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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Biol Psychiatry. 2015 Jul 17;79(9):716–726. doi: 10.1016/j.biopsych.2015.07.005

Figure 4. Stimulus induced GBO due to NMDAR hypofunction in an ISN-PING model.

Figure 4

(A) Co-variation of average spiking activity and GBO power and frequency in an ISN-PING model (Adapted from (82)). The arrows indicate how GBO power changes in response to changes in the activity of PING network. The variation in activity level and GBO properties is plotted in response to changes in the excitatory drive to the PING network, such as in the case of NMDAR hypofunction.

(B) NMDAR hypofunction in PV+ INs modeled as reduced excitation predicts disinhibition and weaker GBO in the model.

(C) Local inhibition circuit in the cortex (97-99). PV+ INs inhibit each other as well as excitatory neurons. SOM+ INs inhibit both PV+ INs and excitatory neurons. VIP+ INs disinhibition excitatory neurons by inhibiting SOM+ INs.

(D) The ISN-PING model predicts reduced power of stimulus-induced GBO if NMDAR hypofunction in SOM+ INs relieves inhibition of both excitatory neurons and PV+ INs such that the average activity is increased in the network.