Abstract
Previous functional magnetic resonance imaging (fMRI) studies demonstrated an abnormally coordinated network functioning in Major Depression Disorder (MDD) during rest. The main monoamine-producing nuclei within midbrain/brainstem are functionally integrated within these specific networks. Therefore, we aimed to investigate the resting-state functional connectivity (RSFC) of these nuclei in 45 MDD patients and differences between patients receiving two different classes of antidepressant drugs. Patients showed reduced RSFC from the ventral tegmental area (VTA) to dorsal anterior cingulate cortex (dACC) and stronger RSFC to the left amygdala and dorsolateral prefrontal cortex (DLPFC). Patients treated with antidepressants influencing noradrenergic and serotonergic neurotransmission showed different RSFC from locus coeruleus to DLPFC compared to patients treated with antidepressants influencing serotonergic neurotransmission only. In the opposite contrast patients showed stronger RSFC from dorsal raphe to posterior brain regions. Enhanced VTA-RSFC to amygdala as a central region of the salience network may indicate an over‐attribution of the affective salience to internally-oriented processes. Significant correlation between decreased VTA-dACC functional connectivity and the BDI-II somatic symptoms indicates an association with diminished volition and behavioral activation in MDD. The observed differences in the FC of the midbrain/brainstem nuclei between two classes of antidepressants suggest differential neural effects of SSRIs and SNRIs.
Highlights
Monoamine-producing midbrain/brainstem nuclei in a large sample of healthy subjects[10]
The functional connectivity was obtained by computing Pearson correlation coefficients
To the best of our knowledge, this is the first time that the functional connectivity of the midbrain and upper brainstem nuclei has been studied in patients with Major Depression Disorder (MDD) during a resting state condition
Summary
Monoamine-producing midbrain/brainstem nuclei in a large sample of healthy subjects[10]. There is strong evidence to assume that the neural circuitry for emotion regulation and social cognition, which strongly relies on the amygdala and distinct medial prefrontal regions, is serotonergically modulated[13, 14], whereas the reward processing neural network, anchored by the VTA, the ventral striatum and the medial prefrontal cortex, is dopaminergically modulated[15]. Alterations in these neural circuits might be associated with different symptoms in MDD such as persistent low mood or anxiety (5-HT associated) or psychomotor speed, apathy and anhedonia (DA associated). We aimed to investigate, whether patients receiving antidepressant drugs modulating the 5-HT neurotransmission (SSRI) differ with regard to the RSFC from the midbrain/brainstem nuclei to patients receiving drugs influencing the 5-HT as well as NA neurotransmission (SNRI/NaSSA)
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