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. Author manuscript; available in PMC: 2010 Oct 13.
Published in final edited form as: Brain Res. 2009 Mar 28;1293:13–23. doi: 10.1016/j.brainres.2009.03.044

Figure 5.

Figure 5

The occurrence of a traumatic event and/or chronic stress leads to increased synaptic 5-HT levels in the amygdala and cortical regions, as well as alterations in dopamine release in the ventral striatum (VST). These effects are at least partially mediated by 5-HT1B receptors. A PTSD-resilience model that implicates a central role for the 5-HT1B receptor would assume that PTSD patients, in contrast to resilient people are unable to downregulate 5-HT1B receptors which will lead to amygdala hyperresponsiveness because of reduced 5-HT activity which may disinhibit excitatory activity by reducing the stimulation of 5HT1A receptors located on pyramidal cells where they inhibit action potential formation, and of 5-HT3 receptors, that are located on GABAergic interneurons where they stimulate GABA release, alterations in dopamine release in the VST and changes in ventromedial prefrontal cortex (vmPFC) function resulting in inadequate top-down governance over the amygdala by the vmPFC which is characteristic for PTSD.