Over the past decade in vitro slice work has revealed much about the cellular and network origins of low gamma (LG, 30–80 Hz) [71] and high gamma (80–200 Hz) activity (see Box 2). LG activity arises primarily due to interactions within the highly-interconnected GABAergic (inhibitory) interneuron network (interneuron network gamma or ING), as well as from network interactions between populations of (excitatory) pyramidal cells and local interneuron networks (pyramidal-interneuron network gamma or PING) [13]. Recent in vivo work employed light-driven activation of interneurons or pyramidal cells to investigate the causal impact of these distinct populations upon gamma activity [72]. This study revealed a cell-type specific double dissociation supporting the ING gamma model. Similarly, it appears that theta activity is also generated locally [73] and is regulated by interneuronal networks [74] with both pyramidal cells and interneurons exhibiting a resonance peak in the theta range due to intrinsic membrane properties [75].
