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Finally, we highlight rodent and human studies supporting the critical involvement of CRTC1 in depression-associated obesity.[This corrects the article DOI 10.3389/fnins.2021.792264.].

Ischemic stroke (IS) is a common disease endangering human life and health. Cerebral ischemia triggers a series of complex harmful events, including excitotoxicity, inflammation and cell death, as well as increased nitric oxide production through the activation of nitric oxide synthase (NOS). Oxidative stress plays a major role in cerebral ischemia and reperfusion. Sphingosine 1-phosphate receptor subtype 3 (S1PR3), a member of S1P's G protein-coupled receptors S1PR1-S1PR5, is involved in a variety of biological effects in the body, and its role in regulating oxidative stress during cerebral ischemia and reperfusion is still unclear.

Transient middle cerebral artery occlusion (tMCAO) mice were selected as the brain ischemia-reperfusion (I/R) injury model. Male C57/BL6 mice were treated with or without a selective S1PR3 inhibition after tMCAO, and changes in infarct volume, Nissl staining, hematoxylin-eosin (H&E) staining and NOS protein, nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA) content after tMCAO were observed.

In the cerebral ischemia-reperfusion model, inhibition of S1PR3 improved the infarct volume and neuronal damage in mice after tMCAO. see more Similarly, inhibition of S1PR3 can reduce the expression of NO synthase subtype neuronal NOS (nNOS) and reduce the production of NO after cerebral ischemia. After cerebral ischemia and reperfusion, the oxidative stress response was enhanced, and after the administration of the S1PR3 inhibitor, the SOD content increased and the MDA content decreased, indicating that S1PR3 plays an important role in regulating oxidative stress response.

Inhibiting S1PR3 attenuates brain damage during I/R injury by regulating nNOS/NO and oxidative stress, which provides a potential new therapeutic target and mechanism for the clinical treatment of IS.

Inhibiting S1PR3 attenuates brain damage during I/R injury by regulating nNOS/NO and oxidative stress, which provides a potential new therapeutic target and mechanism for the clinical treatment of IS.Rett syndrome (RTT) is a neurodevelopmental disorder that represents the most common genetic cause of severe intellectual disability in females. Most patients carry mutations in the X-linked MECP2 gene, coding for the methyl-CpG-binding protein 2 (MeCP2), originally isolated as an epigenetic transcriptional factor able to bind methylated DNA and repress transcription. Recent data implicated a role for glia in RTT, showing that astrocytes express Mecp2 and that its deficiency affects their ability to support neuronal maturation by non-cell autonomous mechanisms. To date, some molecular, structural and functional alterations have been attributed to Mecp2 null astrocytes, but how they evolve over time and whether they follow a spatial heterogeneity are two aspects which deserve further investigations. In this study, we assessed cytoskeletal features of astrocytes in Mecp2 deficient brains by analyzing their arbor complexity and processes in reconstructed GFAP+ cells at different ages, corresponding to peculiar sal astrocytic features. qRT-PCR data corroborated our results, reporting an overall decrement of gene expression, which is area and age-dependent. In conclusion, our data show that Mecp2 deficiency causes structural and molecular alterations in astrocytes, which progress along with the severity of symptoms and diversely occur in the different cerebral regions, highlighting the importance of considering heterogeneity when studying astrocytes in RTT.The Psychomotor Vigilance Test (PVT) is a widely used behavioral attention measure, with the 10-min (PVT-10) and 3-min (PVT-3) as two commonly used versions. The PVT-3 may be comparable to the PVT-10, though its convergent validity relative to the PVT-10 has not been explicitly assessed. For the first time, we utilized repeated measures correlation (rmcorr) to evaluate intra-individual associations between PVT-10 and PVT-3 versions across total sleep deprivation (TSD), chronic sleep restriction (SR) and multiple consecutive days of recovery. Eighty-three healthy adults (mean ± SD, 34.7 ± 8.9 years; 36 females) received two baseline nights (B1-B2), five SR nights (SR1-SR5), 36 h TSD, and four recovery nights (R1-R4) between sleep loss conditions. The PVT-10 and PVT-3 were completed every 2 h during wakefulness. Rmcorr compared responses on two frequently used, sensitive PVT metrics reaction time (RT) via response speed (1/RT) and lapses (RT > 500 ms on the PVT-10 and > 355 ms on the PVT-3) by day (e.g., B2), by study phase (e.g., SR1-SR5), and by time point (1000-2000 h). PVT 1/RT correlations were generally stronger than those for lapses. The majority of correlations (48/50 [96%] for PVT lapses and 38/50 [76%] for PVT 1/RT) were values below 0.70, indicating validity issues. Overall, the PVT-3 demonstrated inadequate convergent validity with the "gold standard" PVT-10 across two different types of sleep loss and across extended recovery. Thus, the PVT-3 is not interchangeable with the PVT-10 for assessing behavioral attention performance during sleep loss based on the design of our study and the metrics we evaluated. Our results have substantial implications for design and measure selection in laboratory and applied settings, including those involving sleep deprivation.

Functional brain imaging has become the dominant approach to the study of brain-behavior relationships. Unfortunately, the behavior half of the equation has been relegated to second-class status when it is not ignored completely. Different approaches to connectivity, based on temporally correlated physiological events across the brain, have ascended in place of behavior. A performance-based analysis has been developed as a simple, basic approach to incorporating specific performance measures obtained during imaging into the analysis of the imaging data identifying clinically relevant regions.

This paper contrasts performance-based lateralized regional cerebral blood flow (CBF) predictors of speech rate during Positron Emission Tomography with the values of these regions and their opposite hemisphere homologs in which a performance-based model was not applied. Five studies were examined two that utilized normal speakers, one that utilized ataxic speakers, and two that examined Parkinsonian speakers.

In egic groups. While the predictors are lateralized consistent with lesion data, the blood flow values of these regions are neither lateralized nor distinguished from their opposite hemisphere homologs in their magnitudes. The consistent differences between regional blood flow values and their corresponding regression coefficients in predicting performance suggests the presence of functional meta-networks that orchestrate the contributions of specific brain regions in support of mental and behavioral functions.The spatial-numerical associations of response codes (SNARC) effect reveals that individuals can represent numbers spatially. In this study, event-related potential (ERP) technology was used to probe the effect of verbal-spatial task instructions on spatial-numerical association coding by using digit parity and magnitude judgment tasks, with the numbers 1-9 (except 5) and Chinese word labels ("left" and "right") as experimental materials. The behavioral results of Experiment 1 showed that the SNARC effect was mainly based on verbal-spatial coding and appeared when the stimulus onset asynchrony (SOA) between the presentation of the verbal labels and the target digit was 0 ms. ERP results did not reveal any significant SNARC-related effects in either the N1 or P3 components. The behavioral results of Experiment 2 again showed that the SNARC effect was dominated by verbal-spatial coding. ERP results showed that significant effects related to verbal-spatial coding were found in both the early positive deflection of the stimulus-locked lateralized readiness potential (S-LRP) and the latency of the response-locked LRP (R-LRP). Hence, in this study, the nature of the spatial coding of the digit magnitudes was influenced by the processing of the word labels and affected both the response selection and response preparation stages.

It is controversially discussed in how far smoking contributes to diabetic polyneuropathy (DPN) in type 2 diabetes (T2D). Diffusion-weighted magnetic resonance neurography (MRN) at 3 Tesla has been shown to provide objective values for structural nerve integrity in patients with T2D. The aim of this study was to investigate the contribution of cigarette smoking on structural nerve integrity in T2D.

This cross-sectional prospective cohort study investigated the structural integrity of the sciatic nerve in 10 smokers, 40 never-smokers, and 20 ex-smokers with T2D and 10 healthy control subjects, using diffusion tensor imaging MRN at 3 Tesla and semi-automated nerve fiber tracking. Results were correlated with clinical, electrophysiological, and serological data.

The sciatic nerve's fractional anisotropy (FA), a parameter for structural nerve integrity, was significantly lower in smokers with T2D when compared to controls (

= 0.002) and never-smokers (

= 0.015), and lower in ex-smokers when compared to DPN due to glycemic stress and less microangiopathy-associated myelin damage in active smokers, while angiopathic effects predominate in ex-smokers. To stop smoking may therefore pose a promising preventive measure to slow the progression of DPN in T2D.

The findings indicate that smoking contributes to sciatic nerve damage in T2D, potentially worsening DPN due to glycemic stress and less microangiopathy-associated myelin damage in active smokers, while angiopathic effects predominate in ex-smokers. To stop smoking may therefore pose a promising preventive measure to slow the progression of DPN in T2D.Neural tissue is a hierarchical multiscale system with intracellular and extracellular diffusion compartments at different length scales. The normal diffusion of bulk water in tissues is not able to detect the specific features of a complex system, providing nonlocal, diffusion measurement averaged on a 10-20 μm length scale. Being able to probe tissues with sub-micrometric diffusion length and quantify new local parameters, transient anomalous diffusion (tAD) would dramatically increase the diagnostic potential of diffusion MRI (DMRI) in detecting collective and sub-micro architectural changes of human tissues due to pathological damage. In DMRI, the use of tAD parameters quantified using specific DMRI acquisition protocols and their interpretation has often aroused skepticism. Although the derived formulas may accurately fit experimental diffusion-weighted data, the relationships between the postulated dynamical feature and the underlying geometrical structure remains elusive, or at most only suggestive. Ththe strongest associations with AxDiam and ELD. On the other hand, α-metrics showed strong associations with SD ax.diam and was significantly related to AxDens, suggesting its ability to quantify local heterogeneity degree in neural tissue. These results elucidate the biophysical mechanism underpinning tAD parameters and show the clinical potential of tAD-imaging, considering that both physiologic and pathologic neurodegeneration translate into alterations of WM morphometry and topology.