Figure 5
From: Mercury-induced toxicity of rat cortical neurons is mediated through N-methyl-D-Aspartate receptors
HgCl 2 enhanced spontaneous inward currents and caused sustained membrane depolarization in pyramidal cortical cells. A. A representative trace of spontaneous synaptic currents recorded before and after the application of HgCl2 (25 μM) from a pyramidal neuron. The cell was held at the potential of −70 mV. Spontaneous inward currents were recorded before (Ai) and during the application of HgCl2. Both the amplitude and frequency of inward current were substantially increased. Robust small, spontaneous events followed the big amplitude of currents as shown in the insert (Aii, indicated by an arrow). B. A representative trace of synaptic currents recorded before and after HgCl2 exposure in the presence of 10 μM of MK 801. Note that application of MK 801 prevented HgCl2 from inducing increase of synaptic currents indicating that NMDA currents was involved in HgCl2 action on cortical neurons (n = 7). C. Membrane potential of a pyramidal cell recorded under current-clamp mode before and after the application of HgCl2 at 25 μM. HgCl2 increased the spontaneous electrical activity and triggered sustained rise in membrane potentials. Subsequent application of MK 801 (10 μM) abolished HgCl2-induced firing of action potentials but did not affect the sustained membrane depolarization. D. A representative trace of membrane potential recorded from a pyramidal cell pretreated with MK 801 for 10 mins before and after HgCl2 exposure,. Pretreatment of cells with MK 801 greatly reduced HgCl2 - induced increase in action potential firing and sustained membrane depolarization. E. Statistical data shows that the increased amplitude of sustained membrane depolarization by HgCl2 (25 μM) in MK 801-treated cells is significantly smaller than that in control cells.