Astroglial gap junctions strengthen hippocampal network activity by sustaining afterhyperpolarization via KCNQ channels
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
38722742
DOI
10.1016/j.celrep.2024.114158
PII: S2211-1247(24)00486-8
Knihovny.cz E-resources
- Keywords
- CP: Neuroscience, KCNQ channels, afterhyperpolarization, astrocytes, bursting, connexins, gap junctions, mathematical modeling, networks, potassium,
- MeSH
- Action Potentials physiology MeSH
- Astrocytes * metabolism MeSH
- Potassium * metabolism MeSH
- KCNQ Potassium Channels * metabolism genetics MeSH
- Hippocampus * metabolism MeSH
- Connexins metabolism genetics MeSH
- Gap Junctions * metabolism MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Nerve Net metabolism MeSH
- Neurons metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Potassium * MeSH
- KCNQ Potassium Channels * MeSH
- Connexins 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.
References provided by Crossref.org
