Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
Changes in Astroglial K + upon Brief Periods of Energy Deprivation in the Mouse Neocortex
Ist Teil von
International journal of molecular sciences, 2022-04, Vol.23 (9), p.4836
Ort / Verlag
Switzerland: MDPI AG
Erscheinungsjahr
2022
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
Malfunction of astrocytic K
regulation contributes to the breakdown of extracellular K
homeostasis during ischemia and spreading depolarization events. Studying astroglial K
changes is, however, hampered by a lack of suitable techniques. Here, we combined results from fluorescence imaging, ion-selective microelectrodes, and patch-clamp recordings in murine neocortical slices with the calculation of astrocytic [K
]. Brief chemical ischemia caused a reversible ATP reduction and a transient depolarization of astrocytes. Moreover, astrocytic [Na
] increased by 24 mM and extracellular [Na
] decreased. Extracellular [K
] increased, followed by an undershoot during recovery. Feeding these data into the Goldman-Hodgkin-Katz equation revealed a baseline astroglial [K
] of 146 mM, an initial K
loss by 43 mM upon chemical ischemia, and a transient K
overshoot of 16 mM during recovery. It also disclosed a biphasic mismatch in astrocytic Na
/K
balance, which was initially ameliorated, but later aggravated by accompanying changes in pH and bicarbonate, respectively. Altogether, our study predicts a loss of K
from astrocytes upon chemical ischemia followed by a net gain. The overshooting K
uptake will promote low extracellular K
during recovery, likely exerting a neuroprotective effect. The resulting late cation/anion imbalance requires additional efflux of cations and/or influx of anions, the latter eventually driving delayed astrocyte swelling.