Abstract
We previously published that activation of peripheral inflammatory response was associated with increased glutamate concentrations in the basal ganglia in depression. However, precise information on neural changes mediating this association has been lacking. To fill this knowledge gap, we undertook an analysis to test if the neural consequences of excess basal ganglia glutamate increases could be profiled using a composite multimodal imaging approach. A data-driven classifier was used to divide a sample of 41 subjects diagnosed with major depression into two groups – a high plasma CRP/high glutamate groups (n = 22) with low plasma CRP/low glutamate subgroup (n = 19). Freesurfer was used to measure morphological alterations and AFNI was used to measure synchronized local neural activity and connectivity of basal ganglia to other brain regions. The high CRP/high glutamate group demonstrated decreased left putamen volume in the context of decreased synchronized neural activity in the basal ganglia and decreased connectivity between ventral striatal-ventromedial prefrontal regions. The neural changes were mapped to behavioral impairments including psychomotor slowing and anhedonia. The combination of above findings predicted high CRP/high glutamate status with high accuracy (sensitivity > 80%, specificity > 80%). We propose that excessive, disarrayed, chaotic signaling induced by an unregulated excess of inflammation-induced glutamate in the basal ganglia might underlie above findings. Identifying neural footprints of glutamate dysregulation induced by inflammatory activation will be discussed.
Published Version
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