To study population-wide changes in neuronal activity following pharmacological manipulation, we used an Axion MEA to record the firing rate of hNGN2-neurons. First, we treated with the GABAA receptor antagonist PTX, which did not increase the firing activity in 21-day-old hNGN2-neurons (Fig. 6C), consistent with the low levels of GAD65/67 we observed in our cultures (Fig. 4D and E). Second, when we applied the AMPA/kainate glutamate receptor antagonist CNQX, the firing rate was decreased (Fig. 6C). Third, treatment with TTX eliminated all firing (Fig. 6C). In aggregate, this data implies that our hNGN2-induced neurons are comprised primarily of excitatory neurons.
