induced sustained elevation of intracellular Ca2+ concentration ([Ca2+]
) in cortical neurons and this rise in [Ca2+]
was inhibited by the NMDA receptor antagonist MK 801. A. Representative traces of changes in fura-2 fluorescence ratio before and after the application of HgCl2 (25 μM) in four different cortical neurons (shown by red, green, blue and black traces). Cells were loaded with fura-2 AM and the ratio of fluorescence intensity, at the 340 and 380 nm excitation wavelengths, was measured B. Representative traces of fura-2 fluorescence ratio recorded before and after application of HgCl2 (25 μM) in four different cortical neurons (shown by red, green, blue and black traces) that were previously exposed to MK 801 (10 μM), an antagonist of NMDA receptors. C. Fold- rises in fura-2 fluorescence ratio induced by HgCl2, after 10 and 15 mins of exposure time, in the absence or presence of MK 801. Note that, HgCl2-induced rise in [Ca2+]i in MK 801-treated neurons was significantly smaller than that in control cells in the period of 10 mins and 15 mins. Arrows indicate the presence of spontaneous Ca2+ transients in cortical neurons under resting conditions.