Figure 3 (IMAGE)

Institute for Basic Science

Figure 3

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Putative molecular mechanism of PTSD treatment. A) In normal mice, NYX-783 acts on the GluN2B subunit of NMDA receptors in glutamatergic neurons, which results in upregulation of BDNF and inhibition of PTSD spontaneous recovery. B) When GluN2B is knocked down in glutamatergic neurons, it eliminated the effectiveness of NYX-783, since the drug no longer has a valid target. C) When GluN2B is knocked down in GABAergic neurons, it lessens the degree of inhibition on the glutamatergic neuron. More glutamate is released, which activates the postsynaptic pyramidal neuron, resulting in a baseline reduction in spontaneous recovery.

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