Altered serotonin and dopamine transporter availabilities in brain of depressed patients upon treatment with escitalopram: A [123I]β-CIT SPECT study

Rominger, Axel; Cumming, Paul; Brendel, Matthias; Xiong, Guoming; Zach, Christian; Karch, Steven B.; Tatsch, Klaus; Bartenstein, Peter; Fougère, Christian la; Koch, Walter; Pogarell, Oliver

doi:10.1016/j.euroneuro.2014.12.010

Cited by 26 publications

(29 citation statements)

References 46 publications

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“…In rats, subchronic administration of fluvoxamine was not associated with significant changes in striatal 123 I-FP-CIT uptake [34]. In humans, higher binding in striatal regions and lower binding in extrastriatal regions was observed after acute treatment of paroxetine [35], while chronic treatment was associated with lower striatal binding [36], which is in line with our findings.…”

Section: Discussionsupporting

confidence: 90%

Extrastriatal 123I-FP-CIT SPECT impairment in Parkinson’s disease – the PPMI cohort

2020

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Background Neuropathological data and nuclear medicine imaging show extensive serotonergic impairment in Parkinson’s disease (PD). We undertook a case-controlled analysis of 123I-FP-CIT SPECT images to measure extrastriatal serotonergic transporters (SERT) in PD using the Parkinson’s Progression Markers Initiative (PPMI) cohort. Methods We included all PD (n = 154) and Control subjects (n = 62) with available 123I-FP-CIT SPECT imaging and high-resolution T1-weighted MRI for coregistration (PD: mean age 61.6 years, 62% male, disease duration 26 months, MDS-UPDRS III score 22). 123I-FP-CIT SPECT images were processed with PETPVE12 using an exploratory voxel-wise analysis including partial-volume effect correction. Linear regressions were performed in the PD group to assess correlations between region of interest 123I-FP-CIT uptake and clinical motor and non-motor impairment. Results Compared to Controls, PD exhibited an uptake reduction in bilateral caudate nucleus, putamen, insula, amygdala and right pallidum (family-wise error (FWE)-corrected p < 0.05). While lower putaminal uptake on the contralateral side to clinically more affected side was associated with higher MDS-UPDRS III score (p = 0.022), we found a trend association between higher geriatric depression scale and lower pallidum uptake (p = 0.09). Higher SCOPA-AUT gastrointestinal subscore was associated with lower uptake in mean putamen and caudate nucleus (p = 0.01 to 0.03), whereas urological subscore was inversely correlated with mean caudate nucleus, putamen, and pallidum uptake (p = 0.002 to 0.03). REM sleep behaviour disorder screening questionnaire was associated with lower 123I-FP-CIT binding in caudate nucleus, putamen and pallidum (all p < 0.05). No significant association was found for Montreal Cognitive Assessment (all p > 0.45) or excessive daytime sleepiness (all p > 0.29). Conclusions In addition to the well-established striatal deficit, this study provides evidence of a major extrastriatal 123I-FP-CIT impairment, and therefore of an altered serotonergic transmission in early PD.

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Section: Discussionsupporting

confidence: 90%

Extrastriatal 123I-FP-CIT SPECT impairment in Parkinson’s disease – the PPMI cohort

2020

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“…DEP were treated with SSRI. Although SRRIs do not bind tightly to DAT (Zhou et al, 2009), they were shown to induce an up-regulation of the DAT protein (Chen and Lawrence, 2003;Kugaya et al, 2003;Rominger et al, 2015). Thus, it cannot be excluded that SSRI treatment may have slightly influenced DAT quantification in depressed patients.…”

Section: Discussionmentioning

confidence: 98%

Dopamine Transporter and Reward Anticipation in a Dimensional Perspective: A Multimodal Brain Imaging Study

Dubol

Trichard

Leroy

et al. 2017

Neuropsychopharmacol.

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Dopamine function and reward processing are highly interrelated and involve common brain regions afferent to the nucleus accumbens, within the mesolimbic pathway. Although dopamine function and reward system neural activity are impaired in most psychiatric disorders, it is unknown whether alterations in the dopamine system underlie variations in reward processing across a continuum encompassing health and these disorders. We explored the relationship between dopamine function and neural activity during reward anticipation in 27 participants including healthy volunteers and psychiatric patients with schizophrenia, depression, or cocaine addiction, using functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) multimodal imaging with a voxel-based statistical approach. Dopamine transporter (DAT) availability was assessed with PET and [C]PE2I as a marker of presynaptic dopamine function, and reward-related neural response was assessed using fMRI with a modified Monetary Incentive Delay task. Across all the participants, DAT availability in the midbrain correlated positively with the neural response to anticipation of reward in the nucleus accumbens. Moreover, this relationship was conserved in each clinical subgroup, despite the heterogeneity of mental illnesses examined. For the first time, a direct link between DAT availability and reward anticipation was detected within the mesolimbic pathway in healthy and psychiatric participants, and suggests that dopaminergic dysfunction is a common mechanism underlying the alterations of reward processing observed in patients across diagnostic categories. The findings support the use of a dimensional approach in psychiatry, as promoted by the Research Domain Criteria project to identify neurobiological signatures of core dysfunctions underling mental illnesses.

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“…34 In the brain of depression animal models, there is dopamine neurotransmitter exhaustion and administration of dopamine antagonists and agonists worsens and improves the symptoms, respectively. 35,36 The NE function is controlling attention by reflecting external stimuli and NE system dysfunction could cause depression. Patients with depression mainly have central nervous system lesions in the hippocampus, prefrontal cortex, striatum, etc.…”

Section: Discussionmentioning

confidence: 99%

<p>Gut Microbiota Regulates Depression-Like Behavior in Rats Through the Neuroendocrine-Immune-Mitochondrial Pathway</p>

Liu¹,

Guo²,

Liu³

et al. 2020

NDT

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Purpose: Gut microbiota affects various physiological functions in the host and has crucial effects on the nervous system. There is increasing evidence of a correlation between gut microbiota and depression; however, the mechanisms underlying the regulation of depression-like behavior by gut microbiota remain unclear. In this study, we assessed the regulatory mechanism of gut microbiota on depression-like behavior in rats. Methods: We transplanted fecal microbiota obtained from patients with depression and healthy individuals into germ-free (GF) rats (n=18) through fecal microbiota transplantation technology. Next, we assessed the affective behavior in the rats using the forced swimming test and a sucrose preference test. We used enzyme-linked immunosorbent assay (ELISA) to determine the hippocampal levels of 5-hydroxytryptamine (5-HT), dopamine (DA), and noradrenaline (NE) and the serum levels of corticosterone (CORT), adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ), interleukin-6 (IL-6), interleukin-1 (IL-1), interleukin-1 (IL-4), and interleukin-1 (IL-10). The mitochondrial morphology of small intestinal epithelial cells was observed through transmission electron microscopy. Results: Rats that received fecal microbiota from patients with depression (depression microbiota) exhibited depression-like behavior. They presented decreased levels of hippocampal neurotransmitters, serum CORT levels, and anti-inflammatory cytokine levels, as well as increased ACTH, CRH, and serum levels of multiple pro-inflammatory cytokines. Observation of the mitochondria ultrastructure showed damaged mitochondria in the intestinal epithelial cells, significant endoplasmic reticulum expansion, and border aggregation of nuclear chromatin. Conclusion: Our findings suggested that the depression-like behaviors induced by the depression microbiota through the neuroendocrine-immune-mitochondrial pathway, which were associated with neuroendocrine disorders, inflammatory responses, and mitochondrial damage.

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Altered serotonin and dopamine transporter availabilities in brain of depressed patients upon treatment with escitalopram: A [123I]β-CIT SPECT study

Cited by 26 publications

References 46 publications

Extrastriatal 123I-FP-CIT SPECT impairment in Parkinson’s disease – the PPMI cohort

Extrastriatal 123I-FP-CIT SPECT impairment in Parkinson’s disease – the PPMI cohort

Dopamine Transporter and Reward Anticipation in a Dimensional Perspective: A Multimodal Brain Imaging Study

<p>Gut Microbiota Regulates Depression-Like Behavior in Rats Through the Neuroendocrine-Immune-Mitochondrial Pathway</p>

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