High extracellular K(+) evokes changes in voltage-dependent K(+) and Na (+) currents and volume regulation in astrocytes.
[K(+)](e) increase accompanies many pathological states in the CNS and evokes changes in astrocyte morphology and glial fibrillary acidic protein expression, leading to astrogliosis. Changes in the electrophysiological properties and volume regulation of astrocytes during the early stages of astrocytic activation were studied using the patch-clamp technique in spinal cords from 10-day-old rats after incubation in 50 mM K(+). In complex astrocytes, incubation in high K(+) caused depolarization, an input resistance increase, a decrease in membrane capacitance, and an increase in the current densities (CDs) of voltage-dependent K(+) and Na(+) currents. In passive astrocytes, the reversal potential shifted to more positive values and CDs decreased. No changes were observed in astrocyte precursors. Under hypotonic stress, astrocytes in spinal cords pre-exposed to high K(+) revealed a decreased K(+) accumulation around the cell membrane after a depolarizing prepulse, suggesting altered volume regulation. 3D confocal morphometry and the direct visualization of astrocytes in enhanced green fluorescent protein/glial fibrillary acidic protein mice showed a smaller degree of cell swelling in spinal cords pre-exposed to high K(+) compared to controls. We conclude that exposure to high K(+), an early event leading to astrogliosis, caused not only morphological changes in astrocytes but also changes in their membrane properties and cell volume regulation.
Neprasova
Helena
H
Department of Neurobiology, Institute of Experimental Medicine, The Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Anderova
Miroslava
M
Petrik
David
D
Vargova
Lydia
L
Kubinova
Sarka
S
Chvatal
Alexandr
A
Sykova
Eva
E
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D048429:Cell Size; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000503:physiopathology; D006863:Hydrogen-Ion Concentration; D007038:Hypotonic Solutions / Q000494:pharmacology; D007150:Immunohistochemistry; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009997:Osmotic Pressure; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000493:pharmacokinetics*; D024642:Potassium Channels, Voltage-Gated / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology*; D013116:Spinal Cord / Q000166:cytology
D005904:Glial Fibrillary Acidic Protein; D007038:Hypotonic Solutions; D024642:Potassium Channels, Voltage-Gated; D015222:Sodium Channels; D012964:Sodium; D011188:Potassium