Astroglial gap junctions strengthen hippocampal network activity by sustaining afterhyperpolarization via KCNQ channels
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
38722742
DOI
10.1016/j.celrep.2024.114158
PII: S2211-1247(24)00486-8
Knihovny.cz E-zdroje
- Klíčová slova
- CP: Neuroscience, KCNQ channels, afterhyperpolarization, astrocytes, bursting, connexins, gap junctions, mathematical modeling, networks, potassium,
- MeSH
- akční potenciály fyziologie MeSH
- astrocyty * metabolismus MeSH
- draslík * metabolismus MeSH
- draslíkové kanály KCNQ * metabolismus genetika MeSH
- hipokampus * metabolismus MeSH
- konexiny metabolismus genetika MeSH
- mezerový spoj * metabolismus MeSH
- myši inbrední C57BL MeSH
- myši knockoutované MeSH
- myši MeSH
- nervová síť metabolismus MeSH
- neurony metabolismus MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- draslík * MeSH
- draslíkové kanály KCNQ * MeSH
- konexiny MeSH
Throughout the brain, astrocytes form networks mediated by gap junction channels that promote the activity of neuronal ensembles. Although their inputs on neuronal information processing are well established, how molecular gap junction channels shape neuronal network patterns remains unclear. Here, using astroglial connexin-deficient mice, in which astrocytes are disconnected and neuronal bursting patterns are abnormal, we show that astrocyte networks strengthen bursting activity via dynamic regulation of extracellular potassium levels, independently of glutamate homeostasis or metabolic support. Using a facilitation-depression model, we identify neuronal afterhyperpolarization as the key parameter underlying bursting pattern regulation by extracellular potassium in mice with disconnected astrocytes. We confirm this prediction experimentally and reveal that astroglial network control of extracellular potassium sustains neuronal afterhyperpolarization via KCNQ voltage-gated K+ channels. Altogether, these data delineate how astroglial gap junctions mechanistically strengthen neuronal population bursts and point to approaches for controlling aberrant activity in neurological diseases.
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