Details

Autor(en) / Beteiligte

• Prossin, Alan R
• Koch, Alisa E
• Campbell, Phillip L
• McInnis, Melvin G
• Zalcman, Steven S
• Zubieta, Jon-Kar

Titel

Association of Plasma Interleukin-18 Levels with Emotion Regulation and μ-Opioid Neurotransmitter Function in Major Depression and Healthy Volunteers

Ist Teil von

• Biological psychiatry (1969), 2011-04, Vol.69 (8), p.808-812

Ort / Verlag

New York, NY: Elsevier Inc

Erscheinungsjahr

2011

Quelle

MEDLINE

Beschreibungen/Notizen

• Background Alterations in central neurotransmission and immune function have been documented in major depression (MDD). Central and peripheral endogenous opioids are linked to immune functioning in animal models, stress-activated, and dysregulated in MDD. We examined the relationship between μ-opioid receptor (OR)-mediated neurotransmission and a proinflammatory cytokine (interleukin [IL]-18). Methods We studied 28 female subjects (14 MDDs, 14 control subjects) with positron emission tomography and [11 C] carfentanil (μ-OR selective) during neutral and sadness states. With a simple regression model in SPM2 (Wellcome Trust, London, England) we identified brain regions where baseline μ-OR availability (nondisplaceable binding potential [BPND ]) and sadness-induced changes in μ-OR BPND were associated with baseline IL-18. Results Baseline IL-18 was greater in MDDs than control subjects [ t (25) = 2.13, p = .04]. In control subjects IL-18 was correlated with negative emotional ratings at baseline and during sadness induction. In MDDs, IL-18 was positively correlated with baseline regional μ-OR BPND and with sadness-induced μ-opioid system activation in the subgenual anterior cingulate, ventral basal ganglia, and amygdala. Conclusions This study links plasma IL-18 with sadness-induced emotional responses in healthy subjects, the diagnosis of MDD, and μ-opioid functioning, itself involved in stress adaptation, emotion regulation, and reward. This suggests that IL-18 represents a marker associated with emotion regulation/dysregulation at least in part through central opioid mechanisms.