Abstract
The dorsal raphe nucleus (DRN) has been repeatedly implicated as having a significant relationship with depression, along with its serotoninergic innervation. However, functional connectivity of the DRN in depression is not well understood. The current study aimed to isolate functional connectivity of the DRN distinct in later life depression (LLD) compared to a healthy age-matched population. Resting state functional magnetic resonance imaging (rsfMRI) data from 95 participants (33 LLD and 62 healthy) were collected to examine functional connectivity from the DRN to the whole brain in voxel-wise fashion. The posterior cingulate cortex (PCC) bilaterally showed significantly smaller connectivity in the LLD group than the control group. The DRN to PCC connectivity did not show any association with the depressive status. The findings implicate that the LLD involves disruption of serotoninergic input to the PCC, which has been suggested to be a part of the reduced default mode network in depression.
Highlights
Disruption of the dorsal raphe nucleus (DRN) is implicated in depression, given that the DRN serves as the major source of 5-HT release in the brain
The later life depression (LLD) group showed significant indications of depression; Beck Depression Inventory (BDI), Global Assessment of Functioning scale (GAF), and SIGH-D 17, as well as their antidepressant medications assessed as imipramine equivalent potency
The results illuminate the serotoninergic dysfunction that may influence LLD pathology, which is independent from the depressive status
Summary
Disruption of the dorsal raphe nucleus (DRN) is implicated in depression, given that the DRN serves as the major source of 5-HT release in the brain. The area of the DRN is reduced in major depression (Matthews and Harrison, 2012). Serotonin transporter dysfunction has been found in the DRN of patients with major depression (Hahn et al, 2014), and binding potentials for the 5-HT1A receptor have been found to be reduced in depression (Drevets et al, 1999). Polymorphisms in 5-HT1A gene have been found to be associated with antidepressants (Kato et al, 2009). Single nucleotide polymorphisms of the 5-HT1A receptor and TPH2 have been suggested to interact with the severity of depression and respond to SSRIs (Serretti et al, 2011; Jacobsen et al, 2012). The DRN is understood to be critical for the actions of antidepressants including
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