Biology subjects

Lee, S. H.

Publications and source records attributed to Lee, S. H..

At least 55 records · Page 3Linked to original sources

bioRxiv2024

Investigation of the Fasciola Cinereum, Absent in BTBR mice, and Comparison with the Hippocampal Area CA2

The arginine vasopressin 1b receptor (Avpr1b) plays an important role in social behaviors including social learning, memory, and aggression, and is known to be a specific marker for the cornu ammonis area 2 (CA2) regions of the hippocampus. The fasciola cinereum (FC) is an anatomical region in which Avpr1b expressing neurons are prominent, but the functional roles of the FC have yet to be investigated. Surprisingly, the FC is absent in the inbred BTBR T+tf/J (BTBR) mouse strain used to study core behavioral deficits of autism. Here, we characterized and compared transcriptomic expression profiles using single nucleus RNA sequencing and identified 7 different subpopulations and heterogeneity within the dorsal CA2 (dCA2) and FC. Mef2c, involved in autism spectrum disorder, is more highly expressed in the FC. Using Hiplex in situ hybridization, we examined the neuroanatomical locations of these subpopulations in the proximal and distal regions of the hippocampus. Anterograde tracing of Avpr1b neurons specific for the FC showed projections to the IG, dCA2, lacunosum molecular layer of CA1, dorsal fornix, septofibrial nuclei, and intermediate lateral septum (iLS). In contrast to the dCA2, inhibition of Avpr1b neurons in the FC by the inhibitory DREADD system during behavioral testing did not impair social memory. We performed single nucleus RNA sequencing in the dCA2 region and compared between wildtype (WT) and BTBR mice. We found that transcriptomic profiles of dCA2 neurons between BTBR and WT mice are very similar as they did not form any unique clusters; yet, we found there were differentially expressed genes between the dCA2s of BTBR and WT mice. Overall, this is a comprehensive study of the comparison of Avpr1b neuronal subpopulations between the FC and dCA2. The fact that FC is absent in BTBR mice, a mouse model for autism spectrum disorder, suggests that the FC may play a role in understanding neuropsychiatric disease.

neuroscience↗

bioRxiv2024

Hypoxia disrupts circadian rhythms in astrocytes and causes synapse engulfment defects

Astrocytes are emerging as key regulators of neuronal synaptic network maturation and function, through control of synaptic pruning. This is important, because individuals with ASD have excess glutamatergic synapses in the cortex, but the biological mechanisms underlying this phenotype remain unclear. Here, we used human cortical organoids (hCO) derived from induced pluripotent stem cells (hiPSCs), to examine the effect of hypoxia on synapse engulfment in human astrocytes at postnatal-equivalent stages of development. We identified that hypoxia significantly inhibits the synaptosome phagocytosis, and that this phenotype is mediated through disruptions in the astrocytic circadian rhythm molecular pathway and subsequent decreased expression of MEGF10. Lastly, we demonstrated that circadian clock disruptions are sufficient to induce these observed phenotypes even in the absence of hypoxia, both in hCOs and within the mouse hippocampus in vivo. Our study uncovers a novel mechanistic link between hypoxia, circadian rhythms disruptions, and synapse pruning by astrocytes, and provides insight into the pathophysiology of ASD, and other neuropsychiatric diseases. Separately, the demonstration of the presence of circadian rhythms in hCOs opens an unprecedented opportunity to dissect the role of circadian clocks in normal brain development and how it contributes to specific diseases of environmental or genetic origin.

neuroscience↗

bioRxiv2024

Modular Phoneme Processing in Human Superior Temporal Gyrus

Modular organization is fundamental to cortical processing, but its presence is human association cortex is unknown. We characterized phoneme processing with 128-1024 channel micro-arrays at 50-200m pitch on superior temporal gyrus of 7 patients. High gamma responses were highly correlated within [~]1.7mm diameter modules, sharply delineated from adjacent modules with distinct time-courses and phoneme-selectivity. We suggest that receptive language cortex may be organized in discrete processing modules.

neuroscience↗

bioRxiv2023

Spatial dissection of cellular heterogeneity and functional crosstalk in the tumor microenvironments of gastric cancers

Spatial transcriptomics offers unprecedented challenges in characterizing tumor ecosystems, encompassing tumor cells and their surrounding tumor microenvironments (TME) along with cellular interactions therein. Here, we conducted Visium-based spatial transcriptomics on nine primary gastric cancers (GC) to translate the spatial organization of GC ecosystems into the functional landscape of cellular crosstalk across malignant, stromal and immune cells. We identified three distinct GC subtypes of 3 immunogenic, 3 epithelial and 3 stromal GCs with elevated infiltration of immune, malignant cells and fibroblasts reflecting the heterogeneity of the cell types and their interactions in GC TME. GC spatial architecture was further delineated into 6 regional compartments with varying degree of TME infiltration, among which the fibroblast-enriched TME was associated with the upregulation of epithelial-to-mesenchymal transformation (EMT) and immune response in malignant and immune cells, respectively. Cell type-specific transcriptional dynamics representing cellular crosstalk between TME cells were further identified, e.g., the infiltration of malignant and endothelial cells promote the cellular proliferations of TME cells whereas the fibroblasts and immune cells are associated with pro-cancer and anti-cancer immunity, respectively. Ligand-receptor analysis further revealed that CCL2-expressing fibroblasts promote the pro-cancer signaling of immune cells including JAK-STAT3 signaling and inflammatory response in tumor-infiltration macrophages. The CCL2+fibroblasts and macrophages with activated JAK-STAT3 signals are co-localized in spatial GC architecture and their co-abundance was associated with unfavorable clinical outcomes. Taken together, GC spatial transcriptomes can be regionally and functionally delineated into functional cellular crosstalk involving multiple cell types with potential clinical relevance, particularly the interaction between CCL2+ fibroblasts and JAK-STAT3+macrophages contributing to cancer-favoring immune contexture in GC TME.

cancer biology↗

bioRxiv2023

Genome-wide exploration of metabolic-based pyrethroid resistance mechanism in Helicoverpa armigera

To elucidate the deltamethrin resistance mechanism in Helicoverpa armigera, we explored mutations at the deltamethrin target site, genomic level variations between insecticide-susceptible and -resistant strains, and differences in gene expression patterns between the strains. Known pyrethroid resistance-associated point mutations within the voltage-gated sodium channel were undetected in the cDNA and gDNA of resistant strains or field populations. The whole-genome de novo assembly of a Korean resistant strain was performed (GCA_026262555.1), and 13 genomes of susceptible and resistant individuals were re-sequenced using field populations. Approximately 3,369,837 variants (SNPs and indels) were compared with our reference H. armigera genome, and 1,032,689 variants were identified from open reading frames. A resistance-specific CYP3 subfamily gene with five variants (CYP321A1v1-v5) was identified in the resistant strains, indicating the potential role of these variants in resistance. RNA-seq analysis identified 36,720 transcripts from 45 Illumina RNA-seq datasets of the fat body, gut, and the rest of the body. Differential gene expression analysis revealed some differently overexpressed detoxification enzyme genes in the resistant strains, particularly cytochrome P450 genes. This finding was consistent with the results of bioassay tests using PBO-based synergists, further supporting the role of detoxification enzymes in resistance. Therefore, H. armigera may acquire deltamethrin resistance through a combination of actions, including the overexpression of various detoxification enzymes, such as CYP3 subfamilies (CYP321A5) and cuticular proteins. The five variants of CYP321A subfamily identified in this study may serve as a basis for understanding insecticide resistance at the molecular level and can be applied as diagnostic markers for resistance. Key MessagesO_LIKnown resistance-related mutations were undetected in all the resistant strains or field populations. C_LIO_LINo specific resistance-associated variations were identified at the genomic level. C_LIO_LIThe expression pattern of the CYP3 subfamily genes was strongly correlated with the level of resistance. C_LIO_LIGenes other than CYP337B3 are also involved in the development of high-level resistance. C_LIO_LIResistance developed as a result of changes in the expression of detoxification genes rather than target site modification through mutation. C_LI

ecology↗

bioRxiv2023

Interleukin-1α links peripheral CaV2.2 channel activation to rapid adaptive increases in heat sensitivity in skin

Neurons have the unique capacity to adapt output in response to changes in their environment. Within seconds, sensory nerve endings can become hypersensitive to stimuli in response to potentially damaging events. The underlying behavioral response is well studied, but several of the key signaling molecules that mediate sensory hypersensitivity remain unknown. We previously discovered that peripheral voltage-gated CaV2.2 channels in nerve endings in skin are essential for the rapid, transient increase in sensitivity to heat, but not to mechanical stimuli, that accompanies intradermal capsaicin. Here we report that the cytokine interleukin-1 (IL-1), an alarmin, is necessary and sufficient to trigger rapid heat and mechanical hypersensitivity in skin. Of 20 cytokines screened, only IL-1 was consistently detected in hind paw interstitial fluid in response to intradermal capsaicin and, similar to behavioral sensitivity to heat, IL-1 levels were also dependent on peripheral CaV2.2 channel activity. Neutralizing IL-1 in skin significantly reduced capsaicin-induced changes in hind paw sensitivity to radiant heat and mechanical stimulation. Intradermal IL-1 enhances behavioral responses to stimuli and, in culture, IL-1 enhances the responsiveness of Trpv1-expressing sensory neurons. Together, our data suggest that IL-1 is the key cytokine that underlies rapid and reversible neuroinflammatory responses in skin.

neuroscience↗

bioRxiv2023

Peripheral gating of pain by glial endozepine

We report that diazepam binding inhibitor (DBI) is a glial messenger mediating satellite glia-sensory neuron crosstalk in the dorsal root ganglion (DRG). DBI is highly and specifically expressed in satellite glia cells (SGCs) of mice, rat and human, but not in sensory neurons or other DRG-resident cells. Knockdown of DBI results in a robust mechanical hypersensitivity without significant effects on other sensory modalities. In vivo overexpression of DBI in SGCs reduces sensitivity to mechanical stimulation and alleviates mechanical allodynia in neuropathic and inflammatory pain models. We further show that DBI acts as a partial agonist and positive allosteric modulator at the neuronal GABAA receptors, particularly strongly effecting those with a high-affinity benzodiazepine binding site. Such receptors are selectively expressed by a subpopulation of mechanosensitive DRG neurons and these are also more enwrapped with DBI-expressing glia, as compared to other DRG neurons, suggesting a mechanism for specific effect of DBI on mechanosensation. These findings identified a new, peripheral neuron-glia communication mechanism modulating pain signalling, which can be targeted therapeutically.

neuroscience↗

bioRxiv2023

The role of positively charged small biomolecules in the aggregation of hyperphosphorylated tau in Alzheimer's disease

Tau proteins have recently drawn attention as a possible cause of Alzheimers disease (AD)-associated neuronal dementia. Hyperphosphorylated tau proteins detach from microtubules, impairing their stability and leading to neuronal degeneration. The present study focuses on understanding the molecular mechanisms behind the aggregation of hyperphosphorylated tau. Since hyperphosphorylated proteins are highly negatively charged, it is implausible that they create the damaging aggregates in the absence of some counteracting positive charge. This study found such an electrostatic (charge-charge) interaction between tau proteins and polyamines, identifying this interaction as crucial to promoting tau aggregation. In this study, we also directly observed the transition over time from tau protein aggregates to fibril structures. These findings challenge existing theories and offer insights into potential therapeutic targets for AD.

biophysics↗

bioRxiv2023

Dynamic decoding of VEGF signaling and coordinated control of multiple phenotypes by the Src-TEM4-YAP pathway

Responses of endothelial cells to elevated levels of Vascular Endothelial Growth Factor (VEGF), frequently accompanying local decrease in oxygen supply, include loosening of cell contacts, rearrangement of cells in the process of vessel remodeling and ultimately, angiogenic growth. How these complex processes, occurring on diverse time scales, are coordinated and how they are guided by a single key signaling input, is still incompletely understood. Here we show that the various phenotypic responses associated with VEGF signaling are controlled at different steps of a pathway involving sequential activation of Src, TEM4, YAP and components of pro-angiogenic Notch signaling. Strikingly, due to feedback regulation at different pathway levels, the functional outcomes are controlled by oscillations of the pathway components occurring on distinct time scales. Deeper pathway layers integrate faster upstream responses and control progressively slower phenotypic outcomes. This signal decoding pathway organization can ensure a high degree of complexity in a vital physiological process.

systems biology↗

bioRxiv2023

Stimulation of median raphe terminals in dorsal CA2 reduces social investigation in male mice specifically investigating social stimulus of ovariectomized female mice

The cornu ammonis area 2 (CA2) region is essential for social behaviors, especially in social aggression and social memory. Recently, we showed that targeted CA2 stimulation of vasopressin presynaptic fibers from the paraventricular nuclei of hypothalamus strongly enhances social memory in mice. In addition, the CA2 area of the mouse hippocampus receives neuronal inputs from other regions including the septal nuclei, the diagonal bands of Broca, supramammillary nuclei, and median raphe nucleus. However, the functions of these projections have been scarcely investigated. A functional role of median raphe (MR) - CA2 projection is supported by the MR to CA2 projections and 82% reduction of hippocampal serotonin (5-HT) levels following MR lesions. Thus, we investigated the behavioral role of presynaptic fibers from the median raphe nucleus projecting to the dorsal CA2 (dCA2). Here, we demonstrate the optogenetic stimulation of 5-HT projections to dCA2 from the MR do not alter social memory, but instead reduce social interaction. We show that optical stimulation of MR fibers excites interneurons in the stratum radiatum (SR) and stratum lacunosum moleculare (SLM) of CA2 region. Consistent with these observations, we show that bath application of 5-HT increases spontaneous GABA release onto CA2 pyramidal neurons and excites presumed interneurons located in the SR/SLM. This is the first study, to our knowledge, which investigates the direct effect of 5-HT release from terminals onto dCA2 neurons on social behaviors. This highlights the different roles for these inputs (i.e., vasopressin inputs regulating social memory versus serotonin inputs regulating social interaction).

neuroscience↗

bioRxiv2023

Genetic and brain similarity independently predict childhood anthropometrics and socioeconomic markers

Linking the developing brain with individual differences in clinical and demographic traits is challenging due to the substantial interindividual heterogeneity of brain anatomy and organization. Here we employ a novel approach that parses individual differences in both cortical thickness and common genetic variants, and assess their effects on a wide set of childhood traits. The approach uses a linear mixed model framework to obtain the unique effects of each type of similarity, as well as their covariance, with the assumption that similarity in cortical thickness may in part be driven by similarity in genetic variants. We employ this approach in a sample of 7760 unrelated children in the ABCD cohort baseline sample (mean age 9.9, 46.8% female). In general, significant associations between cortical thickness similarity and traits were limited to anthropometrics such as height (r2 = 0.11, SE = 0.01), weight (r2 = 0.12, SE = 0.01), and birth weight (r2 = 0.19, SE = 0.01), as well as markers of socioeconomic status such as local area deprivation (r2 = 0.06, SE = 0.01). Analyses of the contribution from common genetic variants to traits revealed contributions across included outcomes, albeit somewhat lower than previous reports, possibly due to the young age of the sample. No significant covariance of the effects of genetic and cortical thickness similarity was found. The present findings highlight the connection between anthropometrics as well as socioeconomic factors and the developing brain, which appear to be independent from individual differences in common genetic variants in this population-based sample. The approach provides a promising framework for analyses of neuroimaging genetics cohorts, which can be further expanded by including imaging derived phenotypes beyond cortical thickness.

neuroscience↗

bioRxiv2023

R2ROC: An efficient method of comparing two or more correlated AUC from out-of-sample prediction using polygenic scores

Polygenic risk scores (PRSs) enable early prediction of disease risk. Evaluating PRS performance for binary traits commonly relies on the area under the receiver operating characteristic curve (AUC). However, the widely used DeLongs method for comparative significance tests suffer from limitations, including computational time and the lack of a one-to-one mapping between test statistics based on AUC and R2. To overcome these limitations, we propose a novel approach that leverages the Delta method to derive the variance and covariance of AUC values, enabling a comprehensive and efficient comparative significance test. Our approach offers notable advantages over DeLongs method, including reduced computation time (up to 150-fold), making it suitable for large-scale analyses and ideal for integration into machine learning frameworks. Furthermore, our method allows for a direct one-to-one mapping between AUC and R2 values for comparative significance tests, providing enhanced insights into the relationship between these measures and facilitating their interpretation. We validated our proposed approach through simulations and applied it to real data comparing PRSs for diabetes and coronary artery disease (CAD) prediction in a cohort of 28,880 European individuals. The PRSs were derived using genome-wide association study summary statistics from two distinct sources. Our approach enabled a comprehensive and informative comparison of the PRSs, shedding light on their respective predictive abilities for diabetes and CAD. This advancement contributes to the assessment of genetic risk factors and personalized disease prediction, supporting better healthcare decision-making.

genetics↗

bioRxiv2023

GxE PRS: Genotype-environment interaction in polygenic risk score models for quantitative and binary traits

The use of polygenic risk score (PRS) models has transformed the field of genetics by enabling the prediction of complex traits and diseases based on an individuals genetic profile. However, the impact of genotype-environment interaction (GxE) on the performance and applicability of PRS models remains a crucial aspect to be explored. Currently, existing GxE PRS models are often inappropriately used, which can result in inflated type 1 error rates and compromised results. In this study, we propose a novel GxE PRS model that correctly incorporates the GxE component to analyze complex traits and diseases. Through extensive simulations, we demonstrate that our proposed model outperforms existing models in terms of controlling type 1 error rates and enhancing statistical power. Furthermore, we apply the proposed model to real data, and report significant GxE effects. Specifically, we highlight the impact of our model on both quantitative and binary traits. For quantitative traits, we uncover the GxE modulation of genetic effects on body mass index (BMI) by alcohol intake frequency (ALC). In the case of binary traits, we identify the GxE modulation of genetic effects on hypertension (HYP) by waist-to-hip ratio (WHR). These findings underscore the importance of employing a robust model that effectively controls type 1 error rates, thus preventing the occurrence of spurious GxE signals. To facilitate the implementation of our approach, we have developed an innovative R software package called GxE PRS, specifically designed to detect and estimate GxE effects. Overall, our study highlights the importance of accurate GxE modeling and its implications for genetic risk prediction, while providing a practical tool to support further research in this area.

genetics↗

bioRxiv2023

An integrated mechanistic and data-driven computational model predicts cell responses to high- and low-affinity EGFR ligands

The biophysical properties of ligand binding heavily influence the ability of receptors to specify cell fates. Understanding the rules by which ligand binding kinetics impact cell phenotype is challenging, however, because of the coupled information transfers that occur from receptors to downstream signaling effectors and from effectors to phenotypes. Here, we address that issue by developing an integrated mechanistic and data-driven computational modeling platform to predict cell responses to different ligands for the epidermal growth factor receptor (EGFR). Experimental data for model training and validation were generated using MCF7 human breast cancer cells treated with the high- and low-affinity ligands epidermal growth factor (EGF) and epiregulin (EREG), respectively. The integrated model captures the unintuitive, concentration-dependent abilities of EGF and EREG to drive signals and phenotypes differently, even at similar levels of receptor occupancy. For example, the model correctly predicts the dominance of EREG over EGF in driving a cell differentiation phenotype through AKT signaling at intermediate and saturating ligand concentrations and the ability of EGF and EREG to drive a broadly concentration-sensitive migration phenotype through cooperative ERK and AKT signaling. Parameter sensitivity analysis identifies EGFR endocytosis, which is differentially regulated by EGF and EREG, as one of the most important determinants of the alternative phenotypes driven by different ligands. The integrated model provides a new platform to predict how phenotypes are controlled by the earliest biophysical rate processes in signal transduction and may eventually be leveraged to understand receptor signaling system performance depends on cell context. One-sentence summaryIntegrated kinetic and data-driven EGFR signaling model identifies the specific signaling mechanisms that dictate cell responses to EGFR activation by different ligands.

systems biology↗

bioRxiv2023

Genetic and transcriptomic analysis of hyphal constriction based on a novel assay method in the rice blast fungus

An ability of fungi to undergo hyphal constriction is important for fungal ecology and diseases. In the rice blast fungus, Magnaporthe oryzae, hyphal constriction is required to traverse host cell junctions through pit fields. However, little is known about genetic underpinnings of hyphal constriction, except the requirement of a mitogen-activated protein kinase, Pmk1. Here we demonstrate that a simple in vitro assay based on nitrocellulose membrane allows investigation of the genetic basis for hyphal constriction. Using the assay, we found that the constriction limit of M. oryzae hypha lies between 0.22 and 0.3 m, and that a histone modification might be involved in hyphal constriction. RNA-seq experiments combining our assay and {Delta}pmk1 showed that hyphal constriction relies on transcriptional changes of genes implicated primarily in membrane and cell wall-related cellular processes in Pmk1-dependent and/or Pmk1-independent manner. Furthermore, our assays with diverse fungal species suggest correlation between hyphal constriction and fungal lifestyles. Our study reveals that hyphal constriction can be induced without host-derived cues and provides molecular and evolutionary insights into a fundamental process to infection of host plant.

microbiology↗

bioRxiv2022

Balance-directed protein engineering of IsPETase enhances both PET hydrolysis activity and thermostability

A mesophilic PETase from Ideonella sakaiensis (IsPETase) has been shown to exhibit high PET hydrolysis activity, but its low thermostability limits its industrial applications. We herein developed an engineering strategy for IsPETase to enhance PET hydrolysis activity, thermostability, and protein folding of the enzyme. Balance-directed Z1-PETase variant outperforms the stability-directed Z2-PETase variant under both mesophilic and thermophilic conditions, although Z2-PETase exhibits higher thermostability than Z1-PETase. The Z1-PETase is also superior to Fast-PETase, Dura-PETase, and LC-CICCG in terms of depolymerization rate regardless of temperature conditions we tested. Thus, maintaining a balance between PET hydrolysis activity and thermostability is essential for the development of high-performance PET hydrolases. In a pH-stat bioreactor, Z1-PETase depolymerized >90% of both transparent and colored post-consumer PET powders within 24 and 8 hours at 40{degrees}C and 55{degrees}C, respectively, demonstrating that the balance-directed IsPETase variant produced herein may be applicable in the bio-recycling of PET.

bioengineering↗

bioRxiv2022

Discovery and biosynthesis of imidazolium antibiotics from a probiotic Bacillus licheniformis

Antibiotic resistance is one of the worlds most urgent public health problems and therefore novel antibiotics to kill drug-resistant bacteria are desperately needed. So far, natural product-derived small molecules have been the major sources for new antibiotics. Here we describe a family of antibacterial metabolites isolated from a probiotic bacterium Bacillus licheniformis. Cross-streaking assay followed by activity-guided isolation yielded a novel antibacterial metabolite bacillimidazole G, which possesses a rare imidazolium ring in the structure, showing MIC values of 0.7-2.6 g/mL against human pathogenic Gram-positive and Gram-negative bacteria including methicillin-resistant Staphylococcus aureus (MRSA) and a lipopolysaccharide(LPS)-lacking Acinetobacter baumannii {Delta}lpxC. Bacillimidazole G also lowered MICs of colistin, a Gram-negative antibiotic, up to 8-fold against wild-type E. coli MG1655 and Acinetobacter baumannii. We propose biosynthetic pathway of the characterized metabolites based on the precursor-feeding studies, chemical biological approach, biomimetic total synthesis, and biosynthetic genes knockout method. TOC/Abstract Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=34 SRC="FIGDIR/small/511033v1_ufig1.gif" ALT="Figure 1"> View larger version (8K): org.highwire.dtl.DTLVardef@184f545org.highwire.dtl.DTLVardef@2a69eorg.highwire.dtl.DTLVardef@8cf13org.highwire.dtl.DTLVardef@530001_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2022

Investigation of neuromodulatory effect of anodal cerebellar transcranial direct current stimulation on the primary motor cortex using functional near-infrared spectroscopy

BackgroundCerebellar brain inhibition (CBI), a neural connection between the cerebellum and primary motor cortex (M1), has been researched as a target pathway for neuromodulation to improve clinical outcomes in various neurological diseases. However, conflicting results of anodal cerebellar transcranial direct current stimulation (acb-tDCS) on M1 excitability indicate that additional investigation is required to examine its precise effect. Objective/HypothesisThis study aimed to gather evidence of the neuromodulatory effect of acb-tDCS on the M1 using functional near-infrared spectroscopy (fNIRS). MethodsSixteen healthy participants were included in this cross-over study. Participants received real and sham acb-tDCS in a random order, with a minimum one-week washout period between them. The anode and cathode were placed on the right cerebellum and the right buccinator muscle, respectively. Stimulation lasted 20 min at an intensity of 2 mA, and fNIRS data were recorded for 42 min (including a 4 min baseline before stimulation and an 18 min post-stimulation duration) using eight channels attached bilaterally on the M1. Resultsacb-tDCS induced a significant decrease in oxyhemoglobin (HbO) concentration (inhibitory effect) in the left (contralateral) M1, whereas it induced a significant increase in HbO concentration (excitatory effect) in the right (ipsilateral) M1 compared to sham tDCS during (p < 0.05) and after stimulation (p < 0.01) in a group level analysis. At the individual level, variations in the response to acb-tDCS were observed. ConclusionOur findings demonstrate the neuromodulatory effects of acb-tDCS on the bilateral M1 in terms of neuronal hemodynamics.

neuroscience↗