gap junctions in the human brain. In mammals, they seem to be preferentially expressed in the cortex and the thalamus, where they may play a role in thalamo-cortical networks.1 Gap junctions are present in relatively high numbers in neurons during early development, and decrease progressively with the maturation of neuronal networks until these rely almost entirely on chemical synapses. Gap junctions between adjacent cells connect their cytoplasm, thereby allowing diffusion of small molecules and ions, providing both chemical and electrical communication. This may result in coupling of membrane voltage between neighbouring cells, and thereby ensure rapid propagation of electric signals through large networks of neurons coupled by few gap junctions, at least in computational models.2 Although the physiological function of gap junctions in information processing is uncertain, they might be expected to enhance synchronized activity in networks of neurons and, if that activity is excitatory, promote epileptogenesis. If confirmed, this hypothesis of gap junctions’ proconvulsive role might lead to using gap junction blockers as antiepileptic drugs. Both experimental and empirical data are available with regard to various compounds that have been documented to block gap junctions,3 such as carbenoxolone, quinidine, retinoic acid, or halogenated inhalation anaesthetic agents (e.g. halothane and isoflurane). However, adverse effects may be a major limitation and markedly inconsistent effects are observed on epileptic activity in function of the paradigm or clinical situation. This may be due to the fact that many of the compounds that impair gap junction conductance have multiple mechanisms of actions – from blocking ion channels to direct antagonism of receptors with either excitatory (e.g. NMDA receptor) or inhibitory (GABAA receptor) effect. It may also be due to other possible roles of gap junctions with regard to epileptogenesis. Gap junctions between glial cells (astrocytes) are also thought to be able to modulate the synchronization of neuronal activity.4 Animal studies suggest that they help sustain coordinated epileptic bursts, making these gap junctions a potential target for treatment. In addition, gap junctions appear to be susceptible to plasticity, which may change their function within neuronal networks. Finally, there is emerging evidence that gap junction signalling and related neuronal synchrony depend on the state (bursting pattern) of the network.5 As a result, according to the state of the network, gap junctional activity might result in either triggering, maintaining, aborting, or reducing the risk of seizure. This is a fast-moving topic, which is becoming increasingly complex. Hopefully, better understanding of the properties and functional implications of gap junctions in the developing human brain may soon create novel opportunities for targeted intervention against epilepsy and possibly other conditions involving neuronal synchronization and desynchronization." @default.
• W2562266950 created "2017-01-06" @default.
• W2562266950 creator A5064086819 @default.
• W2562266950 date "2016-12-08" @default.
• W2562266950 modified "2023-10-18" @default.
• W2562266950 title "Gap junctions in epilepsy: for better or worse" @default.
• W2562266950 cites W1977060982 @default.
• W2562266950 cites W1980027718 @default.
• W2562266950 cites W2171891895 @default.
• W2562266950 cites W2290008274 @default.
• W2562266950 cites W2409281493 @default.
• W2562266950 doi "https://doi.org/10.1111/dmcn.13290" @default.
• W2562266950 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28340280" @default.
• W2562266950 hasPublicationYear "2016" @default.
• W2562266950 type Work @default.
• W2562266950 sameAs 2562266950 @default.
• W2562266950 citedByCount "0" @default.
• W2562266950 crossrefType "journal-article" @default.
• W2562266950 hasAuthorship W2562266950A5064086819 @default.
• W2562266950 hasBestOaLocation W25622669501 @default.
• W2562266950 hasConcept C112592302 @default.
• W2562266950 hasConcept C131584629 @default.
• W2562266950 hasConcept C151730666 @default.
• W2562266950 hasConcept C158157758 @default.
• W2562266950 hasConcept C169760540 @default.
• W2562266950 hasConcept C170493617 @default.
• W2562266950 hasConcept C17077164 @default.
• W2562266950 hasConcept C185592680 @default.
• W2562266950 hasConcept C191897082 @default.
• W2562266950 hasConcept C192562407 @default.
• W2562266950 hasConcept C200170125 @default.
• W2562266950 hasConcept C2777348757 @default.
• W2562266950 hasConcept C2778186239 @default.
• W2562266950 hasConcept C2779343474 @default.
• W2562266950 hasConcept C2908872077 @default.
• W2562266950 hasConcept C55493867 @default.
• W2562266950 hasConcept C79879829 @default.
• W2562266950 hasConcept C86803240 @default.
• W2562266950 hasConcept C95444343 @default.
• W2562266950 hasConceptScore W2562266950C112592302 @default.
• W2562266950 hasConceptScore W2562266950C131584629 @default.
• W2562266950 hasConceptScore W2562266950C151730666 @default.
• W2562266950 hasConceptScore W2562266950C158157758 @default.
• W2562266950 hasConceptScore W2562266950C169760540 @default.
• W2562266950 hasConceptScore W2562266950C170493617 @default.
• W2562266950 hasConceptScore W2562266950C17077164 @default.
• W2562266950 hasConceptScore W2562266950C185592680 @default.
• W2562266950 hasConceptScore W2562266950C191897082 @default.
• W2562266950 hasConceptScore W2562266950C192562407 @default.
• W2562266950 hasConceptScore W2562266950C200170125 @default.
• W2562266950 hasConceptScore W2562266950C2777348757 @default.
• W2562266950 hasConceptScore W2562266950C2778186239 @default.
• W2562266950 hasConceptScore W2562266950C2779343474 @default.
• W2562266950 hasConceptScore W2562266950C2908872077 @default.
• W2562266950 hasConceptScore W2562266950C55493867 @default.
• W2562266950 hasConceptScore W2562266950C79879829 @default.
• W2562266950 hasConceptScore W2562266950C86803240 @default.
• W2562266950 hasConceptScore W2562266950C95444343 @default.
• W2562266950 hasIssue "1" @default.
• W2562266950 hasLocation W25622669501 @default.
• W2562266950 hasLocation W25622669502 @default.
• W2562266950 hasOpenAccess W2562266950 @default.
• W2562266950 hasPrimaryLocation W25622669501 @default.
• W2562266950 hasRelatedWork W2067877248 @default.
• W2562266950 hasRelatedWork W2097674439 @default.
• W2562266950 hasRelatedWork W2137836504 @default.
• W2562266950 hasRelatedWork W2145676527 @default.
• W2562266950 hasRelatedWork W2315459921 @default.
• W2562266950 hasRelatedWork W2399067859 @default.
• W2562266950 hasRelatedWork W4200484545 @default.
• W2562266950 hasRelatedWork W4232035013 @default.
• W2562266950 hasRelatedWork W4248869517 @default.
• W2562266950 hasRelatedWork W4254411729 @default.
• W2562266950 hasVolume "59" @default.
• W2562266950 isParatext "false" @default.
• W2562266950 isRetracted "false" @default.
• W2562266950 magId "2562266950" @default.
• W2562266950 workType "article" @default.