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. Author manuscript; available in PMC: 2009 Jan 8.
Published in final edited form as: Nat Neurosci. 2008 Mar 2;11(4):450–456. doi: 10.1038/nn2060

Figure 6. Oligodendrocyte precursor glia with and without INa respond differently to ischaemia.

Figure 6

a Response of a P7 OPC lacking INa to simulated ischaemia (0 mM Mg2+ enhances detection of NMDA receptor currents, -40 mV), and block of glutamate-mediated component of current by 200 μM AP5 and 25 μM NBQX. b As a, but for a cell with INa, showing spontaneous synaptic currents (circles) contribute to the response. The greater noise in the trace for the INa cell reflects the presence of synaptic input which is lacking in the no INa cell, and the presence of a larger number of glutamate-gated channels in the INa cell. c Ischaemia-evoked inward current and current suppressed by glutamate receptor blockers (at 500-800 sec after starting ischaemia, ± s.e.m.) in INa and no INa cells. Analysing the current inhibition as a percentage of the ischaemia-induced current showed the same difference between the INa and no INa cells: in INa cells the inhibition was 71.5 ± 9.7% of the ischaemia-evoked current, while in no INa cells it was 24.0 ± 15.2% (significantly different, P = 0.035). d Frequency of inward and outward spontaneous synaptic currents at -40 mV in 4 cells after 1 min ischaemia (relative to pre-ischaemia). Cs-gluconate internal, ECl -87 mV, in a-d. e Labelling of P7 slice for NG2 (green), Na+ channels (red, or yellow/orange where overlapping with NG2) and with propidium iodide (mauve) after 1 hour’s ischaemia, showing death of an INa cell and no death of a no INa cell. f Percentage of NG2 positive INa cells and no INa cells killed in control conditions (no ischaemia, 103 NG2 expressing cells), after 1 hour’s ischaemia (166 cells), or after 1 hour’s ischaemia in the presence of 25 μM NBQX, 50 μM D-AP5, 50 μM MK-801 and 100 μM 7-chlorokynurenate (7-CK) (173 cells). All P values are for comparison with INa cells in ischaemia without blockers.