Astrocyte-neuron circuits in epilepsy.
Adenosine
Astrocytes
Epilepsy
Glia
Metabolism
Therapy
Journal
Neurobiology of disease
ISSN: 1095-953X
Titre abrégé: Neurobiol Dis
Pays: United States
ID NLM: 9500169
Informations de publication
Date de publication:
04 2023
04 2023
Historique:
received:
19
12
2022
revised:
20
02
2023
accepted:
27
02
2023
pubmed:
4
3
2023
medline:
23
3
2023
entrez:
3
3
2023
Statut:
ppublish
Résumé
The epilepsies are a diverse spectrum of disease states characterized by spontaneous seizures and associated comorbidities. Neuron-focused perspectives have yielded an array of widely used anti-seizure medications and are able to explain some, but not all, of the imbalance of excitation and inhibition which manifests itself as spontaneous seizures. Furthermore, the rate of pharmacoresistant epilepsy remains high despite the regular approval of novel anti-seizure medications. Gaining a more complete understanding of the processes that turn a healthy brain into an epileptic brain (epileptogenesis) as well as the processes which generate individual seizures (ictogenesis) may necessitate broadening our focus to other cell types. As will be detailed in this review, astrocytes augment neuronal activity at the level of individual neurons in the form of gliotransmission and the tripartite synapse. Under normal conditions, astrocytes are essential to the maintenance of blood-brain barrier integrity and remediation of inflammation and oxidative stress, but in epilepsy these functions are impaired. Epilepsy results in disruptions in the way astrocytes relate to each other by gap junctions which has important implications for ion and water homeostasis. In their activated state, astrocytes contribute to imbalances in neuronal excitability due to their decreased capacity to take up and metabolize glutamate and an increased capacity to metabolize adenosine. Furthermore, due to their increased adenosine metabolism, activated astrocytes may contribute to DNA hypermethylation and other epigenetic changes that underly epileptogenesis. Lastly, we will explore the potential explanatory power of these changes in astrocyte function in detail in the specific context of the comorbid occurrence of epilepsy and Alzheimer's disease and the disruption in sleep-wake regulation associated with both conditions.
Identifiants
pubmed: 36868484
pii: S0969-9961(23)00072-4
doi: 10.1016/j.nbd.2023.106058
pmc: PMC10334651
mid: NIHMS1914871
pii:
doi:
Substances chimiques
Adenosine
K72T3FS567
Glutamic Acid
3KX376GY7L
Types de publication
Review
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
106058Subventions
Organisme : NINDS NIH HHS
ID : F32 NS117792
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS065957
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS103740
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS127846
Pays : United States
Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest DB is co-founder and CDO of PrevEp Inc.
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