Neuroscience最新文献

Prepulse inhibition (PPI) refers to the phenomenon in which a weak sensory stimulus before a strong one significantly reduces the startle reflex caused by the strong stimulus. Perceptual spatial separation, a phenomenon where auditory cues from the prepulse and background noise are distinguished in space, has been shown to enhance PPI. This study aims to investigate the neural modulation mechanisms of PPI by the spatial separation between the prepulse stimulus and background noise, particularly in the deep superior colliculus (deepSC). The experiment used 11 anesthetized male Sprague-Dawley rats, with electrodes implanted in the left deepSC nd the right inferior colliculus (IC). The prepulse stimulus was a segment of narrowband noise, with interaural time differences adjusted so that the prepulse stimulus and background noise were perceived as either ipsilaterally leading or contralaterally leading, resulting in perceptual spatial fusion or spatial separation. The results showed that under conditions of spatial separation, the stimulus-response coherence of the envelope and fine structure components of the prepulse stimulus in the deepSC was significantly enhanced, the response of the deepSC to the stimulus was significantly reduced in the presence of the prepulse stimulus, and the envelope component of the prepulse stimulus was positively correlated with the inhibitory effect. The above results suggest that perceptual spatial dissociation can significantly enhance the expression of deepSC, particularly the precision of the envelope component, thereby significantly affecting the electrophysiological response of PPI.

The diagnosis and analysis of major depressive disorder (MDD) faces some intractable challenges such as dataset limitations and clinical variability. Resting-state functional magnetic resonance imaging (Rs-fMRI) can reflect the fluctuation data of brain activity in a resting state, which can find the interrelationships, functional connections, and network characteristics among brain regions of the patients. In this paper, a brain functional connectivity matrix is constructed using Pearson correlation based on the characteristics of multi-site Rs-fMRI data and brain atlas, and an adaptive propagation operator graph convolutional network (APO-GCN) model is designed. The APO-GCN model can automatically adjust the propagation operator in each hidden layer according to the data features to control the expressive power of the model. By adaptively learning effective information in the graph, this model significantly improves its ability to capture complex graph structural patterns. The experimental results on Rs-fMRI data from 1601 participants (830 MDD and 771 HC) and 16 sites of REST-meta-MDD project show that the APO-GCN achieved a classification accuracy of 91.8%, outperforming those of the state-of-the-art classifier methods. The classification process is driven by multiple significant brain regions, and our method further reveals functional connectivity abnormalities between these brain regions, which are important biomarkers of classification. It is worth noting that the brain regions identified by the classifier and the networks involved are consistent with existing research results, which suggest that the pathogenesis of depression may be related to dysfunction of multiple brain networks.

Bayesian brain theory, a computational framework grounded in the principles of Predictive Processing (PP), proposes a mechanistic account of how beliefs are formed and updated. This theory assumes that the brain encodes a generative model of its environment, made up of probabilistic beliefs organized in networks, from which it generates predictions about future sensory inputs. The difference between predictions and sensory signals produces prediction errors, which are used to update belief networks. In this article, we introduce the fundamental principles of Bayesian brain theory, and show how the brain dynamics of prediction are associated with the generation and evolution of beliefs.

Media multitasking has become pervasive in our daily lives, yet its impact on cognitive abilities remains contentious, with more evidence supporting adverse effects (scattered attention hypothesis) than benefits (trained attention hypothesis). Recent studies have increasingly focused on the training effects of behavioral training on anticipatory brain functions, which involve cognitive and motor preparation before stimulus onset, assessed using event-related potentials (ERPs). This study investigated whether media multitasking enhances anticipatory brain functions and how task difficulty influences this relationship. Participants performed a response discrimination task where they detected targets among distractors, with salient and nonsalient targets manipulating task difficulty. Behavioral results indicated faster response times and comparable accuracy in heavy media multitaskers (HMM) compared to light media multitaskers (LMM) across both salient and nonsalient conditions, suggesting that media multitasking can expedite responses without sacrificing accuracy. The larger Bereitschaftspotential (BP) amplitude observed in HMM compared to LMM reflects heightened motor preparation in HMM, consistent with their quicker responses. The larger prefrontal negativity (pN) and P3 amplitudes in the nonsalient condition for HMM indicate increased cognitive preparation before stimulus onset and heightened attention control after stimulus onset. Our results suggest that HMM can flexibly adjust resource allocation based on task demands to maintain their response speed advantage. These findings suggest that LMM may possess a relatively steady acceleration/brake system, whereas HMM exhibit a more adaptable system capable of responding flexibly to diverse situations. Overall, these results underscore the training effects of media multitasking on anticipatory brain functions, supporting the trained attention hypothesis.

Incidences of seizure after e-cigarette use in adolescents and young adults have been reported, raising the concern about the risk of nicotine overconsumption. Few previous studies have investigated the effects of nicotine at high doses on brain and behavior in adolescent animals. In this study, the effects of a 15-day repeated nicotine treatment at a daily dose of 2 mg/kg body weight were investigated in adolescent and adult male rats. Nicotine treatment abolished body weight gain in the adults, but did not affect the body weight significantly in the adolescents. Only the nicotine-treated adolescents showed significant changes in brain anatomy 1 day post-treatment, which manifested as a significant reduction of whole-brain gray matter (GM) volume, a further reduction of regional GM volume in the medial prefrontal cortex (mPFC) and altered GM volume covariations between the mPFC and a number of brain regions. The mPFC of nicotine-treated adolescent rats did not exhibit evident signs of neuronal degeneration and reactive astrocytosis, but showed a significantly decreased expression of presynaptic marker synaptophysin (SYN), along with a significantly increased oxidative stress and a significantly elevated expressions of microglial marker ionized calcium binding adaptor molecule 1 (IBA1). Together, these results suggested that repeated nicotine overdosing may shift regional redox, modulate microglia-mediated pruning, and give rise to structural/connectivity deficits in the mPFC of adolescent male rats.

This study explored surface brain morphometry in type 1 diabetes including focus on painful diabetic peripheral neuropathy (DPN). Brain MRI was obtained from 56 individuals with diabetes (18 without DPN, 19 with painless DPN, 19 with painful DPN) and 20 healthy controls. Cortical thickness, sulcus depth, and gyrification were analysed globally and regionally in each group and in the combined diabetes group. Associations with clinical characteristics and pain were assessed. Globally, cortical thickness was reduced in the combined diabetes group and in painful DPN compared to healthy controls. No differences in sulcus depth and gyrification were found. Several regions, including the middle frontal gyrus showed reduced cortical thickness in the combined diabetes- and painful DPN group. The postcentral gyrus exhibited reduced cortical thickness in painful DPN compared to healthy controls, and reduced sulcus depth compared to painless DPN correlating with higher pain intensity. Cortical thinning manifested across the brain cortex in diabetes, especially for painful DPN. Altered postcentral gyrus morphometry may be associated with neuropathic pain. Assessing cortical morphometry may be critical for comprehending central neuropathy and the manifestation of painful DPN in diabetes.

Diabetic peripheral neuropathy (DPN) is the most common form of diabetic neuropathy, representing 75% of cases and posing a substantial public health challenge. Emerging evidence from animal studies indicates that stem cell therapy holds significant promise as a potential treatment for diabetic neuropathy. Nevertheless, a comprehensive evaluation of the safety and efficacy of stem cell therapy for DPN in animal studies remains outstanding. A systematic search of MEDLINE, Embase, Scopus, the Web of Science, and the CENTRAL was performed. The time period was up to January 31, 2024. All animal studies investigating the stem cell therapy for treating DPN were included. A random-effects model to combine effect sizes in our meta-analysis was applied. 29 out of the 5431 records met the eligibility criteria. In these studies, stem cell therapy improved motor and sensory nerve conduction velocity, compound muscle action potential (CMAP), and sciatic nerve blood flow. Post-treatment, mechanical and thermal nociceptive thresholds decreased. Rats had significant improvement in axonal circularity, nerve growth factor, and transforming growth factor beta 1; mice had significant increase in weight, CMAP, and angiopoietin 1. The stem cell subgroup analysis showed that dental pulp stem cells had the greatest effects across all parameters, while bone marrow mononuclear cells had strong biochemical responses. Stem cell therapy demonstrates promising efficacy in ameliorating neuropathic symptoms in DPN animal models. Human patient studies and targeted treatment procedures for specific neuropathic disorders are advocated to improve therapeutic outcomes.

Virtual reality (VR) technology has emerged as a ground-breaking tool in neuroscience, revolutionizing our understanding of neuroplasticity and its implications for neurological rehabilitation. By immersing individuals in simulated environments, VR induces profound neurobiological transformations, affecting neuronal connectivity, sensory feedback mechanisms, motor learning processes, and cognitive functions. These changes highlight the dynamic interplay between molecular events, synaptic adaptations, and neural reorganization, emphasizing the potential of VR as a therapeutic intervention in various neurological disorders. This comprehensive review delves into the therapeutic applications of VR, focusing on its role in addressing multiple conditions such as stroke, traumatic brain injuries, phobias, and post-traumatic stress disorder. It highlights how VR can enhance motor recovery, cognitive rehabilitation, and emotional resilience, showcasing its potential as an innovative and effective tool in neurological rehabilitation. Integrating molecular neuroscience with VR technology allows for a deeper understanding of the molecular mechanisms underlying neuroplasticity, opening doors to personalized interventions and precise treatment strategies for individuals with neurological impairments. Moreover, the review emphasizes the ethical considerations and challenges that come with implementing VR-based interventions in clinical practice, stressing the importance of data privacy, informed consent, and collaborative interdisciplinary efforts. By leveraging advanced molecular imaging techniques, VR-based research methodologies, and computational modelling, the review envisions a future where VR technology plays a central role in revolutionizing neuroscience research and clinical neurorehabilitation, ultimately providing tailored and impactful solutions for individuals facing neurological challenges.

It is becoming increasingly recognized that, in addition to psychological stress, unbalanced maternal nutritional habits can threaten fetal brain development. Maternal obesity is one of the most pressing public health problems facing the world today, as about 40% of pregnant women are obese or gain excessive weight worldwide. This condition can negatively impact offspring's brain development, increasing the risk for autism spectrum disorders, cognitive deficits, attention deficit hyperactivity disorder, as well as anxiety and depression. In the context of fetal development, nutritional interventions may represent a feasible and safe approach for preventing the negative effects of maternal obesity. We argue that maternal Omega-3 supplementation, among the many dietary strategies available, is especially promising as it buffers oxidative stress and inflammation, both recognized as candidate mechanisms underlying the negative long-term effects of maternal obesity on the offspring. Notwithstanding the current knowledge, both preclinical studies and clinical trials are needed to refine current strategies addressing dietary content and length of administration according to individual characteristics and needs.

Neurodegenerative diseases are a group of disorders characterized by progressive degeneration of discrete groups of neurons causing severe disability. The main risk factor is age, hence their incidence is rapidly increasing worldwide due to the rise in life expectancy. Although the causes of the disease are not identified in about 90% of the cases, in the last decades there has been great progress in understanding the basis for neurodegeneration. Different pathological mechanisms including oxidative stress, mitochondrial dysfunction, alteration in proteostasis and inflammation have been addressed as important contributors to neuronal death. Despite our better understanding of the pathophysiology of these diseases, there is still no cure and available therapies only provide symptomatic relief. In an effort to discover new therapeutic approaches, natural products have aroused interest among researchers given their structural diversity and wide range of biological activities. In this review, we focus on three plant-derived compounds with promising neuroprotective potential that have been traditionally used by folk medicine: the flavonoid quercetin (QCT), the phytocannabinoid cannabidiol (CBD)and the tryptamine N,N-dimethyltryptamine (DMT). These compounds exert neuroprotective effects through different mechanisms of action, some overlapping, but each demonstrating a principal biological activity: QCT as an antioxidant, CBD as an anti-inflammatory, and DMT as a promoter of neuroplasticity. This review summarizes current knowledge on these activities, potential therapeutic benefits of these compounds and their limitations as candidates for neuroprotective therapies. We envision that treatments with QCT, CBD, and DMT could be effective either when combined or when targeting different stages of these diseases.