Neural Plasticity最新文献

Low-frequency oscillatory activity (3-9 Hz) and increased synchrony in the basal ganglia (BG) are recognized to be crucial for Parkinsonian tremor. However, the dynamical mechanism underlying the tremor-related oscillations still remains unknown. In this paper, the roles of the indirect and hyperdirect pathways on synchronization and tremor-related oscillations are considered based on a modified Hodgkin-Huxley model. Firstly, the effects of indirect and hyperdirect pathways are analysed individually, which show that increased striatal activity to the globus pallidus external (GPe) or strong cortical gamma input to the subthalamic nucleus (STN) is sufficient to promote synchrony and tremor-related oscillations in the BG network. Then, the mutual effects of both pathways are analysed by adjusting the related currents simultaneously. Our results suggest that synchrony and tremor-related oscillations would be strengthened if the current of these two paths are in relative imbalance. And the network tends to be less synchronized and less tremulous when the frequency of cortical input is in the theta band. These findings may provide novel treatments in the cortex and striatum to alleviate symptoms of tremor in Parkinson's disease.

Throughout life, sensory systems adapt to the sensory environment to provide optimal responses to relevant tasks. In the case of a developing system, sensory inputs induce changes that are permanent and detectable up to adulthood. Previously, we have shown that rearing rat pups in a complex acoustic environment (spectrally and temporally modulated sound) from postnatal day 14 (P14) to P28 permanently improves the response characteristics of neurons in the inferior colliculus and auditory cortex, influencing tonotopical arrangement, response thresholds and strength, and frequency selectivity, along with stochasticity and the reproducibility of neuronal spiking patterns. In this study, we used a set of behavioral tests based on a recording of the acoustic startle response (ASR) and its prepulse inhibition (PPI), with the aim to extend the evidence of the persistent beneficial effects of the developmental acoustical enrichment. The enriched animals were generally not more sensitive to startling sounds, and also, their PPI of ASR, induced by noise or pure tone pulses, was comparable to the controls. They did, however, exhibit a more pronounced PPI when the prepulse stimulus was represented either by a change in the frequency of a background tone or by a silent gap in background noise. The differences in the PPI of ASR between the enriched and control animals were significant at lower (55 dB SPL), but not at higher (65-75 dB SPL), intensities of background sound. Thus, rearing pups in the acoustically enriched environment led to an improvement of the frequency resolution and gap detection ability under more difficult testing conditions, i.e., with a worsened stimulus clarity. We confirmed, using behavioral tests, that an acoustically enriched environment during the critical period of development influences the frequency and temporal processing in the auditory system, and these changes persist until adulthood.

Sensory gating is a neurophysiological measure of inhibition that is characterized by a reduction in the P₅₀, N₁₀₀, and P₂₀₀ event-related potentials to a repeated identical stimulus. It was proposed that abnormal sensory gating is involved in the neural pathological basis of some severe mental disorders. Since then, the prevailing application of sensory gating measures has been in the study of neuropathology associated with schizophrenia and so on. However, sensory gating is not only trait-like but can be also state-like, and measures of sensory gating seemed to be affected by several factors in healthy subjects. The objective of this work was to clarify the roles of acute stress and gender in sensory gating. Data showed acute stress impaired inhibition of P₅₀ to the second click in the paired-click paradigm without effects on sensory registration leading to worse P₅₀ sensory gating and disrupted attention allocation reflected by attenuated P₂₀₀ responses than control condition, without gender effects. As for N₁₀₀ and P₂₀₀ gating, women showed slightly better than men without effects of acute stress. Data also showed slightly larger N₁₀₀ amplitudes across clicks and significant larger P₂₀₀ amplitude to the first click for women, suggesting that women might be more alert than men.

Neurofeedback training has shown benefits in clinical treatment and behavioral performance enhancement. Despite the wide range of applications, no consensus has been reached about the optimal training schedule. In this work, an EEG neurofeedback practical experiment was conducted aimed at investigating the effects of training intensity on the enhancement of the amplitude in the individual upper alpha band. We designed INTENSIVE and SPARSE training modalities, which differed regarding three essential aspects of training intensity: the number of sessions, the duration of a session, and the interval between sessions. Nine participants in the INTENSIVE group completed 4 sessions with 37.5 minutes each during consecutive days, while nine participants in the SPARSE group performed 6 sessions of 25 minutes spread over approximately 3 weeks. As a result, regarding the short-term effects, the upper alpha band amplitude change within sessions did not significantly differ between the two groups. Nonetheless, only the INTENSIVE group showed a significant increase in the upper alpha band amplitude. However, for the sustained effects across sessions, none of the groups showed significant changes in the upper alpha band amplitude across the whole course of training. The findings suggest that the progression within session is favored by the intensive design. Therefore, based on these findings, it is proposed that training intensity influences EEG self-regulation within sessions. Further investigations are needed to isolate different aspects of training intensity and effectively confirm if one modality globally outperforms the other.

Flaccid paralysis in the upper extremity is a severe motor impairment after stroke, which exists for weeks, months, or even years. Electroacupuncture treatment is one of the most widely used TCM therapeutic interventions for poststroke flaccid paralysis. However, the response to electroacupuncture in different durations of flaccid stage poststroke as well as in the topological configuration of the cortical network remains unclear. The objectives of this study are to explore the disruption of the cortical network in patients in different durations of flaccid stage and observe dynamic network reorganization during and after electroacupuncture. Resting-state networks were constructed from 18 subjects with flaccid upper extremity by partial directed coherence (PDC) analysis of multichannel EEG. They were allocated to three groups according to time after flaccid paralysis: the short-duration group (those with flaccidity for less than two months), the medium-duration group (those with flaccidity between two months and six months), and the long-duration group (those with flaccidity over six months). Compared with short-duration flaccid subjects, weakened effective connectivity was presented in medium-duration and long-duration groups before electroacupuncture. The long-duration group has no response in the cortical network during electroacupuncture. The global network measures of EEG data (sPDC, mPDC, and N) indicated that there was no significant difference among the three groups. These results suggested that the network connectivity reduced and weakly responded to electroacupuncture in patients with flaccid paralysis for over six months. These findings may help us to modulate the formulation of electroacupuncture treatment according to different durations of the flaccid upper extremity.

It was reported that acupuncture could treat Alzheimer's disease (AD) with the potential mechanisms remaining unclear. The aim of the study is to explore the effect of the combination stimulus of Hegu (LI4) and Taichong (LR3) on the resting-state brain networks in AD, beyond the default network (DMN). Twenty-eight subjects including 14 AD patients and 14 healthy controls (HCs) matched by age, gender, and educational level were recruited in this study. After the baseline resting-state MRI scans, the manual acupuncture stimulation was performed for 3 minutes, and then, another 10 minutes of resting-state fMRI scans was acquired. In addition to the DMN, five other resting-state networks were identified by independent component analysis (ICA), including left frontal parietal network (lFPN), right frontal parietal network (rFPN), visual network (VN), sensorimotor network (SMN), and auditory network (AN). And the impaired connectivity in the lFPN, rFPN, SMN, and VN was found in AD patients compared with those in HCs. After acupuncture, significantly decreased connectivity in the right middle frontal gyrus (MFG) of rFPN (P = 0.007) was identified in AD patients. However, reduced connectivity in the right inferior frontal gyrus (IFG) (P = 0.047) and left superior frontal gyrus (SFG) (P = 0.041) of lFPN and some regions of the SMN (the left inferior parietal lobula (P = 0.004), left postcentral gyrus (PoCG) (P = 0.001), right PoCG (P = 0.032), and right MFG (P = 0.010)) and the right MOG of VN (P = 0.003) was indicated in HCs. In addition, after controlling for the effect of acupuncture on HCs, the functional connectivity of the right cerebellum crus I, left IFG, and left angular gyrus (AG) of lFPN showed to be decreased, while the left MFG of IFPN and the right lingual gyrus of VN increased in AD patients. These findings might have some reference values for the interpretation of the combination stimulus of Hegu (LI4) and Taichong (LR3) in AD patients, which could deepen our understanding of the potential mechanisms of acupuncture on AD.

Traumatic brain injury (TBI) is characterized by a complex pattern of abnormalities in resting-state functional connectivity (rsFC) and network dysfunction, which can potentially be ameliorated by rehabilitation. In our previous randomized controlled trial, we found that a 3-month neurological music therapy intervention enhanced executive function (EF) and increased grey matter volume in the right inferior frontal gyrus (IFG) in patients with moderate-to-severe TBI (N = 40). Extending this study, we performed longitudinal rsFC analyses of resting-state fMRI data using a ROI-to-ROI approach assessing within-network and between-network rsFC in the frontoparietal (FPN), dorsal attention (DAN), default mode (DMN), and salience (SAL) networks, which all have been associated with cognitive impairment after TBI. We also performed a seed-based connectivity analysis between the right IFG and whole-brain rsFC. The results showed that neurological music therapy increased the coupling between the FPN and DAN as well as between these networks and primary sensory networks. By contrast, the DMN was less connected with sensory networks after the intervention. Similarly, there was a shift towards a less connected state within the FPN and SAL networks, which are typically hyperconnected following TBI. Improvements in EF were correlated with rsFC within the FPN and between the DMN and sensorimotor networks. Finally, in the seed-based connectivity analysis, the right IFG showed increased rsFC with the right inferior parietal and left frontoparietal (Rolandic operculum) regions. Together, these results indicate that the rehabilitative effects of neurological music therapy after TBI are underpinned by a pattern of within- and between-network connectivity changes in cognitive networks as well as increased connectivity between frontal and parietal regions associated with music processing.

Introduction: We studied the impact of vibratory stimulation on the electrophysiological features of digital sensory nerve action potential (SNAP).

Methods: The antidromic digit 3 SNAP was recorded in 19 healthy adults before, during, and after applying a vibration to either 3rd or 5th metacarpal phalangeal joint (MCPJ) at 60 Hz and amplitude of 2 mm. 100% supramaximal stimulus intensity was performed in 5 subjects (randomly selected from the 19 subjects) where the SNAP sizes were recorded.

Results: The amplitude of digit 3 SNAP declined to 58.9 ± 8.6% when a vibration was applied to MCPJ digit 3. These impacts did not change by increasing the electrical stimulus intensity. The SNAP regained its baseline value immediately after the cessation of vibration stimulation. The magnitude of size reduction of digit 3 SNAP was less when vibration was moved to from MCPJ of digit 3 to MCPJ of digit 5. Discussion. The marked drop of the SNAP size during vibratory stimulation reflects the decreased responsiveness of Aβ afferents to electrical stimulation, which deserve further investigation in the study of focal vibration in neurorehabilitation.

Resiniferatoxin is an ultrapotent capsaicin analog that mediates nociceptive processing; treatment with resiniferatoxin can cause an inflammatory response and, ultimately, neuropathic pain. Hepatoma-derived growth factor, a growth factor related to normal development, is associated with neurotransmitters surrounding neurons and glial cells. Therefore, the study aims to investigate how blocking hepatoma-derived growth factor affects the inflammatory response in neuropathic pain. Serum hepatoma-derived growth factor protein expression was measured via ELISA. Resiniferatoxin was administrated intraperitoneally to induce neuropathic pain in 36 male Sprague-Dawley rats which were divided into three groups (resiniferatoxin+recombinant hepatoma-derived growth factor antibody group, resiniferatoxin group, and control group) (n = 12/group). The mechanical threshold response was tested with calibration forceps. Cell apoptosis was measured by TUNEL assay. Immunofluorescence staining was performed to detect apoptosis of neuron cells and proliferation of astrocytes in the spinal cord dorsal horn. RT-PCR technique and western blot were used to measure detect inflammatory factors and protein expressions. Serum hepatoma-derived growth factor protein expression was higher in the patients with sciatica compared to controls. In resiniferatoxin-group rats, protein expression of hepatoma-derived growth factor was higher than controls. Blocking hepatoma-derived growth factor improved the mechanical threshold response in rats. In dorsal root ganglion, blocking hepatoma-derived growth factor inhibited inflammatory cytokines. In the spinal cord dorsal horn, blocking hepatoma-derived growth factor inhibited proliferation of astrocyte, apoptosis of neuron cells, and attenuated expressions of pain-associated proteins. The experiment showed that blocking hepatoma-derived growth factor can prevent neuropathic pain and may be a useful alternative to conventional analgesics.

Background: Nowadays, acute intracerebral hemorrhage stroke (AICH) still causes higher mortality. Liangxue Tongyu Formula (LXTYF), originating from a traditional Chinese medicine (TCM) prescription, is widely used as auxiliary treatment for AICH.

Objective: To dig into the multicomponent, multitarget, and multipathway mechanism of LXTYF on treating AICH via network pharmacology and RNA-seq.

Methods: Network pharmacology analysis was used by ingredient collection, target exploration and prediction, network construction, and Gene Ontology (GO) and KEGG analysis, with the Cytoscape software and ClusterProfiler package in R. The RNA-seq data of the AICH-rats were analyzed for differential expression and functional enrichments. Herb-Compound-Target-Pathway (H-C-T-P) network was shown to clarify the mechanism of LXTYF for AICH.

Results: 76 active ingredients (quercetin, Alanine, kaempferol, etc.) of LXTYF and 376 putative targets to alleviate AICH (PTGS2, PTGS1, ESR1, etc.) were successfully identified. The protein-protein interaction (PPI) network indicated the important role of STAT3. The functional enrichment of GO and KEGG pathway showed that LXTYF is most likely to influence MAPK and PI3K-Akt signaling pathways for AICH treatment. From the RNA-seq of AICH-rats, 583 differential mRNAs were identified and 14 of them were consistent with the putative targets of LXTYF for AICH treatment. The KEGG pathway enrichment also implied that the MAPK signaling pathway was the most correlated one among all the related signaling pathways. Many important targets with expression changes of LXTYF for AICH treatment and their related pathways are great markers of antioxidation, anti-inflammatory, antiapoptosis, and lowering blood pressure, which indicated that LXTYF may play mutiroles in the mechanisms for AICH treatment.

Conclusion: The LXTYF attenuates AICH partially by antioxidation, anti-inflammatory, and antiapoptosis and lowers blood pressure roles through regulating the targets involved MAPK, calcium, apoptosis, and TNF signaling pathway, which provide notable clues for further experimental validation.