have been employed to investigate the disruption of normal network waves and oscillations in the brain caused by the absence of certain ion channels in neurons. In one particular case, Simeone et al. studied the effect of the delayed rectifier potassium channel α-subunit Kv1.1 to the oscillations in the hippocampus shown in Figures 9A–C (Simeone et al., 2013). By reducing or eliminating the expression of Kv1.1 in the axons of the hippocampal tri-synaptic pathway, the authors were able to observe an increase in occurrence of fast ripples (80–200 Hz bandwidth, 50% longer duration) and high frequency oscillations associated with epilepsy, as shown in Figure 9C. Similar applications have been done using HDMEAs. Medrihan et al. (2014) showed that the absence of synapsin II (Syn II), a protein related to epilepsy, decreases tonic inhibition in mouse hippocampal slices, thus increasing synchronized bursts (see Figures 9D,E). THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol; gaboxadol), a selective agonist of δ subunit-containing GABAA receptors, restores tonic inhibition.
