Neuroscience最新文献

There is mounting evidence for the involvement of the immune system, neuroinflammation and disturbed gut microbiota, or dysbiosis, in attentive-deficit/hyperactivity disorder (ADHD). Gut dysbiosis is strongly implicated in many physical, autoimmune, neurological, and neuropsychiatric conditions, however knowledge of its particular pathogenic role in ADHD is sparse. As such, this narrative review examines and synthesizes the available evidence related to inflammation, dysbiosis, and neural processes in ADHD. Minimal differences in microbiota diversity measures between cases and controls were found, however many relative abundance differences were observed at all classification levels (phylum to strain). Compositional differences of taxa important to key gut-brain axis pathways, in particular Bacteroides species and Faecalibacterium, may contribute to inflammation, brain functioning differences, and symptoms, in ADHD. We have identified one possible model of ADHD etiopathogenesis involving systemic inflammation, an impaired blood-brain barrier, and neural disturbances as downstream consequences of gut dysbiosis. Nevertheless, studies conducted to date have varied degrees of methodological rigour and involve diverse participant characteristics and analytical techniques, highlighting a need for additional research.

Background: Opioid-induced hyperalgesia (OIH) is a serious complication during the pain treatment. Ketamine has been commonly reported to treat OIH, but the mechanisms remain unclear. Gut microbiota is recently recognized as one of the important mechanisms underlying the occurrence and treatment of OIH. However, whether ketamine enantiomers could alleviate OIH through gut microbiota that still needs to be clarified.

Methods: The OIH model was established by morphine injection for 3 consecutive days, followed by hierarchical clustering analysis of behavioral results into susceptible or resilient group. Broad-spectrum antibiotic cocktail (ABx) was used to eradicated the gut microbiota of mice. Subsequently, fecal microbiota transplantation (FMT) was performed. S- or R-ketamine was administered as pretreatment 30 min before morphine injection. Fecal samples were collected for 16S rRNA gene sequencing after completion of all behavioral tests.

Results: Approximately 60% of the mice developed OIH after morphine exposure with abnormal locomotion and anxiety-like behaviors. Pseudo germ-free mice treated with ABx did not develop hyperalgesia, whereas pseudo germ-free mice that received fecal microbiota transplantation from OIH mice developed hyperalgesia. Interestingly, S-ketamine but not R-ketamine rescued mice from OIH. The principal co-ordinates analysis (PCoA) suggested that the distribution of gut microbiota differed among the groups. Importantly, levels of Enterobacteriaceae were increased in OIH susceptible group, while decreased after S-ketamine treatment.

Conclusion: S-ketamine but not R-ketamine was able to alleviate morphine-induced OIH, and this mechanism is probably related to decreasing the levels of gut Enterobacteriaceae.

Most activities of daily life involve some degree of coordinated, bimanual activity from the upper limbs. However, compared to single-handed movements, bimanual movements are processed, learned, and controlled from both hemispheres of the brain. Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique that enhances motor learning by modulating the activity of movement-associated brain regions. While effective in simple, single-handed tasks, tDCS has shown mixed results in complex bimanual tasks. This study investigated the effects of bilateral M1 anodal tDCS (biM1 a-tDCS) on learning and cortical excitability during a customized, bimanual racing videogame task. Thirty-six right-handed adults completed three lab visits (∼48 h apart), practicing the task while receiving either biM1 a-tDCS or SHAM tDCS. Cortical excitability was measured with transcranial magnetic stimulation (TMS) and electromyography (EMG) before and after the first visit. Though all subjects demonstrated improvements over the course of the study, our analyses revealed significantly faster rates of learning on days 1 & 2, but not day 3, of practice in subjects receiving biM1 a-tDCS. Moreover, perhaps due to differences in baseline gaming experience and aptitude, this effect appeared to be stronger in female subjects. Interestingly, no significant differences in corticomotor excitability were observed between conditions. Though biM1 a-tDCS did not appear to impact corticomotor excitability, our results contribute to the growing body of evidence which seems to suggest that multifocal tDCS protocols may be superior to traditional, single-site tDCS for the enhancement of bimanual motor learning.

Cerebrolysin (CBL) is a combination of neurotrophic peptides and amino acids derived from pig brains. CBL can cross the blood-brain barrier (BBB) and its biological effect is similar to the effect of endogenous neurotrophic effects. The mechanism of action of CBL is related to the induction of neurogenesis, neuroplasticity, neuroprotection, and neurotrophicity. Therefore, CBL may be effective against the development and progression of neurodegenerative diseases such as Alzheimer disease (AD) and cerebrovascular disorders such as vascular dementia (VD). Moreover, many studies highlighted that CBL is effective in the improvement of cognitive impairment in patients with neurodegenerative diseases. However, the underlying neuroprotective effects of CBL against the VD neuropathology were not fully elucidated. Thus, this review aims to discuss the possible therapeutic efficacy of CBL in the management of VD. In conclusion, CBL could be effective therapeutic strategy in preventing and treating VD by targeting neuroinflammation, BBB injury, and chronic cerebral hypoperfusion.

Scopolamine is the secondary metabolite of the Datura stramonium and act as a muscarinic receptor antagonist. Previous studies showed that scopolamine caused attention and memory deficit. However, the effects of scopolamine on specific cognitive functions, such as fear learning and social recognition, remain poorly understood. Here, we demonstrate the effects of scopolamine on fear learning, social memory, and neural activity in zebrafish, providing a novel perspective on its impact on cognitive and social behaviors. Here, we used equal number of male and female zebrafish as an animal model and performed a series of behavioral tests after treatment with scopolamine (100 µM and 200 µM) for 1 h to evaluate social and cognitive functions. Treatment with scopolamine increased locomotion activity, reduced the level of anxiety in the novel tank diving test, and impaired memory retrieval in the active avoidance test. Scopolamine also increased the preference for newly introduced fish in the social recognition test. In situ hybridization of c-fos mRNA showed that scopolamine decreased the neural activity of the telencephalic regions that are crucial for social, cognitive, and memory functions. Our results demonstrate the effects of scopolamine on fear learning and social recognition in adult zebrafish.

While our understanding of the neurobiological mechanisms underlying cocaine and opiate reward has historically been dopamine-focused, evidence from genetic and pharmacological approaches indicates that µ-opioid receptors (MORs) in the striatum are important contributors. Within the striatum, MORs are expressed in both dopamine D1-receptor and D2-receptor expressing GABAergic medium spiny neurons (MSNs), as well as in interneurons and various afferents. Thus, it remains unclear how these distinct MOR populations regulate drug reward. To address this, we generated mice with a targeted deletion of MORs from dopamine D2 receptor-expressing MSNs (D2-MORKO) and tested the locomotor and conditioned rewarding effects of cocaine and morphine. D2-MORKO mice showed blunted acquisition of cocaine place preference and suppressed expression of preference when tested in the presence of cocaine. Conversely, the acute and sensitized locomotor responses to cocaine and morphine, as well as morphine conditioned place preference, were normal in D2-MORKOs. This indicates MORs expressed in D2-MSNs facilitate cocaine reward. Further, these data suggest these MORs play divergent roles in cocaine and morphine reward.

Insect research has significantly advanced neuroscience by addressing fundamental questions, with groundbreaking discoveries emerging from research carried out in Uruguay. Powered by technological advances, the field has seen milestones in ultrastructure, neuronal and synaptic structure, and complex behavioral findings. Key contributions include the first formal description of chemical synapses, the identification of synaptic vesicle origins in the endoplasmic reticulum, and pioneering work on eye induction and development. Uruguay's research has also provided critical insights into neural degeneration and repair mechanisms, the functional microanatomy of the visual pathway, and mechanoreception. This review highlights four decades of Uruguayan legacy in insect neuroscience, underscoring how a small, yet vibrant, community of researchers has embraced interdisciplinary collaborations and innovative methodologies. Additionally, this review addresses the evolving role of women in the field and the collaborative spirit that has propelled scientific discovery, marking a critical juncture in the development of insect neuroscience. Despite limited resources, Uruguay has played a pivotal role in advancing our understanding of brain organization, neuronal-glial interactions, and connectomics, making lasting contributions to both local and global neuroscience.

Purpose: The neuropathologic mechanisms of sudden sensorineural hearing loss (SSNHL) are unknown. The aim of this study was to investigate the alterations of neurovascular coupling (NVC) in patients with SSNHL and its association with hematologic inflammatory factors.

Methods: The amplitude of low-frequency fluctuations (ALFF), fractional amplitude of low-frequency fluctuations (fALFF), regional homogeneity (ReHo), and degree centrality (DC) were calculated in 48 patients with SSNHL and 54 age-, gender-, and education-matched healthy control (HC), and also utilized the arterial spin labeling imaging (ASL) to calculate cerebral blood flow (CBF). Four indices of NVC (CBF-ALFF, CBF-fALFF, CBF-ReHo, and CBF-DC) in the whole brain gray matter as well as the NVC ratio were compared between two groups. In addition, correlation analyses were performed with inflammatory factors for the NVC indexes at the global level and regional level, respectively.

Results: The NVC at global level was lower in SSNHL group than in HC, except for CBF-ALFF. At the regional level, most of the brain regions with abnormal NVC in SSNHL patients involved auditory and sensorimotor language centers and limbic system compared to HC. In addition, both at the global and regional levels, NVC metrics were shown to correlate with partial inflammatory factors or hematologic parameters, including platelet-lymphocyte ratio (PLR), neutrophil-lymphocyte ratio (NLR), systemic immunoinflammatory index (SII), blood platelet count (PLT), and lymphocyte count (Lym).

Conclusion: From the view of the NVC metrics, these findings provide new perspectives on the neuropathologic mechanisms and clinical treatment of SSNHL.