کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4178809 | 1276515 | 2009 | 4 صفحه PDF | دانلود رایگان |

BackgroundDopamine (DA) system dysfunction is implicated in the pathophysiology of major depressive disorder (MDD). We sought to determine if cigarette smokers with a history of MDD and current mild depressive symptoms have abnormal smoking-induced DA release (measured indirectly as change in 11C-raclopride binding potential [BPND]).MethodsFifty-six cigarette smokers either with (n = 10) or without (n = 46) a history of MDD (MDD+ and MDD−, respectively) underwent bolus-plus-continuous-infusion 11C-raclopride positron emission tomography, during which they smoked a regular cigarette. Presmoking to postsmoking changes in 11C-raclopride BPND were compared between groups. Also, correlations were determined between change in BPND and depression, anxiety, and withdrawal rating scale scores for the MDD+ group.ResultsThe MDD+ group had a significantly greater reduction in 11C-raclopride BPND (−16.3%) than the MDD− group (−8.4%) (analysis of covariance [ANCOVA], p = .03). Significant negative correlations were found between depression/anxiety and change in 11C-raclopride BPND (r = −.77, p < .01 and r = −.74, p = .01, respectively).ConclusionsMDD+ smokers have greater smoking-induced DA release than MDD− smokers, and higher depression/anxiety levels are associated with greater smoking-induced DA release. These findings support the theory that MDD+ smokers have DA system dysfunction, including heightened smoking-induced DA release.
Journal: Biological Psychiatry - Volume 66, Issue 9, 1 November 2009, Pages 898–901