McCabe C, Mishor Z. Antidepressant medications reduce subcortical-cortical resting-state functional connectivity in healthy volunteers. Neuroimage 57: 1317-1323

Department of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK.
NeuroImage (Impact Factor: 6.36). 05/2011; 57(4):1317-23. DOI: 10.1016/j.neuroimage.2011.05.051
Source: PubMed


Studies have revealed abnormalities in resting-state functional connectivity in those with major depressive disorder specifically in areas such as the dorsal anterior cingulate, thalamus, amygdala, the pallidostriatum and subgenual cingulate. However, the effect of antidepressant medications on human brain function is less clear and the effect of these drugs on resting-state functional connectivity is unknown.
Forty volunteers matched for age and gender with no previous psychiatric history received either citalopram (SSRI; selective serotonergic reuptake inhibitor), reboxetine (SNRI; selective noradrenergic reuptake inhibitor) or placebo for 7 days in a double-blind design. Using resting-state functional magnetic resonance imaging and seed based connectivity analysis we selected the right nucleus accumbens, the right amygdala, the subgenual cingulate and the dorsal medial prefrontal cortex as seed regions. Mood and subjective experience were also measured before and after drug administration using self-report scales.
Despite no differences in mood across the three groups, we found reduced connectivity between the amygdala and the ventral medial prefrontal cortex in the citalopram group and the amygdala and the orbitofrontal cortex for the reboxetine group. We also found reduced striatal–orbitofrontal cortex connectivity in the reboxetine group.
These data suggest that antidepressant medications can decrease resting-state functional connectivity independent of mood change and in areas known to mediate reward and emotional processing in the brain. We conclude that hypothesis-driven seed based analysis of resting-state fMRI supports the proposition that antidepressant medications might work by normalising the elevated resting-state functional connectivity seen in depressed patients.

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    • "Psychotropic medication likely influenced past DMN studies in ASD. For example, SSRIs reduced MPFC functional connectivity to medial temporal regions in healthy adults (McCabe and Mishor, 2011). Treatment with atypical antipsychotics in schizophrenia (Sambataro et al., 2010), and stimulants or SNRIs in ADHD (Marquand et al., 2011; Wilson et al., 2013) have increased PCC–MPFC functional connectivity. "
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    • "Beyond its sympathetic property and peripheral effects within the autonomic nervous system, noradrenaline is one of the classical central neurotransmitters that plays a pivotal role in the pathophysiology of affective disorders (Schildkraut and Kety, 1967; Delgado and Moreno, 2000). There is only one study that previously investigated the impact of REB on rs-FC, revealing reduced striatal-orbitofrontal cortex connectivity compared to placebo (McCabe and Mishor, 2011). However, the intuitive influence of REB on the NE-pathway, as well as local resting state alterations, have not been investigated to date. "
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