Store Ca2+ depletion enhances NMDA responses in cultured human astrocytes.
NMDA produced whole-cell membrane currents in cultured human astrocytes. The currents were not inhibited by the selective NMDA receptor antagonist, APV, while they were partially inhibited by the broad G-protein inhibitor, GDPbetaS. NMDA-induced currents were enhanced by either the microsomal Ca2+/ATPase inhibitors, thapsigargin and cyclopiazonic acid, or the ATP-uncoupler, dinitrophenol (DNP). In the Ca2+ assay, NMDA increased intracellular calcium concentration. The increase was inhibited by 26% in Ca2+-free extracellular solution, and it was not inhibited by APV. The results of the present study suggest that NMDA responses in human astrocytes are regulated by store Ca2+ depletion-associated signal.
Nishizaki
T
T
Department of Physiology, Department of Neurosurgery, Kobe University School of Medicine, 7-5-1 kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Matsuoka
T
T
Nomura
T
T
Kondoh
T
T
Tamaki
N
N
Okada
Y
Y
D001253:Astrocytes / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology; D002478:Cells, Cultured; D006801:Humans; D016202:N-Methylaspartate / Q000502:physiology*; D018408:Patch-Clamp Techniques
D016202:N-Methylaspartate; D002118:Calcium