Primary hemifacial spasm involves central network reorganization, but white matter functional alterations remain unclear. We acquired resting-state functional magnetic resonance imaging data from 89 left-sided patients, 92 right-sided patients, and 124 healthy controls. Patients exhibited widespread abnormalities in tracts including the corpus callosum, superior longitudinal fasciculus, and corona radiata. Notably, this remodeling was highly asymmetric: left-sided patients primarily showed increased local neural activity in prefrontal pathways, whereas right-sided patients exhibited increased global network centrality across interhemispheric tracts. Furthermore, these alterations displayed distinct frequency preferences, and certain functional instabilities were exclusively captured by dynamic metrics rather than static analyses. These findings demonstrate that the disorder is associated with time-varying, frequency-specific, and asymmetric white matter functional reorganization, highlighting the value of dynamic and multi-frequency approaches in decoding its pathophysiology.
Mild cognitive impairment (MCI) is associated with early, regionally selective neurodegenerative changes that may affect socioemotional functioning before atrophy becomes widespread. This study examined whether structural brain alterations in MCI relate to facial emotion recognition performance. Sixty adults (30 MCI, 30 healthy controls), aged 50–86 years, completed neuropsychological testing, the Facial emotion composite Task, and structural MRI. Whole-brain voxel-based morphometry revealed no significant gray matter volume differences between groups. However, targeted region-of-interest ROI analyses demonstrated lower right amygdala and bilateral hippocampal volumes in patients with MCI. Cortical thickness analyses identified two regions with lower thickness in MCI: the right superior parietal lobule and the left posterior insula. A significant Group × Sadness interaction indicated that the association between left superior parietal gray matter volume and sadness recognition differed between groups. Follow-up analyses of the extracted values showed a positive association in MCI, although this within-group association did not reach statistical significance, and a significant inverse association in HCs. These findings suggest that early MCI involves selective thinning in association cortices supporting attention and salience processing. The sadness-specific interaction indicates that patients with MCI may rely on preserved superior parietal structure during sadness recognition, a pattern that is consistent with structural reserve accounts, although this interpretation remains speculative given the cross-sectional design.
Reward Sensitivity refers to individual differences in the perception, evaluation, and emotional response to potential or acquired rewarding stimuli. Future self-continuity refers to the degree of psychological connection, identification, and consistency that individuals perceive between their present self and future self. Although both constructs are known to critically influence intertemporal decision-making and self-control, the shared neurobiological mechanisms linking them remain largely unexplored. To address this question, we used voxel-based morphometry and resting-state functional connectivity analyses to investigate the neural basis underlying the association between reward sensitivity and future self-continuity. Behavioral results showed reward sensitivity exhibited a significant negative correlation with future self-continuity. Moreover, voxel-based morphometry (VBM) revealed that reward sensitivity was negatively associated with gray matter volume in the dorsomedial prefrontal cortex (dmPFC). Furthermore, resting-state functional connectivity (RSFC) analysis demonstrated that the functional connectivity between the dmPFC and the ventrolateral prefrontal cortex (vlPFC) was positively correlated with reward sensitivity. Ultimately, mediation analysis revealed a positive indirect effect, indicating that this dmPFC-vlPFC connectivity acted as a protective neural factor in the negative relationship between reward sensitivity and future self-continuity. In conclusion, the current research offered novel insights into the impact of reward sensitivity on future self-continuity, advancing our understanding of this behavioral connection from a neurobiological perspective.
In the mediodorsal thalamus (MD), neurons of the medial (MD-M) and lateral (MD-L) subnuclei project to the medial prefrontal cortex (mPFC) to control complementary aspects of behavior, with MD-M supporting more of the social/emotional domain and MD-L promoting cognitive functions. Our recent work shows that MD-M and MD-L have differences in hyperpolarization-activated, cyclic nucleotide-gated (HCN) pacemaker channels that may enable their distinct roles in behavior. Low HCN channel activity in MD-M neurons makes them relatively sensitive and responsive to inputs, while higher HCN channel activity makes MD-L neurons more specific and selective for which inputs it transforms into outputs. Knockout (KO) of the fragile X syndrome-related gene Fmr1 decreased the activity of HCN channels in MD-L but not MD-M neurons, making MD-L neurons more like MD-M cells physiologically. We sought to understand if these Fmr1-related changes in MD function were accompanied by changes in subcellular structure. Here, we assessed the dendritic morphology of MD neurons in adult Fmr1 KO and wildtype (WT) littermate mice. In acute ex vivo brain slices, we filled MD neurons with biocytin via whole cell recording pipettes. We used Neurolucida to trace the dendrites, performed quantitative analysis of dendritic architecture, compared MD-M and MD-L neurons in wildtype mice, and compared WT to KO mice for each subnucleus. In WT mice, MD-M neurons showed more distal dendritic branching compared with MD-L neurons. In Fmr1 KO mice, MD-M neurons lost their distal dendritic branching and exhibited significant reductions in multiple measures of dendritic complexity compared to WT controls (total dendritic length, number of nodes, and number of terminals), while MD-L neurons showed no morphological differences between WT and KO animals. Notably, these morphological changes show a double dissociation with our previous physiological findings: MD-M neurons exhibit structural but not functional changes, while MD-L neurons show functional but not structural changes in Fmr1 KO mice. Together, these findings suggest that FMRP regulates structure and function through independent, circuit-specific mechanisms in thalamocortical neurons, with implications for understanding the diverse cellular and network consequences of Fmr1 loss in fragile X syndrome.
The cingulate cortex plays a central role in emotion, motivation, decision-making and motor control, yet its internal organization in the macaque brain remains debated. In the present study, we examined the cyto- and receptor architectonic organization of the macaque cingulate cortex and provide a 3D parcellation of the identified areas in both surface and volumetric representations. Multivariate receptor analyses consistently separated areas of the anterior cingulate cortex (ACC) and anterior midcingulate cortex (aMCC) from those of the posterior midcingulate cortex (pMCC) and posterior cingulate cortex (PCC), supporting the definition of four principal cingulate regions in the macaque brain. These regions are characterized by distinct receptor balances: the ACC is enriched with glutamatergic and monoaminergic receptors; the aMCC exhibits high densities of modulatory receptors; the pMCC is characterized by overall lowest receptor densities; and the PCC displays intermediate receptor densities with relatively higher GABAA and M3 receptors. Within the ACC, receptor architecture revealed differentiation of subgenual, gyral and sulcal portions, while the PCC contained subdivisions corresponding to dorsal and ventral PCC. Cytoarchitectonic and receptor analyses further demonstrated that cortex along the dorsal bank of the cingulate sulcus (cgs) contains distinct cingulate areas extending from the sulcal fundus onto the dorsal wall, indicating that it forms part of the cingulate cortex rather than the frontal cortex or a transitional zone between those regions. Together, these findings provide a comprehensive anatomical and neurochemical framework for the macaque cingulate cortex and address the long-standing controversy regarding the dorsal bank of the cgs.
