Abstract
In posttraumatic stress disorder (PTSD), the anterior insula (AI) is hyperresponsive to trauma cues and negative emotions. Recent research suggests that the AI exerts inhibitory control over reward circuitry including the nucleus accumbens. We are unaware of prior reports of the role of glutamatergic activity in the AI on reward processing in PTSD. We hypothesized that elevated right AI glutamate would be associated with anhedonia and faster devaluation of delayed rewards (accelerated delay discounting).
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