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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Trends Cogn Sci. 2012 Nov 8;16(12):584–592. doi: 10.1016/j.tics.2012.10.008

Figure 2. DMN deactivation findings across clinical, pharmacological and computational approaches.

Figure 2

(a) We identified a set of regions (2 example foci shown) where patients (red) relative to healthy controls (blue) failed to show sustained activation (top) as well as appropriate suppression (bottom) during delayed WM [32]. This finding was present even in the context of matched performance. (b) Regions closely corresponding to FPCN and the DMN were modulated by an NMDA-receptor antagonist ketamine (red) relative to placebo control condition (blue) [37]. We highlight two regions with a similar pattern of modulation as observed in schizophrenia. (c) A computational model of WM, comprised of task-activated (top) and task-deactivated (bottom) modules highlighting a possible mechanism for deactivation (see Box 3), followed by results. We tested whether ‘disinhibition’ via reduced NMDA receptor conductance onto GABA cells (E–I) (small red arrow) would resemble activation/deactivation BOLD findings under ketamine and observations in schizophrenia. Figures adapted with permission from [32] and [37].