Neural Plasticity最新文献

Neurofeedback (NFB) is a relatively novel approach to the treatment of tinnitus, and prior studies have demonstrated that the increases in alpha activity rather than reduced delta power seem to drive these NFB-related improvements in tinnitus symptoms. The present study was therefore designed to explore whether the implementation of an alpha training protocol with a portable neurofeedback apparatus would achieve improvements in tinnitus patient symptoms. In this study, 38 tinnitus patients underwent NFB training while 18 were enrolled in a control group. The study was single-blinded such that only participants were not aware of their group assignments. Those in the NFB group underwent 15 NFB training sessions over 5 weeks, in addition to pre- and posttraining tests including the Tinnitus Handicap Inventory (THI), Tinnitus Handicap Questionnaire (THQ), visual analog scales (VAS), electroencephalography (EEG), and functional magnetic resonance imaging (fMRI). Our result find that when the THI, THQ, and VAS scores of patients in the two groups were assessed after a 5-week training period, these scores were unchanged in control patients whereas they had significantly improved in the NFB group patients. EEG analyses revealed that the alpha band was increased in the occipital lobe following NFB treatment, while fMRI indicated an increase in regional homogeneity (ReHo) in the right frontal lobe of patients in the NFB group after treatment that was negatively correlated with THI and VAS scores. The results of this analysis indicate that alpha NFB training can be effectively used to reduce tinnitus-related distress and sound perception in patients.

Background: Transient ischemic attack (TIA) is a known risk factor for stroke. Abnormal alterations in the low-frequency range of the gray matter (GM) of the brain have been studied in patients with TIA. However, whether there are abnormal neural activities in the low-frequency range of the white matter (WM) in patients with TIA remains unknown. The current study applied two resting-state metrics to explore functional abnormalities in the low-frequency range of WM in patients with TIA. Furthermore, a reinforcement learning method was used to investigate whether altered WM function could be a diagnostic indicator of TIA.

Methods: We enrolled 48 patients with TIA and 41 age- and sex-matched healthy controls (HCs). Resting-state functional magnetic resonance imaging (rs-fMRI) and clinical/physiological/biochemical data were collected from each participant. We compared the group differences between patients with TIA and HCs in the low-frequency range of WM using two resting-state metrics: amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (fALFF). The altered ALFF and fALFF values were defined as features of the reinforcement learning method involving a Q-learning algorithm.

Results: Compared with HCs, patients with TIA showed decreased ALFF in the right cingulate gyrus/right superior longitudinal fasciculus/left superior corona radiata and decreased fALFF in the right cerebral peduncle/right cingulate gyrus/middle cerebellar peduncle. Based on these two rs-fMRI metrics, an optimal Q-learning model was obtained with an accuracy of 82.02%, sensitivity of 85.42%, specificity of 78.05%, precision of 82.00%, and area under the curve (AUC) of 0.87.

Conclusion: The present study revealed abnormal WM functional alterations in the low-frequency range in patients with TIA. These results support the role of WM functional neural activity as a potential neuromarker in classifying patients with TIA and offer novel insights into the underlying mechanisms in patients with TIA from the perspective of WM function.

Small extracellular vesicles (sEVs) secreted by mesenchymal stem cells (MSCs) have shown great therapeutic potential in cerebral ischemia-reperfusion injury (CIRI). In this study, we firstly performed a systematic review to evaluate the efficacy of MSCs-derived sEV for experimental cerebral ischemia/reperfusion injury. 24 studies were identified by searching 8 databases from January 2012 to August 2022. The methodological quality was assessed by using the SYRCLE 's risk of bias tool for animal studies. All the data were analyzed using RevMan 5.3 software. As a result, the score of study quality ranged from 3 to 9 in a total of ten points. Meta-analyses showed that MSCs-derived sEVs could effectively alleviate neurological impairment scores, reduced the volume of cerebral infarction and brain water content, and attenuated neuronal apoptosis. Additionally, the possible mechanisms of MSCs-derived sEVs for attenuating neuronal apoptosis were inhibiting microglia-mediated neuroinflammation. Thus, MSCs-derived sEVs might be regarded as a novel insight for cerebral ischemic stroke. However, further mechanistic studies, therapeutic safety, and clinical trials are required. Systematic review registration. PROSPERO CRD42022312227.

Angelman syndrome (AS) is a rare neurodevelopmental disorder characterized by severe developmental delay, motor impairment, language and cognition deficits, and often with increased seizure activity. AS is caused by deficiency of UBE3A, which is both an E3 ligase and a cofactor for transcriptional regulation. We previously showed that the small conductance potassium channel protein SK2 is a UBE3A substrate, and that increased synaptic SK2 levels contribute to impairments in synaptic plasticity and fear-conditioning memory, as inhibition of SK2 channels significantly improved both synaptic plasticity and fear memory in male AS mice. In the present study, we investigated UBE3a-mediated regulation of synaptic plasticity and fear-conditioning in female AS mice. Results from both western blot and immunofluorescence analyses showed that synaptic SK2 levels were significantly increased in hippocampus of female AS mice, as compared to wild-type (WT) littermates. Like in male AS mice, long-term potentiation (LTP) was significantly reduced while long-term depression (LTD) was enhanced at hippocampal CA3-CA1 synapses of female AS mice, as compared to female WT mice. Both alterations were significantly reduced by treatment with the SK2 inhibitor, apamin. The shunting effect of SK2 channels on NMDA receptor was significantly larger in female AS mice as compared to female WT mice. Female AS mice also showed impairment in both contextual and tone memory recall, and this impairment was significantly reduced by apamin treatment. Our results indicate that like male AS mice, female AS mice showed significant impairment in both synaptic plasticity and fear-conditioning memory due to increased levels of synaptic SK2 channels. Any therapeutic strategy to reduce SK2-mediated inhibition of NMDAR should be beneficial to both male and female patients.

Background: Hemiplegic shoulder pain (HSP) is a common symptom for post-stroke patients, which has a severely adverse impact on their rehabilitation outcomes. However, the cause of HSP has not been clearly identified due to its complicated multifactorial etiologies. As possible causes of HSP, the abnormality of both muscular electrical activity and blood perfusion remains lack of investigations.

Objective: This study aimed to analyze the alteration of muscular electrical activity and blood perfusion of upper extremity in patients with HSP by using surface electromyography (sEMG) and laser speckle contrast imaging (LSCI) measurement techniques, which may provide some insight into the etiology of HSP.

Methods: In this observational and cross-sectional study, three groups of participants were recruited. They were hemiplegic patients with shoulder pain (HSP group), hemiplegic patients without shoulder pain (HNSP group), and healthy participants (Healthy group). The sEMG data and blood perfusion data were collected from all the subjects and used to compute three different physiological measures, the root-mean-square (RMS) and median-frequency (MDF) parameters of sEMG recordings, and the perfusion unit (PU) parameter of blood perfusion imaging.

Results: The RMS parameter of sEMG showed significant difference (p < 0.05) in the affected side between HSP, HNSP, and Healthy groups. The MDF parameter of sEMG and PU parameter of blood perfusion showed no significant difference in both sides among the three groups (p > 0.05). The RMS parameter of sEMG showed a statistically significant correlation with the pain intensity (r = -0.691, p =0.012).

Conclusion: This study indicated that the muscular electrical activity of upper extremity had a correlation with the presence of HSP, and the blood perfusion seemed to be no such correlation. The findings of the study suggested an alternative way to explore the mechanism and treatment of HSP.

The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG granule cell layer (GCL) widening due to granule cell dispersion has been reported under hyperexcitation conditions in animal models as well as in patients with mesial temporal lobe epilepsy, but also in patients with no apparent relation to epilepsy. Strikingly, it is unclear whether the presence and severity of GCL widening along time affect synaptic processing arising from the PP and alter the performance in hippocampal-mediated behaviors. To evaluate the above, we injected excitotoxic kainic acid (KA) unilaterally into the DG of mice and analyzed the evolution of GCL widening at 10 and 30 days post injection (dpi), while analyzing if KA-induced GCL widening affected in vivo long-term potentiation (LTP) in the PP-DG pathway, as well as the performance in learning and memory through contextual fear conditioning. Our results show that at 10 dpi, when a subtle GCL widening was observed, LTP induction, as well as contextual fear memory, were impaired. However, at 30 dpi when a pronounced increase in GCL widening was found, LTP induction and contextual fear memory were already reestablished. These results highlight the plastic potential of the DG to recover some of its functions despite a major structural alteration such as abnormal GCL widening.

Attention deficit hyperactivity disorder (ADHD) is a common mental disorder in children, which is related to inattention and hyperactivity. These symptoms are associated with abnormal interactions of brain networks. We used resting-state functional magnetic resonance imaging (rs-fMRI) based on the graph theory to explore the topology property changes of brain networks between an ADHD group and a normal group. The more refined AAL_1024 atlas was used to construct the functional networks with high nodal resolution, for detecting more subtle changes in brain regions and differences among groups. We compared altered topology properties of brain network between the groups from multilevel, mainly including modularity at mesolevel. Specifically, we analyzed the similarities and differences of module compositions between the two groups. The results found that the ADHD group showed stronger economic small-world network property, while the clustering coefficient was significantly lower than the normal group; the frontal and occipital lobes showed smaller node degree and global efficiency between disease statuses. The modularity results also showed that the module number of the ADHD group decreased, and the ADHD group had short-range overconnectivity within module and long-range underconnectivity between modules. Moreover, modules containing long-range connections between the frontal and occipital lobes disappeared, indicating that there was lack of top-down control information between the executive control region and the visual processing region in the ADHD group. Our results suggested that these abnormal regions were related to executive control and attention deficit of ADHD patients. These findings helped to better understand how brain function correlates with the ADHD symptoms and complement the fewer modularity elaboration of ADHD research.

Introduction: Action observation therapy (AOT) is a mirror neuron-based approach that has been recently used in poststroke rehabilitation. The main goal of this study was to investigate the effectiveness of AOT of occupations and tasks that are meaningful for chronic stroke patients on occupational performance, upper-extremity function, and corticospinal changes.

Method: A randomized control trial was designed to compare between experimental (n = 13) and control groups (n = 14). In both groups, the execution of meaningful tasks was practiced, but the videos of those tasks were just shown to the experiment group. Instead, patients in the control group watched nature videos as a placebo. Clinical outcomes were evaluated using the Canadian Occupational Performance Measure (COPM), Fugl-Meyer Assessment (FMA), Action Research Arm Test (ARAT), and Box-Block Test (BBT) on 3 occasions: baseline, post (at 4 weeks), and follow-up (at 8 weeks). The assessments of central motor conduction time (CMCT) for abductor policis brevis (APB) and extensor indicis (EI) were only recorded at baseline and posttreatment. Both assessors of clinical and neurophysiological outcomes were blinded to the allocation of subjects.

Result: Finally, the results of outcomes in 24 patients who completed the study were analyzed. In both groups, significant improvements after treatment were seen for most outcomes (p ≤ 0.05). These changes were persistent until follow-up. There were significant differences in COPM performance (p = 0.03) and satisfaction (p = 0.001) between the experimental and control groups. In contrast, other clinical assessments such as FMA, ARAT, and BBT did not show significant differences between the two treatments (p ≥ 0.05). The results of CMCT related to APB showed a more significant change in the experiment group compared to the control group (p = 0.022). There was no difference in change detected between the two groups for CMCT related to EI after treatments.

Conclusion: Observation and execution of meaningful activities can enhance the effects of simply practicing those activities on occupational performance/satisfaction and corticospinal excitability poststroke.

Electroacupuncture (EA) therapy has been widely reported to alleviate neuropathic pain with few side effects in both clinical practice and animal studies worldwide. However, little is known about the comparison of the therapeutic efficacy among the diverse EA schemes used for neuropathic pain. The present study is aimed at investigating the therapeutic efficacy discrepancy between the single and combined-acupoint EA and to reveal the difference of mechanisms behind them. Electroacupuncture was given at both Zusanli (ST36) and Huantiao (GB30) in the combined group or ST36 alone in the single group. Paw withdrawal mechanical threshold (PWMT) was measured to determine the pain level. Electrophysiology was performed to detect the effects of EA on synaptic transmission in the spinal dorsal horn of the vGlut2-tdTomato mice. Spinal contents of endogenous opioids, endocannabinoids, and their receptors were examined. Inhibitors of CBR (cannabinoid receptor) and opioid receptors were used to study the roles of opioid and endocannabinoid system (ECS) in EA analgesia. We found that combined-acupoint acupuncture provide stronger analgesia than the single group did, and the former inhibited the synaptic transmission at the spinal level to a greater extent than later. Besides, the high-intensity stimulation at ST36 or normal stimulation at two sham acupoints did not mimic the similar efficacy of analgesia in the combined group. Acupuncture stimulation in single and combined groups both activated the endogenous opioid system. The ECS was only activated in the combined group. Naloxone totally blocked the analgesic effect of single-acupoint EA; however, it did not attenuate that of combined-acupoint EA unless coadministered with CBR antagonists. Hence, in the CCI-induced neuropathic pain model, combined-acupoint EA at ST36 and GB30 is more effective in analgesia than the single-acupoint EA at ST36. EA stimulation at GB30 alone neither provided a superior analgesic effect to EA treatment at ST36 nor altered the content of AEA, 2-AG, CB1 receptor, or CB2 receptor compared with the CCI group. Activation of the ECS is the main contributor of the better analgesia by the combined acupoint stimulation than that induced by single acupoint stimulation.