Psychomotor disturbance (PmD) is prevalent in major depressive disorder (MDD), with neural substrates implicated in disrupted motor circuits and the interaction to non-motor cortex. Our objective is to explore the functional connectivity pattern underlying PmD using functional magnetic resonance imaging (fMRI).

A total of 150 patients with MDD and 91 healthy controls (HCs) were included in this study. The patients were categorized into psychomotor (pMDD, n = 107) and non-psychomotor (npMDD, n = 43) groups based on the Hamilton Depression Rating Scale. Seed-based connectivity (SBC) analysis was conducted using predefined somatomotor and cerebellar network (SMN and CN) coordinates as seeds, to assess group differences and symptom correlations. Subsequently, we correlated the group-contrast SBC map with existing neurotransmitter maps to explore the neurochemical basis.

In pMDD patients compared to HC, we observed decreased connectivity, especially between the SMN and frontal cortex, within the bilateral SMN, and between the CN and right precentral cortex. Meanwhile, connectivity increased between the SMN and the middle cingulate cortex and between the CN and left precentral cortex in pMDD relative to npMDD and HC. Connectivity between the SMN and angular gyrus was positively correlated with the severity of PmD. Additionally, the aberrant SBC patterns in pMDD were linked to the distribution of dopamine D1 and D2 receptors.

This study provides insights into the aberrant connectivity within the motor circuits and its interactions with non-motor regions in PmD. It also suggests a potential role for dopaminergic dysregulation in the connectivity abnormalities associated with PmD.

Negative symptoms (NS) represent a core aspect of schizophrenia with a huge impact on real life functioning. Dysfunctions within the dopaminergic cortico-striatal circuits have been documented in subjects with schizophrenia (SCZ) and hypothesized as possible neurobiological mechanisms underlying some domains of NS.

We investigated relationships between the resting-state functional connectivity (RS-FC) of the ventro-tegmental area (VTA) and NS.

Resting-state fMRI data were recorded in 35 SCZ, recruited within the Italian Network for Research on Psychoses. We performed partial correlations between RS-FC and NS (evaluated with the Brief Negative Symptom Scale) controlling for possible sources of secondary negative symptoms.

We found that the experiential domain correlated with the RS-FC of the VTA with the left ventro-lateral prefrontal cortex (lVLPFC) (r=0.372, p=0.039), while the Expressive deficit domain correlated with the RS-FC of the VTA with the left dorso-lateral prefrontal cortex (lDLPFC) (r= 0.470, p .008). Looking at subdomains, only the avolition (r= 0.418, p=0.019) and the blunted affect (r= 0.465, p=.008) showed the same correlations of the domains to which they belong.

According to our findings, separate dysfunctional neuronal circuits could underpin distinct negative symptom subdomains. A better understanding of neurobiological dysfunctions underlying NS could help to design new treatments, targeting different NS subdomains.

Convergent studies provide support for abnormalities in the structure and functioning of the prefrontal cortex (PFC) and the amygdala, the key components of the neural system that subserves emotional processing in major depressive disorder (MDD). We used resting-state functional magnetic resonance imaging (fMRI) to examine potential amygdala–PFC functional connectivity abnormalities in treatment-naive subjects with MDD.

Resting-state fMRI data were acquired from 28 individuals with MDD and 30 healthy control (HC) subjects. Amygdala–PFC functional connectivity was compared between the MDD and HC groups.

Decreased functional connectivity to the left ventral PFC (VPFC) from the left and right amygdala was observed in the MDD group, compared with the HC group (p < 0.05, corrected).

The treatment-naive subjects with MDD showed decreased functional connectivity from the amygdala to the VPFC, especially to the left VPFC. This suggests that these connections may play an important role in the neuropathophysiology of MDD at its onset.