Ischemic stroke, a serious neurological disease, is associated with cell death, axonal and dendritic plasticity, and other activities. Anti-inflammatory, anti-apoptotic, promote dendritic and synaptic plasticity are critical therapeutic targets after ischemic stroke. Fibroblast growth factor-2 (FGF2), which is involved in the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/CAMP response element (CRE)-binding protein (CREB) pathway, has been shown to facilitate dendritic and synaptic plasticity. Salidroside (Sal) has been reported to have anti-inflammatory, anti-oxidative, and anti-apoptotic effects; however, the underlying mechanisms of Sal in promoting dendritic and synaptic plasticity remain unclear. Here, the anti-inflammatory, anti-apoptotic, dendritic and synaptic plasticity effects of Sal were investigated in vitro in PC12 cells under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions and in vivo in rats with middle cerebral artery occlusion/reperfusion (MCAO/R). We investigated the role of Sal in promoting dendritic and synaptic plasticity in the ischemic penumbra and whether the FGF2-mediated cAMP/PKA/CREB pathway was involved in this process. The present study demonstrated that Sal could significantly inhibit inflammation and apoptosis, and promote dendritic and synaptic plasticity. Overall, our study suggests that Sal is an effective treatment for ischemic stroke that functions via the FGF2-mediated cAMP/PKA/CREB pathway to promote dendritic and synaptic plasticity.

No abstract

No abstract

BackgroundMotor imagery training might be helpful in stroke rehabilitation. This study explored if a specific modulation of movement-related regions is related to motor imagery (MI) ability.MethodsTwenty-three patients with subcortical stroke and 21 age-matched controls were recruited. They were subjectively screened using the Kinesthetic and Visual Imagery Questionnaire (KVIQ). They then underwent functional magnetic resonance imaging (fMRI) while performing three repetitions of different motor tasks (motor execution and MI). Two separate runs were acquired [motor execution tasks (ME and rest) and motor imagery (MI and rest)] in a block design. For the different tasks, analyses of cerebral activation and the correlation of motor/imagery task-related activity and KVIQ scores were performed.ResultsDuring unaffected hand (UH) active grasp movement, we observed decreased activations in the contralateral precentral gyrus (PreCG), contralateral postcentral gyrus (PoCG) [p < 0.05, family wise error (FWE) corrected] and a positive correlation with the ability of FMA-UE (PreCG: r = 0.46, p = 0.028; PoCG: r = 0.44, p = 0.040). During active grasp of the affected hand (AH), decreased activation in the contralateral PoCG was observed (p < 0.05, FWE corrected). MI of the UH induced significant activations of the contralateral superior frontal gyrus, opercular region of the inferior frontal gyrus, and ipsilateral ACC and deactivation in the ipsilateral supplementary motor area (p < 0.05, AlphaSim correction). Ipsilateral anterior cingulate cortex (ACC) activity negatively correlated with MI ability (r = =–0.49, p = 0.022). Moreover, we found significant activation of the contralesional middle frontal gyrus (MFG) during MI of the AH.ConclusionOur results proved the dominant effects of MI dysfunction that exist in stroke during the processing of motor execution. In the motor execution task, the enhancement of the contralateral PreCG and PoCG contributed to reversing the motor dysfunction, while in the MI task, inhibition of the contralateral ACC can increase the impaired KVIQ ability. The bimodal balance recovery model can explain our results well. Recognizing neural mechanisms is critical to helping us formulate precise strategies when intervening with electrical or magnetic stimulation.

No abstract

No abstract

Introduction Numerous resting-state functional magnetic resonance imaging (fMRI) researches have indicated that large-scale functional and structural remodeling occurs in the whole brain despite an intact sensorimotor network after carpal tunnel syndrome (CTS). Investigators aimed to explore alterations of the global and nodal properties that occur in the whole brain network of patients with CTS based on topographic theory. Methods Standard-compliant fMRI data were collected from 27 patients with CTS in bilateral hands and 19 healthy control subjects in this cross-sectional study. The statistics based on brain networks were calculated the differences between the patients and the healthy. Several topological properties were computed, such as the small-worldness, nodal clustering coefficient, characteristic path length, and degree centrality. Results Compared to those of the healthy controls, the global properties of the CTS group exhibited a decreased characteristic path length. Changes in the local-level properties included a decreased nodal clustering coefficient in 6 separate brain regions and significantly different degree centrality in several brain regions that were related to sensorimotor function and pain. Discussion The study suggested that CTS reinforces global connections and makes their networks more random. The changed nodal properties were affiliated with basal ganglia-thalamo-cortical circuits and the pain matrix. These results provided new insights for improving our understanding of abnormal topological theory in relation to the functional brain networks of CTS patients. Perspective This article presents that the CTS patients’ brain with a higher global efficiency. And the significant alterations in several brain regions which are more related to pain and motor processes. The results provided effective complements to the neural mechanisms underlying CTS.

No abstract