Neuroscience
-
The development and exacerbation of depression and anxiety are associated with exposure to repeated psychosocial stress. Stress is known to affect the bidirectional communication between the nervous and immune systems leading to elevated levels of stress mediators including glucocorticoids (GCs) and catecholamines and increased trafficking of proinflammatory immune cells. Animal models, like the repeated social defeat (RSD) paradigm, were developed to explore this connection between stress and affective disorders. ⋯ Recently, the observation that these monocytes have the ability to traffic to the brain perivascular spaces and parenchyma have provided mechanisms by which these peripheral cells may contribute to the prolonged anxiety-like behavior associated with RSD. The data that have been amassed from the RSD paradigm and others recapitulate many of the behavioral and immunological phenotypes associated with human anxiety disorders and may serve to elucidate potential avenues of treatment for these disorders. Here, we will discuss novel and key data that will present an overview of the neuroendocrine, immunological and behavioral responses to social stressors.
-
Motor feedback usually engages distinct sensory and cognitive processes based on different feedback conditions, e.g., the real and sham feedbacks. It was thought that these processes may rely on the functional connectivity among the brain networks. However, it remains unclear whether there is a difference in the network connectivity between the two feedback conditions. ⋯ Using independent component analysis and functional connectivity analysis, we found that as compared with the sham feedback, the real feedback recruited stronger negative connectivity between the executive network (EN) and the posterior default mode network (pDMN). More intriguingly, the left frontal parietal network (lFPN) exhibits positive connectivity with the pDMN in the real feedback while in the sham feedback, the lFPN shows connectivity with the EN. These results suggest that the connectivity among EN, pDMN, lFPN could differ depending on the real and sham feedbacks, and the lFPN may balance the competition between the pDMN and EN, thus supporting the sensory and cognitive processes of the motor feedback.
-
Hemifacial spasm (HFS) is a peripheral nerve disorder which impacts the living quality of patients both psychologically and physically. Whether HFS has structural changes under these specific stressors including psychological and physiological conditions in the CNS remains largely unknown. In the current study, voxel-based morphometry (VBM) was used to evaluate changes in gray matter (GM) by using T1-weighted imaging in 25 HFS patients and 25 demographically similar healthy volunteers. ⋯ Additionally, the GM volume changes in the amygdala did not exhibit any significant between-group differences with HAMA and HAMD scores as covariates. Our results suggested that HFS probably led to GM volume abnormalities of the CNS. We indicated that the GM volume changes of the amygdala may be highly related to emotional factors.
-
Necrostatin-1 (Nec-1) is an inhibitor of necroptosis, playing an important role in inhibition of pathological death in the central nervous system (CNS). Our earlier study suggests that Nec-1 protects the injured spinal cord. In this study, we found that Nec-1 reduces the elevated Ca(2+) concentration in mitochondria post-injury and preserves the remarkably decreased mitochondrial membrane potential (MMP) level post-spinal cord injury (SCI). ⋯ It also inhibits the up-regulation of mitochondrial fusion genes Mnf1, Mnf2 within 6h post-injury and adjusts the abnormal expression of mitochondrial fission gene Fis1. All these results indicate the improvement of mitochondrial functions in injured spinal cord after the treatment of Nec-1. This research revealed the mechanisms of functional protection of Nec-1 by mitigating mitochondrial dysfunction post-SCI.
-
Both central and peripheral sympathetic nervous systems contribute to the cardiovascular effects of dexmedetomidine (DMED), a highly selective and widely used a2-adrenoceptor agonist for sedation, analgesia, and stress management. The central sympatholytic effects are augmented by peripheral inhibition of sympathetic ganglion transmission. The mechanism is not clear. ⋯ In conclusion, DMED dose-dependently inhibits INa and IACh in rat SCG neurons by preferential binding to the inactivated state of the Na(+) channels and the closed state (resting) of nAChR channels respectively. Both inhibitions are a2-adrenoceptor independent. Furthermore, the nAChR channels in rat SCG neurons are much more sensitive to inhibition by DMED than Na(+) channels.