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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Neurobiol Dis. 2016 Jan 4;88:29–43. doi: 10.1016/j.nbd.2015.12.019

Figure 1. Hypoxia and/or systemic inflammation increase the spontaneous firing rate.

Figure 1

A) Representative picture of a thalamocortical slice on a MEA prepared from a mouse of the P8–10 age group. B) Spike sorting of individual action potentials recorded over a 10 minute period from the slice in (A) on each of the 60 electrodes show low activity present in all cortical layers and in the hippocampus. Some electrodes could record the activity of more than one neuron. C), D), and E) Evolution of the MUA (in Hz) for neurons located in cortical layers 2 to 6 during 5 minutes recordings in ACSF with 8 mM KCl in representative slices from the P8–10 group (C), the P13–16 group (D), and the P28–30 group (E). For each condition, a raster plot shows the MUA on all MEA electrodes located in all layers of the Barrel cortex (bottom) with the total spike frequency of all these channels (bin: 1 sec, top). Note the peaks of activity corresponding to epileptiform events. Spikes occurring during these events were not counted in the spontaneous firing rate. F) Average firing rate per layers of the Barrel cortex recorded in thalamocortical slices from mice of P8–10 (left), 13–16 (middle) and P28–30 age groups (right) treated with all four conditions: SHAM (dark grey), HYPO (blue), INFL (red) and HYPO+INFL (green). G) The mean cortical firing rate in a ten minute recording period per slice and condition is plotted as box and whisker plots. For each age group, the mean firing rate is plotted for 3 mM (open boxes) and 8 mM (filled boxes) KCl ACSF. The numbers of slices recorded per condition are represented on the top of the graph.