Neural Plasticity最新文献

Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.

Objective: This study is aimed at exploring alteration in motor-related effective connectivity in individuals with transient ischemic attack (TIA).

Methods: A total of 48 individuals with TIA and 41 age-matched and sex-matched healthy controls (HCs) were recruited for this study. The participants were scanned using MRI, and their clinical characteristics were collected. To investigate motor-related effective connectivity differences between individuals with TIA and HCs, the bilateral primary motor cortex (M1) was used as the regions of interest (ROIs) to perform a whole-brain Granger causality analysis (GCA). Furthermore, partial correlation was used to evaluate the relationship between GCA values and the clinical characteristics of individuals with TIA.

Results: Compared with HCs, individuals with TIA demonstrated alterations in the effective connectivity between M1 and widely distributed brain regions involved in motor, visual, auditory, and sensory integration. In addition, GCA values were significantly correlated with high- and low-density lipoprotein cholesterols in individuals with TIA.

Conclusion: This study provides important evidence for the alteration of motor-related effective connectivity in TIA, which reflects the abnormal information flow between different brain regions. This could help further elucidate the pathological mechanisms of motor impairment in individuals with TIA and provide a new perspective for future early diagnosis and intervention for TIA.

Neuronal apoptosis is an important factor in the etiology of Alzheimer's disease (AD). Aerobic exercise (AE) enhances learning and memory, improves cognitive impairment, increases telomere binding protein expression, and decreases apoptosis regulators, but it remains unclear whether it can improve cognitive impairment caused by neuronal apoptosis in AD. Therefore, this study investigated whether an 8-week running table exercise intervention could reduce apoptosis and improve cognitive function in the hippocampal neurons of AD model mice. After the exercise intervention, we evaluated the learning memory ability (positioning, navigation, and spatial search) of mice using a Morris water labyrinth, Nissl staining, immunohistochemistry, and protein application to detect hippocampal PI3K/Akt/GSK-3β signaling pathway protein and hippocampal neuronal cell apoptosis protein B cell lymphoma 2 (Bcl-2) and apoptosis-promoting protein bcl-2-related X (Bax) protein expression. The results showed that aerobic exercise improved the location and spatial exploration ability of mice, increased the number of PI3K- and p-Akt-positive cells, increased the expression of PI3K, p-Akt, and bcl-2 proteins, decreased the expression of GSK-3β and Bax proteins, and increased the bcl-2/Bax ratio of mice. The results suggest that aerobic exercise can reduce apoptosis and improve cognitive function in AD mice. The molecular mechanism may involve activation of the PI3K/Akt/GSK-3β signaling pathway.

Background: Repetitive transcranial magnetic stimulation (rTMS) has been widely used in the treatment of neuropathic orofacial pain (NOP). The consistency of its therapeutic efficacy with the optimal protocol is highly debatable.

Objective: To assess the effectiveness of rTMS on pain intensity, psychological conditions, and quality of life (QOL) in individuals with NOP based on randomized controlled trials (RCTs).

Methods: We carefully screened and browsed 5 medical databases from inception to January 1, 2022. The study will be included that use of rTMS as the intervention for patients with NOP. Two researchers independently completed record retrieval, data processing, and evaluation of methodological quality. Quality and evidence were assessed using the PEDro scores and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system.

Results: Six RCTs with 214 participants were included in this systematic review: 2 studies were considered level 1 evidence, and 4 were considered level 2 evidence. Six studies found that high-frequency rTMS had a pain-relieving effect, while 4 studies found no improvement in psychological conditions and QOL. Quality of evidence (GRADE system) ranged from moderate to high. No significant side effects were found.

Conclusions: There is moderate-to-high evidence to prove that high-frequency rTMS is effective in reducing pain in individuals with NOP, but it has no significant positive effect on psychological conditions and QOL. High-frequency rTMS can be used as an alternative treatment for pain in individuals with NOP, but further studies will be conducted to unify treatment parameters, and the sample size will be expanded to explore its influence on psychological conditions and QOL.

Background: Electroacupuncture (EA) has benefits for neuropathic pain. However, the underlying mechanisms are still unknown. The current study explores the underlying mechanisms of EA in neuropathic pain of chronic constriction injury (CCI) rats. Material/Methods. Overall, 126 Sprague-Dawley (200-250 g) rats were divided into nine groups randomly: the sham-operated, CCI, CCI+EA, CCI+sham EA, CCI+NS, CCI+AAV-NC, CCI+AAV-miR-206-3p, CCI+EA+NS, and CCI+EA+AAV-miR-206-3p groups. The animals were sacrificed 14 days postsurgery. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) tests were used to determine differences in neurobehavioral manifestations. qPCR, western blotting, and immunofluorescence (IF) were carried out to detect the expression levels of miR-206-3p, BDNF, BAX/Bcl-2, TNF-α, and IL-6. Nissl staining was measured to observe morphological changes in neurons. Transmission electron microscopy (TEM) was employed to evaluate microscopic changes in dorsal horn synapses.

Results: Hyperalgesia was reduced markedly by EA in the CCI model. The expression level of miR-206-3p was elevated, whereas the expression levels of BDNF, BAX/Bcl-2, TNF-α, and IL-6 were decreased in EA-treated CCI rats. However, a miR-206-3p inhibitor partially abrogated the analgesic effect of EA and resulted in poor behavioral performance and the BDNF, BAX/Bcl-2, TNF-α, and IL-6 expression was elevated as well.

Conclusions: EA can relieve neuropathic pain by regulating the miR-206-3p/BDNF pathway, thus exerting anti-inflammatory and antiapoptotic effect.

Hippocampal neuronal damage likely underlies cognitive impairment in vascular dementia (VaD). PPARγ coactivator-1α (PGC-1α) is a master regulator of mitochondrial biogenesis. However, the role and the precise mechanism of how PGC-1α alleviates hippocampal neuronal injury remain unknown. To address this question, HT-22 cells, an immortalized hippocampal neuron cell line, with or without PGC-1α overexpression were subjected to oxygen-glucose deprivation (OGD), which mimics the circumstance of chronic cerebral hypoperfusion in VaD. After OGD, cell viability was assessed using the MTS assay. The mitochondrial function and reactive oxygen species (ROS) were both detected. ChIP-Seq analysis was employed to discover the underlying molecular mechanism of PGC-1α-mediated neuroprotective effects. Our results showed that mitochondrial membrane potentials were increased and ROS production was decreased in PGC-1α overexpressing cells, which increased cell viability. The further bioinformatics analysis from ChIP-Seq data indicated that PGC-1α may participate in the regulation of apoptosis, autophagy, and mitophagy pathways in HT-22 cells. We found that PGC-1α promoted the LC3-II formation and reduced the neuronal apoptosis determined by TUNEL staining. In addition, PGC-1α upregulated the expressions of mitochondrial antioxidants, including SOD2, Trx2, and Prx3. In summary, our findings indicate that PGC-1α may attenuate OGD-induced hippocampal neuronal damage by regulating multiple mechanisms, like autophagy and mitochondrial function. Thus, PGC-1α may be a potential therapeutic target for hippocampal damage associated with cognitive impairment.

The analysis of structural covariance has emerged as a powerful tool to explore the morphometric correlations among broadly distributed brain regions. However, little is known about the interactions between the damaged primary motor cortex (M1) and other brain regions in stroke patients with motor deficits. This study is aimed at investigating the structural covariance pattern of the ipsilesional M1 in chronic subcortical stroke patients with motor deficits. High-resolution T1-weighted brain images were acquired from 58 chronic subcortical stroke patients with motor deficits (29 with left-sided lesions and 29 with right-sided lesions) and 50 healthy controls. Structural covariance patterns were identified by a seed-based structural covariance method based on gray matter (GM) volume. Group comparisons between stroke patients (left-sided or right-sided groups) and healthy controls were determined by a permutation test. The association between alterations in the regional GM volume and motor recovery after stroke was investigated by a multivariate regression approach. Structural covariance analysis revealed an extensive increase in the structural interactions between the ipsilesional M1 and other brain regions in stroke patients, involving not only motor-related brain regions but also non-motor-related brain regions. We also identified a slightly different pattern of structural covariance between the left-sided stroke group and the right-sided stroke group, thus indicating a lesion-side effect of cortical reorganization after stroke. Moreover, alterations in the GM volume of structural covariance brain regions were significantly correlated to the motor function scores in stroke patients. These findings indicated that the structural covariance patterns of the ipsilesional M1 in chronic subcortical stroke patients were induced by motor-related plasticity. Our findings may help us to better understand the neurobiological mechanisms of motor impairment and recovery in patients with subcortical stroke from different perspectives.

Background: Tai chi (TC) has received increased attention in stroke rehabilitation, yet services are greatly underutilized. An increasing number of systematic reviews and meta-analyses (SRs/MAs) have begun to investigate the effects of TC on balance function in stroke patients. The aim of this current study was to systematically collate, appraise, and synthesize the results of these SRs/MAs using a systematic overview.

Methods: Eight databases were searched: PubMed, Cochrane Library, Embase, Web of Science, CNKI, SinoMed, Chongqing VIP, and Wanfang Data. SRs/MAs of TC on balance function in stroke patients were included. Literature selection, data extraction, and assessment of the review quality were performed by two independent reviewers. Methodological quality was assessed by the Assessing the Methodological Quality of Systematic Reviews 2 (AMSTAR-2), reporting quality by Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), and evidence quality by Grading of Recommendations, Assessment, Development, and Evaluation (GRADE).

Results: Nine SRs/MAs were included in this study. For methodological quality, what resulted in unsatisfactory methodological quality was noncompliance with critical item 4 (using a comprehensive literature search strategy) and critical item 7 (providing the list of excluded research literature). For reporting quality, what resulted in unsatisfactory reporting quality was inadequate reporting of Q1 (protocol and registration), Q8 (search), Q15 (risk of bias across studies), Q16 (additional analyses), Q22 (risk of bias across studies), Q23 (additional analysis), and Q27 (funding). For GRADE, the evidence quality was high in 0, moderate in 3, low in 11, and very low in 6. Risk of bias was the most common factor leading to downgrading of evidence, followed by inconsistency, imprecision, publication bias, and indirectness.

Conclusions: TC may have beneficial effects on balance function in stroke survivors; however, this finding is limited by the generally low methodology, reporting quality, and evidence quality for published SRs/MAs.

Ischemic stroke and traumatic brain injury (TBI) are among the leading causes of death and disability worldwide with impairments ranging from mild to severe. Many therapies are aimed at improving functional and cognitive recovery by targeting neural repair but have encountered issues involving efficacy and drug delivery. As a result, therapeutic options for patients are sparse. Neurotrophic factors are one of the key mediators of neural plasticity and functional recovery. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) serve as potential therapeutic options to increase neural repair and recovery as they promote neuroprotection and regeneration. BDNF and NGF have demonstrated the ability to improve functional recovery in preclinical and to a lesser extent clinical studies. Direct and indirect methods to increase levels of neurotrophic factors in animal models have been successful in improving postinjury outcome measures. However, the translation of these studies into clinical trials has been limited. Preclinical experiments have largely failed to result in significant impacts in clinical research. This review will focus on the administration of these neurotrophic factors in preclinical and clinical stroke and TBI and the challenges in translating these therapies from the bench to the clinic.

Chronic pain patients often develop mental disorders, and anxiety disorders are common. We hypothesize that the comorbid anxiety results from an imbalance between the reward and antireward system due to persistent pain, which leads to the dysfunction of the pain and anxiety regulatory system. In this review, we will focus on changes in neuroplasticity, especially in neural circuits, during chronic pain and anxiety as observed in animal studies. Several neural circuits within specific regions of the brain, including the nucleus accumbens, lateral habenular, parabrachial nucleus, medial septum, anterior cingulate cortex, amygdala, hippocampus, medial prefrontal cortex, and bed nucleus of the stria terminalis, will be discussed based on novel findings after chemogenetic or optogenetic manipulation. We believe that these animal studies provide novel insights into human conditions and can guide clinical practice.