Journal of neurophysiology最新文献

Vagus nerve stimulation (VNS) has been commonly employed for the functional rehabilitation of stroke patients. This study aimed to investigate the therapeutic effects of transcranial direct current stimulation on the vagus nerve (TDCSVN) in improving dysphagia in stroke patients. Patients experiencing dysphagia following a stroke were diagnosed with dysphagia by a water swallow test. Swallowing function was evaluated with the standard swallowing scale score and the functional dysphagia scale. Serum levels of interleukin (IL)-1β and IL-8 were measured with enzyme-linked immunosorbent assays. TDCSVN treatment resulted in a significantly greater reduction in both the standard swallowing scale and functional dysphagia scale scores compared to conventional treatment. Furthermore, TDCSVN treatment led to a notable increase in hemoglobin and albumin levels, suggesting a more substantial improvement in dysphagia compared to conventional methods. Additionally, TDCSVN treatment was more effective in decreasing serum levels of IL-1β and IL-8 in dysphagic patients after a stroke. TDCSVN treatment demonstrated a significant inhibitory effect on inflammatory cytokines, resulting in a more pronounced improvement in dysphagia among stroke patients.NEW & NOTEWORTHY The present study demonstrates that transcranial direct current stimulation on the vagus nerve (TDCSVN) treatment shows a significant inhibitory effect on the production of inflammatory factors, resulting in a more pronounced improvement in dysphagia among stroke patients.

Microglia are the resident immune cells of the central nervous system (CNS), which have been classically viewed as involved in CNS responses to damage and tissue repair. However, microglia are constantly sensing neuronal network activity and changes in the CNS milieu, establishing complex state-dependent microglia-neuron interactions that impact their functions. By doing so, microglia perform a wide range of physiological roles, including brain homeostasis maintenance, control of neural connectivity, network function modulation, as well as functional and morphological plasticity regulation in health and disease. Here, the author reviews recent evidence of the modulations induced by microglia, a highly heterogeneous cell type, on synaptic and intrinsic neuronal properties, and on neuronal network patterns during perinatal development and adulthood. The reviewed evidence clearly indicates that microglia are important, if not essential, for brain function and plasticity in both health and disease.

The brain is a complex neural network whose functional dynamics offer valuable insights into behavioral performance and health. Advances in fMRI have provided a unique window into studying human brain networks, providing us with a powerful tool for clinical research. Yet many questions about the underlying correlates between spontaneous fMRI and neural activity remain poorly understood, limiting the impact of this research. Cross-species studies have proven essential in deepening our understanding of how neuronal activity is coupled to increases in local cerebral blood flow, changes in blood oxygenation, and the measured fMRI signal. In this article, we review some fundamental mechanisms implicated in neurovascular coupling. We then examine neurovascular coupling within the context of spontaneous cortical functional networks and their dynamics, summarizing key findings from mechanistic studies in rodents. In doing so, we highlight the nuances of the neurovascular coupling that ultimately influences the interpretation of derived hemodynamic functional networks, their dynamics, and the neural underpinnings they represent.

Performance of a task involves the engagement of various brain areas, as evidenced by the effects of lesions of particular brain areas and the results of functional neuroimaging and neurophysiological studies. Here, we tested the hypothesis that overall task performance would depend on the level of ongoing, resting-state change in synaptic activity of participating areas, such that the degree of success of the outcome would be higher, the higher the resting-state activation. For that purpose, we used 248-sensor magnetoencephalography (MEG) in healthy people to obtain estimates of resting-state synaptic activity in various areas and then correlated those estimates to the average performance score in three visuospatial tasks assessed outside the MEG session using the Montreal Cognitive Assessment (MoCA), namely, the trails, cube, and clock drawing (TCCD) tasks. We found that the average success score in these tasks covaried positively with the level of resting-state neural activity of three broad area clusters, namely, 1) right cerebellum, occipital, and parietal cortical regions (strongest association), 2) right inferior frontal, middle and posterior temporal regions, and 3) left middle frontal region. The dependence of the outcome of task performance on the activation state of areas in the absence of action, i.e., in resting-state, points to a priming role in facilitating task performance. NEW & NOTEWORTHY Does successful task performance depend on the resting-state, background activity of brain areas involved? We used magnetoencephalography to obtain estimates of this activity that we then correlated with the average score of performing three visuospatial tasks outside the magnetoencephalography session. Task performance correlated positively with resting-state activity mostly in right-sided brain regions, broadly agreeing with existing knowledge from neuropsychological and other studies. These results point to a priming effect of background neural activity on task performance.

Parkinson's disease (PD) is a prevalent and challenging neurodegenerative disorder, and may involve impaired autophagy. Nuclear factor erythroid-2-related factor 2 (Nrf2) is crucial for regulating autophagy-related genes and maintaining cellular homeostasis. Electroacupuncture (EA), a complementary and alternative therapy for PD, has gained widespread clinical application. In this study, we investigate whether EA at Baihui (GV20) and Taichong (LR3) acupoints modulates autophagy through the Nrf2 pathway, providing neuroprotection in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice. Using wild-type and Nrf2 knockout (KO) mice, we examined EA's effects on dopaminergic neuron survival, α-synuclein expression, motor function and the underlying mechanisms. Results showed that EA treatment significantly reduced dopaminergic neuron loss and α-synuclein expression, and improved motor deficits while restoring autophagy, as evidenced by increased autophagy markers (Atg7, LC3II) and decreased p62 levels. Transmission electron microscopy confirmed a rise in autophagosomes and lysosomes in the MPTP + EA group. EA also enhanced nuclear Nrf2 expression and activated Nrf2 signaling. Importantly, Nrf2 KO mice did not exhibit neuroprotection or increased autophagy-related proteins following EA treatment. In conclusion, our research demonstrated that EA ameliorated defective autophagy and activated the Nrf2 signaling pathway, which collectively contribute to its neuroprotective effects against MPTP-induced neurotoxicity.NEW & NOTEWORTHY In this study, we explored the potential mechanism of electroacupuncture (EA) therapy at the GV20 and LR3 acupoints of Parkinson's disease (PD). We demonstrated EA therapy's neuroprotective effect on PD, through ameliorating defective autophagy and activating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway whereas the regulation of EA on autophagy was absent in Nrf2 knockout (KO) mice. Our study not only provides new insights into the therapeutic mechanisms of EA but also suggests a promising strategy for PD treatment.

Animals must deal with numerous perturbations, oftentimes concurrently. In this study, we examine the effects of two perturbations, high extracellular potassium and elevated temperature, on the resilience of the pyloric rhythm of the crab, Cancer borealis. At control temperatures (11°C), high potassium saline (2.5× K⁺) depolarizes the neurons of the stomatogastric ganglion (STG), and the pyloric rhythm becomes quiescent. Over minutes, while remaining depolarized in high potassium, the pyloric network neurons adapt, and resume their spiking and bursting activity. We compared adaptation to high potassium applications at 20°C to those seen at 11°C. At 20°C, the intracellular waveforms of the neuronal activity seen in high potassium more closely resemble activity in control saline, and adaptation and recovery occur more rapidly. Spike and burst thresholds were measured using slow ramps of injected current from hyperpolarized to depolarized values of membrane potential in the presence of high potassium and at both temperatures. The maximal burst frequencies in control saline were higher at 20°C and subthreshold bursts occurred at a more hyperpolarized membrane potential at 20°C. In high potassium, subthreshold bursts were seen at 20°C, but not at 11°C, whereas spike thresholds were similar at the two temperatures. At both temperatures, a second application of high potassium showed substantially more rapid adaptation than did the first application. Together, these data show that the adaptation to high potassium saline is enhanced by high temperature.NEW & NOTEWORTHY Multiple applications of high potassium saline to the pyloric rhythm of the crab, Cancer borealis show a history-dependent adaptation process that is enhanced at high temperatures.

Social and sensory experiences across the lifespan can shape social interactions; however, experience-dependent plasticity is widely studied within discrete life stages. In the socially monogamous zebra finch, in which females use learned vocal signals to identify individuals and form long-lasting pair bonds, developmental exposure to song is key for females to show species-typical song perception and preferences. Although adult mating experience can still lead to pair-bonding and song preference learning even in birds with limited previous song exposure ("song-naive"), whether similarities in adult behavioral plasticity between normally reared and song-naive females reflect convergent patterns of neural activity is unknown. We investigated this using expression of a marker of neural activity and plasticity [phosphorylated S6 (pS6)] in mated normally reared and song-naive females in response to song from either their mate, a neighbor, or an unfamiliar male. We found that, in portions of a secondary auditory region (the caudomedial nidopallium, NCM) and in dopaminergic neurons of the caudal ventral tegmental area, hearing the mate's song significantly increased pS6 expression in females from both rearing conditions. In contrast, within other NCM subregions, song identity drove different patterns of pS6 expression depending on the rearing condition. These data suggest that developmental experiences can have long-lasting impacts on the neural signatures of behaviors acquired in adulthood and that socially driven behavioral plasticity in adults may arise through both shared and divergent neural circuits depending on an individual's developmental experiences.NEW & NOTEWORTHY Social and sensory experiences across the lifespan can shape social interactions. Female zebra finches form long-lasting social bonds with a male mate and preferences for his song; however, few studies have investigated how neural responses to the mate's song compare to responses to familiar or unfamiliar songs. We found multiple regions that differentially respond to the song of the mate, and, in some of these regions, responses were modulated by the female's previous auditory experience.

The loss of a sensory modality triggers a phenomenon known as cross-modal plasticity, where areas of the brain responsible for the lost sensory modality are reorganized and repurposed to the benefit of the remaining modalities. After perinatal or congenital deafness, superior visual motion detection abilities have been psychophysically identified in both humans and cats, and this advantage has been causally demonstrated to be mediated by reorganized auditory cortex. In our study, we investigated visually evoked potentials (VEPs) in response to motion-onset stimuli of varying speeds in both hearing and perinatally deafened cats under light anesthesia. Although the peak latencies did not differ between the two groups, we observed significantly greater VEP amplitudes in deaf cats, specifically in the P1 component and the signal power of the overall waveform. Through sigmoidal modeling, we identified that the speed offset and steepness at the threshold for 50% maximum neural activity was unchanged, showing that neuronal activity was modulated by motion speeds in a comparable manner between the hearing and deaf subjects and the deaf had greater potentials at all dot speeds. Our results suggest that the increased cortical activity by the auditory and visual cortices of deaf cats may account for their superior behavioral advantage in motion detection and indicates that cross-modal plasticity plays a significant role in the cortical processing of motion. NEW & NOTEWORTHY The present study investigated cross-modal plasticity after perinatal deafness in cats using motion-onset visually evoked potentials. Deaf animals were observed to have significantly greater evoked potentials in both peak components and the signal power of the overall waveforms. These results are discussed in relation to prior studies on deaf subjects in both human and animal research on evoked potentials and psychophysics.

It has long been known that a neural circuit situated in the spinal cord of mammals is independently capable of generating and modulating locomotor movements. Following its initial discovery over a century ago, a great deal of research has been focused on characterizing this neural circuit to determine how it is able to elicit movement. For much of the 20th century, difficulty in identifying individual component interneurons that comprised this neural circuit resulted in it being considered a powerful but mysterious "black box." In this article, we will review the development of a number of innovative experimental approaches that have brought us to the current state of research in the field, where we are able to identify populations that comprise this neural circuit, pinpoint their specific function, and image their activity in real time during a locomotor task.

Glioblastoma (GBM), a highly aggressive brain tumor predominantly affecting individuals over 40, often co-occurs with sleep disorders. However, the causal relationship remains unclear. This study employed a bidirectional Mendelian randomization (MR) approach to investigate the causal links between sleep traits/disorders and GBM. Sleep trait and disorder data were obtained from the IEU Open GWAS Project, while GBM data came from the Finn cohort. Primary analysis utilized the inverse-variance weighted (IVW) method, complemented by MR-Egger, weighted median, and weighted mode methods. MR pleiotropy residual sum and outlier (MR-PRESSO) was applied to detect potential outliers, and MR-Egger regression explored horizontal pleiotropy, with Cochran's Q test assessing heterogeneity. IVW analysis indicated a significant negative association between sleep duration and GBM risk [odds ratio (OR) = 0.13; 95% confidence interval (CI) = 0.02-0.80; P = 0.027). Conversely, GBM was positively associated with evening chronotype (OR = 1.0094; 95% CI = 1.0034-1.0154; P = 0.002). No significant associations were found for other sleep traits or disorders. Midday napping showed potential pleiotropy, and significant heterogeneity was noted in the reverse analysis. MR-PRESSO identified no outliers. Shorter sleep duration may elevate GBM risk, and GBM might influence circadian preference toward eveningness. Further studies are warranted to validate these findings.NEW & NOTEWORTHY This study employs a bidirectional Mendelian randomization approach to explore the causal relationship between various sleep traits, sleep disorders, and glioblastoma (GBM). We found that shorter sleep duration may increase GBM risk, while GBM may shift individuals toward an evening chronotype. No significant relationships were observed for other sleep traits or any of the sleep disorders. These findings illuminate the complex interplay between sleep and GBM, highlighting the need for further investigation into their correlations.