Inhibitory interneurons are particularly sensitive to NMDA receptor antagonists (70, 112, 113). In combination with findings of altered expression of NMDA receptors within these interneurons, it is well-supported that inhibitory interneurons, particularly those expressing the calcium-binding protein parvalbumin, are a locus for dysfunction in schizophrenia (shown in Figure 2) (84, 114, 115). A number of studies have shown that parvalbumin+ cells are critical to the generation and maintenance of the GBO (106, 113, 116, 117). These interneurons have extremely fast-spiking properties and their rapid synaptic activation is consistent with the frequency required for entrainment of the GBO (118). Parvalbumin+ cells also show the strongest coupling to the gamma oscillation cycle relative to other interneuron types (e.g., calbindin, calrentin) (119, 120). Parvalbumin+ interneurons are typically fast-spiking and provide perisomatic inhibition onto excitatory pyramidal cells. Parvalbumin+ interneurons can present morphologically as either basket (project to the soma and proximal dendrites of neurons) or chandelier cells (project to the initial axon segment of neurons) as illustrated in Figure 3. While both parvalbumin+ basket and chandelier cells are active during GBO, parvalbumin+ basket cell activity is more strongly coupled with the GBO (121). Studies have also shown that GBO power is markedly reduced by opioid receptor activation, which dampens the activity of synaptic inputs from parvalbumin basket cells onto pyramidal neurons but does not affect chandelier neurons (122). These findings emphasize the critical importance of parvalbumin+ basket cells specifically to the generation of the GBO and their dysfunction in schizophrenia. In support of this, it has been shown that reductions in the firing rate of parvalbumin+ interneurons via optogenetics can reduce the power of GBO (114). Conversely, non-rhythmic stimulation provided to parvalbumin+ interneurons can increase the power of the GBO.