bioRxiv Science⌕ Search

Biology subjects

Yin, X.

Publications and source records attributed to Yin, X..

At least 37 records · Page 2Linked to original sources

Sodium Selenite Alleviates Hyperglycemia-aggravated Cerebral Ischemic Injury by Mediating Apoptosis through the Fas/FasL Signaling Pathway

ObjectiveTo investigate the intervention mechanism of sodium selenite in alleviating hyperglycemia-induced cerebral ischemia/reperfusion (I/R) injury through the Fas/FasL/NF-{kappa}B/PUMA pathway. MethodsThe SD rat model of hyperglycemia-induced cerebral I/R injury and the HT22 cell model of high-glucose oxygen deprivation/reoxygenation (OD/R) were constructed to systematically evaluate the neuroprotective effect of sodium selenite and its regulatory effect on the Fas/FasL/NF-{kappa}B/PUMA pathway. ResultsThe infarct volume, neurological dysfunction, metabolic level, and apoptosis level in the HG group were significantly higher than those in the NG group. Sodium selenite improved the infarct volume, neurological dysfunction, metabolic level, and apoptosis level in the HG group, and regulated the Fas/FasL/PUMA apoptotic pathway to alleviate injury. In vitro experiments showed that sodium selenite significantly improved morphological damage caused by high-glucose OD/R, increased cell viability, and reduced the expression of apoptotic factors. The application of Fas and FasL inhibitors and knockdown of PUMA expression indicated that sodium selenite alleviated cell apoptosis by inhibiting the activation of the Fas/FasL/PUMA pathway. ConclusionSodium selenite alleviates hyperglycemia-exacerbated cerebral I/R injury by regulating the Fas/FasL/NF-{kappa}B/PUMA signaling pathway.

pathology↗

Iterative delivery of mRNA by MEFI

Conventional therapeutic mRNA delivery systems are inherently single-use, limiting expression potency, duration, and penetration across biological barriers. To address this, we engineered the mRNA Exporting and Ferrying Implement (MEFI), a platform that enables iterative cell-to-cell transfer of cargo mRNA, allowing a single mRNA molecule to be utilized multiple times across various cells. MEFI encodes a fusion protein that assembles virus-like particles (VLPs) and encapsulates both itself and cargo mRNA into these VLPs, orchestrating reproduction of VLPs from targeted cells and continuous intercellular spreading. MEFI significantly amplified cargo protein expression in the transfected cell populations ([~]20-fold) and in organs ([~]500-fold in lung) from mice administered systemically. Notably, through intramuscular injection of naked plasmids, MEFI promoted robust ([~]20-fold) and durable ([~]2-month) cargo expression, interorgan mRNA transfer, and successful crossing of the blood-brain barrier. Moreover, modified MEFI demonstrated cell-type-specific targeting, mediating the elimination of antigen-expressing cells. Collectively, MEFI establishes a modular platform for enhancing mRNA delivery, leveraging the concept of iterative delivery of mRNA. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=138 SRC="FIGDIR/small/667827v2_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@14522c2org.highwire.dtl.DTLVardef@1ecfa7dorg.highwire.dtl.DTLVardef@1314347org.highwire.dtl.DTLVardef@1380cc7_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Rpl13a snoRNAs Downregulate Smooth Muscle Cell COX4I2 and Promote Neointimal Hyperplasia

BACKGROUNDReactive oxygen species (ROS) augment the activation of vascular smooth muscle cells (SMCs) and promote neointimal hyperplasia evoked by arterial injury or atherogenesis. We have previously shown that small nucleolar RNAs (snoRNAs) from the Rpl13a locus are key regulators of cellular ROS levels. METHODSUsing mice deficient in the Rpl13a snoRNAs, we tested whether these snoRNAs regulate SMC activation in vitro and in vivo. Carotid endothelial denudation was used to provoke neointimal hyperplasia in wild-type (WT) and snoRNA knockout (snoKO) mice, which lack all four intronically-encoded Rpl13a snoRNAs. Primary SMCs from WT and snoKO mice were used for in vitro functional and proteomic analyses. HEK293T cells with specific snoRNA deletions were used to test for snoRNA-guided 2-O-methylation of mRNA. RESULTSArterial ROS levels, inflammation, and carotid artery neointimal hyperplasia were reduced in snoKO compared with WT mice. In vitro, snoKO SMCs demonstrated lower ROS levels and less migration, proliferation, and inflammatory signaling than WT SMCs. Reduced ROS levels in snoKO SMCs and aortas correlated with upregulation of the mitochondrial protein COX4I2, which is associated with reduced mitochondrial ROS under normoxic conditions. Deleting the snoRNA U32A in human HEK293T cells decreased 2-O-methylation of COX4I2 mRNA and upregulated COX4I2 protein without changing COX4I2 mRNA levels. Silencing Cox4i2 in snoKO SMCs upregulated SMC ROS to WT levels. CONCLUSIONSRpl13a snoRNAs are important drivers of SMC activation and neointimal hyperplasia. Rpl13a snoRNAs augment SMC ROS levels, at least in part, by post-transcriptional downregulation of COX4I2 expression.

molecular biology↗

Population-specific brain charts reveal Chinese-Western differences in neurodevelopmental trajectories

Human brain charts provide unprecedented opportunities for decoding neurodevelopmental milestones and establishing clinical benchmarks for precision brain medicine 1-7. However, current lifespan brain charts are primarily derived from European and North American cohorts, with Asian populations severely underrepresented. Here, we present the first population-specific brain charts for China, developed through the Chinese Lifespan Brain Mapping Consortium (Phase I) using neuroimaging data from 43,037 participants (aged 0-100 years) across 384 sites nationwide. We establish the lifespan normative trajectories for 296 structural brain phenotypes, encompassing global, subcortical, and cortical measures. Cross-population comparisons with Western brain charts (based on data from 56,339 participants aged 0-100 years) reveal distinct neurodevelopmental patterns in the Chinese population, including prolonged cortical and subcortical maturation, accelerated cerebellar growth, and earlier development of sensorimotor regions relative to paralimbic regions. Crucially, these Chinese-specific charts outperform Western-derived models in predicting healthy brain phenotypes and detecting pathological deviations in Chinese clinical cohorts. These findings highlight the urgent need for diverse, population-representative brain charts to advance equitable precision neuroscience and improve clinical validity across populations.

neuroscience↗

CDK12 condensation in nuclear speckles confers sensitivity to cyclin K molecular glue degraders

Transcriptional machinery often operates in the configuration of biomolecular condensates, presenting emerging opportunities to develop therapies targeting transcriptionally addicted malignancies. In this study, we discovered that cyclin-dependent kinase 12 (CDK12), a key regulator of transcription elongation, formed dynamic liquid-like droplets within nuclear speckles, a process enhanced by high CDK12 expression and CDK12 inhibitor treatment. Recognizing this unique property, we rationally designed ZSQ253, a modular cyclin K molecular glue degrader that coupled binding moieties for both CDK12 and DDB1. By promoting phase separation-driven assembly and subsequent proteasomal degradation of the CDK12-cyclin K complex, ZSQ253 interfered with oncogenic transcription and demonstrated potent antitumor capability. Further structure-guided optimization yielded HQY1428, a derivative with a multi-site gluing effect and improved drug activity. Given the frequent genomic co-amplification of CDK12 and ERBB2 across diverse human cancers, we showed that combining HQY1428 with HER2 inhibitors provided synergistic therapeutic benefits. Collectively, our findings establish CDK12 condensation within nuclear speckles as an exploitable vulnerability, and introduce a novel mechanism of action underlying cyclin K molecular glue degraders.

cancer biology↗

Altered Interpersonal Neural Synchronization during Social Interaction After Shared Excluded Experiences in Depressed Adolescents

BackgroundMajor depressive disorder (MDD) is common in adolescents, and the special development stage, during which adolescents brain and neuroendocrine system develop intensively, makes it subtly difficult to develop prevention and treatment strategies for depressed adolescents compared with depressed adults. Meanwhile, public psychosocial stressors significantly influence adolescents mental health and social interaction, rendering it essential to explore how a shared psychosocial stressor, i.e., shared excluded experiences, influences social interaction in depressed adolescents. MethodsWe designed a 4-player cyberball game to probe adolescents responses to shared excluded experiences and explore the underlying interpersonal neural synchronization (INS) with functional near-infrared spectroscopy (fNIRS). ResultsWe found that shared excluded experiences could enhance adolescents social interaction preferences but decreased INS in each pair of excluded adolescents, which indicates a reduced willingness to interact with others after the exclusion. However, no significantly different behavioral responses to the shared excluded experiences were found in depressed adolescents compared to adolescents as healthy controls (HC). Further analyses revealed that adolescents with MDD experienced more negative feelings than HC after exclusion. Of note, adolescents with MDD demonstrated stronger INS than HC, indicating the potential empathic stress in depressed adolescents. In addition, there existed altered brain-behavioral association patterns in responses to shared excluded experiences in depressed adolescents. ConclusionsIn summary, our study gives us deeper insights into how a shared psychosocial stressor impacts the INS in depressed adolescents, and it might be demonstrated that INS could be more sensitive than behavioral responses to detect social interaction deficits in depressed adolescents.

neuroscience↗

China Autism Brain Imaging Consortium: Charting Brain Growth in Chinese Children with Autism

Autism Spectrum Disorder (ASD) is a lifelong neurodevelopmental condition characterized by atypical brain growth. While advances in neuroimaging and openly sharing large-sample datasets such as the Autism Brain Imaging Data Exchange (ABIDE) have improved understanding of ASD, most studies focus on adolescents and adults, with early brain development-critical for diagnosis and intervention-remaining underexplored. Existing research predominantly involves Western samples, offering limited insight and generalizability into non-Caucasian populations. We introduce the China Autism Brain Imaging Consortium (CABIC) (https://php.bdnilab.com/resources/), a grassroots effort by researchers across the country to aggregate previously collected multi-site structural MRI datasets and phenotypic information from 1,451 autistic children and 1,119 typically developing children, covering an age range from early childhood to school age (1.0 - 12.92 years). Here, we present this resource and depict brain growth charts to push forward a more comprehensive understanding of the brain development in Chinese autism children. We constructed brain growth charts that reveal a developmental shift in autistic children, transitioning from early overgrowth to delayed maturation. Regional analyses identified distinct atypical trajectories across specific brain regions. Individual deviation scores quantified inter-subject variability, characterizing the heterogeneity of brain development in ASD. Comparative analyses between CABIC and ABIDE highlighted differences potentially attributable to ethnicity and culture, advancing our understanding of cross-population neurodevelopmental diversity. CABIC MRI datasets will be shared publicly to foster investigation of the potential neural mechanisms underlying ASD in non-Western populations and support efforts toward precision medicine for autistic individuals across diverse backgrounds.

neuroscience↗

VPS13D mutations disrupt mitochondrial homeostasis and locomotion in Caenorhabditis elegans

Mitochondria control cellular metabolism, serve as hubs for signaling and organelle communication, and are important for the health and survival of cells. VPS13D encodes a cytoplasmic lipid transfer protein that regulates mitochondrial morphology, mitochondria and endoplasmic reticulum (ER) contact, quality control of mitochondria. VPS13D mutations have been reported in patients displaying ataxic and spastic gait disorders with variable age of onset. Here we used CRISPR/Cas9 gene editing to create VPS13D related-spinocerebellar ataxia-4 (SCAR4) missense mutations and C-terminal deletion in VPS13Ds orthologue vps-13D in C. elegans. Consistent with SCAR4 patient movement disorders and mitochondrial dysfunction, vps-13D mutant worms exhibit locomotion defects and abnormal mitochondrial morphology. Importantly, animals with a vps-13D deletion or a N3017I missense mutation exhibited an increase in mitochondrial unfolded protein response (UPRmt). The cellular and behavioral changes caused by VPS13D mutations in C. elegans advance the development of animal models that are needed to study SCAR4 pathogenesis.

genetics↗

Action mechanism of a novel agrichemical quinofumelin against Fusarium graminearum

Modern fungicides have made significant contributions to crop disease management, but the development of resistant fungal strains has caused their failure in disease control. Therefore, developing fungicides with novel action mechanisms is the most effective measure to manage resistance. Quinofumelin, a novel quinoline fungicide, exhibits exceptional antifungal activity against phytopathogens. However, there is currently no available information on its mechanism of action. Here, we used transcriptome and metabolome analysis to observe a co-enrichment pattern of differentially expressed genes (DEGs) and differentially accumulated metabolites (DAMs) within pyrimidine biosynthesis pathway (PBP), identifying down-regulation of dihydroorotate dehydrogenase (DHODH). Exogenous uridine monophosphate (UMP), uridine or uracil (metabolites in PBP) successfully restored quinofumelin-induced inhibition of mycelial growth in Fusarium graminearum and Fusarium asiaticum. Additionally, the deletion of FgDHODHII was determined to be lethal; however, mycelial growth of {Delta}FgDHODHII mutants could be restored by adding UMP, uridine or uracil. These findings indicate that the deficiencies in FgDHODHII are functionally equivalent to complete inhibition of its activity by quinofumelin. Finally, molecular docking, surface plasmon resonance (SPR) and microscale thermophoresis (MST) results strongly support the precise interaction between quinofumelin and FgDHODHII. Collectively, these findings provide compelling evidence for the involvement of de novo uracil biosynthesis as mechanism of action for quinofumelin while identifying FgDHODHII as its specific target.

pathology↗

A novel method for in vivo assessment of soft tissue weight in bivalves

Aquaculture has been playing an increasingly important role in supplying proteins. To satisfy the rapidly growing demands for quality aquatic foods, the efficiency of aquaculture production needs to be improved. One strategy to achieve more efficient aquaculture production is to produce high-yielding seeds through breeding programs, for which in vivo assessment of target traits is indispensable to prevent candidate parents from being sacrificed for measurement and to track dynamically changing yield-related traits. Farmed mollusks, most of which are bivalves, rank the second among all aquatic animals in aquaculture production. Bivalves with heavier soft tissue, the major edible part, are preferable, target species for breeding and farming. A prerequisite for obtaining such species is to make accurate but nondestructive assessments of soft tissue weight, which cannot be accomplished using traditional dissection- or imaging-based methods. To resolve this issue, we take advantage of the complex relationships among shell dimension- and weight-related traits to construct classical, shell dimension- or wet weight-based models and novel, shell surface area-based models for in vivo assessment of soft tissue weight in Zhikong scallop (Chlamys farreri) and yesso scallop (Patinopecten yessoensis). Overall, soft tissue weight estimated by wet weight-involving models are highly correlated with observed values, indicating wet weight as a key proxy for soft tissue weight. While some models incorporating wet weight tend to systematically over- or under-estimate soft tissue weight despite the strong association between actual and estimated values, the novel, shell surface area-based model, MLR-log10Sshell-RR, generates accurate estimates free of systematic biases across populations of different ages for both species, suggesting it as a promising approach for in vivo assessment of soft tissue weight for scallops and other bivalves with bilaterally symmetrical shells.

genetics↗

UTX Epigenetically Imposes a Cytolytic Effector Program in Autoreactive Stem-like CD8+ T cell Progenitors

Type 1 Diabetes Mellitus (T1D) is a chronic disease caused by an unremitting autoimmune attack on pancreatic beta cells. This autoimmune chronicity is mediated by stem-like progenitor CD8+ T cells that continually repopulate the pool of beta cell-specific cytolytic effectors. Factors governing the conversion of progenitors to effectors, however, remain unclear. T1D has been linked to a chromosomal region (Xp13-p11) that contains the epigenetic regulator UTX, which suggests a key role for UTX in T1D pathogenesis. Here, we show that T cell-specific UTX deletion in NOD mice protects against T1D development. In T cells of NOD mice and T1D patients, UTX ablation resulted in the accumulation of CD8+ progenitor cells with concomitant deficiency of effectors, suggesting a key role for UTX in poising progenitors for transition to effectors. Mechanistically, UTXs role in T1D was independent of its inherent histone demethylase activity but instead relied on binding with transcription factors (TCF1 and STAT3) to co-regulate genes important in the maintenance and differentiation of progenitor CD8+ T cells. Together, these findings identify a critical role for UTX in T1D and the UTX:TCF1:STAT3 complex as a therapeutic target for terminating the long-lived autoimmune response.

immunology↗

PlateletBase: A Comprehensive Knowledgebase for Platelet Research and Disease Insights

Platelets are vital in many pathophysiological processes, yet there is a lack of a comprehensive resource dedicated specifically to platelet research. To fill this gap, we have developed PlateletBase, a knowledge base aimed at enhancing the understanding and study of platelets and related diseases. Our team retrieved information from various public databases, specifically extracting and analyzing RNA-seq data from 3,711 samples across 41 different conditions available on NCBI. PlateletBase offers six analytical and visualization tools, enabling users to perform gene similarity analysis, pair correlation, multi-correlation, expression ranking, clinical information association, and gene annotation for platelets. The current version of PlateletBase includes 10,278 genomic entries, 31,758 transcriptomic entries, 4,869 proteomic entries, 2,614 omics knowledge entries, 1,833 drugs, 97 platelet resources, 438 diseases/traits, and six analysis modules. Each entry has been carefully curated and supported by experimental evidence. Additionally, PlateletBase features a user-friendly interface designed for efficient querying, manipulation, browsing, visualization, and analysis of detailed platelet protein and gene information. Case study results, such as those from gray platelet syndrome and angina pectoris, demonstrate that this tool can aid in identifying diagnostic biomarkers and exploring disease mechanisms, significantly advancing research in platelet functionality and its applications. PlateletBase is accessible at http://plateletbase.clinlabomics.org.cn/.

bioinformatics↗

Deep Ensemble Model for Quantitative Optical Property and Chromophore Concentration Images of Biological Tissues

The ability to quantify widefield tissue optical properties (OPs, i.e., absorption and scattering) has major implications on the characterization of various physiological and disease processes. However, conventional image processing methods for tissue optical properties are either limited to qualitative analysis, or have tradeoffs in speed and accuracy. The key to quantification of optical properties is the extraction of amplitude maps from reflectance images under sinusoidal illumination of different spatial frequencies. Conventional three-phase demodulation (TPD) method has been demonstrated for the mapping of OPs, but it requires as many as 14 measurement images for accurate OP extraction, which leads to limited throughput and hinders practical translation. Although single-phase demodulation (SPD) method has been proposed to map OPs with a single measurement image, it is typically subject to image artifacts and decreased measurement accuracy. To tackle those challenges, here we develop a deep ensemble model (DEM) that can map tissue optical properties with high accuracy in a single snapshot, increasing the measurement speed by 14x compared to conventional TPD method. The proposed method was validated with measurements on an array of optical phantoms, ex vivo tissues, and in vivo tissues. The errors for OP extraction were 0.83 {+/-} 5.0% for absorption and 0.40 {+/-} 1.9% for reduced scattering, dramatically lower than that of the state-of-the-art SPD method (2.5 {+/-} 15% for absorption and -1.2 {+/-} 11% for reduced scattering). It was further demonstrated that while trained with data from a single wavelength, the DEM can be directly applied to other wavelengths and effectively obtain optical property and chromophore concentration images of biological tissues. Together, these results highlight the potential of DEM to enable new capabilities for quantitative monitoring of tissue physiological and disease processes.

biophysics↗

Processing negative words in pun-humor: dynamic representation of mixed feelings blending amusement and negativity

This study aims to investigate whether amusement and negativity counteract each other or are jointly intensified during the online processing of negative keywords in pun-humor sentences, and how mixed feelings blending these two emotional states are dynamically experienced over time. Participants read three types of sentences that included the same negative words as keywords: pun-humor (negative words can generate humorous effects by resonating with the context), non-humor (negative words seamlessly align with the context), and nonsensical (negative words cannot be integrated with the context) sentences. The behavioral ratings revealed that compared with non-humor and nonsensical sentences, pun-humor sentences evoked stronger amusement and intensified negative feelings, indicating that pun-humor sentences containing negative keywords can effectively elicit mixed feelings that encompass conflicting emotional states. The ERP results showed that the N400 (300-500 ms) elicited by negative words in pun-humor sentences was comparable to that in non-humor sentences, suggesting that negative words were connected contextually in both sentence types. Besides, negative words elicited greater LPC (600-800 ms) in pun-humor sentences than in non-humor and nonsensical sentences, suggesting that pun-humor sentences require additional semantic processing and more elaborate emotional processing. Moreover, the representational similarity analysis (RSA) results revealed that in pun-humor sentences, the representation of negativity persisted for a longer duration, and it occurred and peaked earlier than that of amusement. This implies that within the dynamic representation of mixed feelings, negativity was experienced first, whereas amusement was subsequently felt within a brief period, during which negativity was not offset but rather continued to be represented over a longer time span, resulting in the simultaneous presence of both amused and negative feelings. Taken together, these findings show that mixed feelings elicited during the online processing of negative keywords in pun-humor sentences can be dynamically experienced in a way that aligns with the highly simultaneous pattern and that negativity can be experienced before amusement during the dynamic representation of mixed feelings.

neuroscience↗

Generating snoRNA-guided Programmable 2'O-methylation

Small nucleolar RNAs (snoRNAs) are critical in guiding post-transcriptional modifications like 2-O-methylation (Nm), which play crucial roles in downstream processes such as splicing and translation. This study tests a novel method for Nm validation, addressing a significant gap in modern Nm research, and offers insight into the intricacies of snoRNA-guided Nm. While mapping of Nm modifications has seen significant improvement within the past decade, no major techniques have been able to validate these potential sites. Additionally, many mapping techniques lack consensus among proposed Nm sites, especially on mRNAs. Without a proper validation technique, Nm research lags compared to its peer post-transcriptional modifications. The RNase H-based Nm-VAQ assay used here quantifies 2-O-methylation at single nucleotide resolution across various RNA species including rRNA, snRNA, and mRNA. Its optimization for mRNA allows for an unprecedented way to study the effects of Nm modifications in low abundance transcripts. Utilizing this, the study also explores the potential of creating synthetic snoRNAs to guide Nm modifications. Exogenous snoRNAs are shown to rescue Nm in genetic knockout models and can be mutated to guide Nm at any location along the target RNA transcript. Preliminary work indicates that synthetic snoRNAs demonstrate the ability to modify luciferase, impacting translation efficiency. Targeting an exon increases mRNA abundance but decreases protein expression, consistent with previous findings on Pxdn mRNA. These findings set the scene for novel understanding of the relationship between snoRNA abundance, 2-O-methylation efficiency, and Nms impact on gene expression.

molecular biology↗

Probabilistic Fine-mapping of Putative Causal Genes

Integrative genetic analysis of molecular and complex trait data, including colocalization analysis and transcriptome-wide association studies (TWAS), has shown promise in linking GWAS findings to putative causal genes (PCGs) underlying complex diseases. However, existing methods have notable limitations: TWAS tend to produce an excess of false-positive PCGs, while colocalization analysis often lacks sufficient statistical power, resulting in many false negatives. This paper introduces a probabilistic fine-mapping method, INTERFACE, which is designed to identify putative causal genes while accounting for direct variant-to-trait effects within genomic regions harboring multiple gene candidates. INTERFACE lever-ages interpretable, data-informed priors that incorporate both colocalization and TWAS evidence, enhancing the sensitivity and specificity of PCG inference and setting it apart from existing methods. Additionally, INTERFACE implements analytical measures to improve the accuracy of gene-to-trait effect estimation. We apply INTERFACE to METSIM plasma metabolite GWASs and UK Biobank pQTL data to identify causal genes regulating blood metabolite levels and demonstrate the unique biological insights INTERFACE provides.

genetics↗

Why do bats fly into cave doors? Inattentional blindness in echolocating animals

Echolocating bats can navigate complex 3D environments by integrating prior knowledge of spatial layouts and real-time sensory cues. This study demonstrates that inattentional blindness to sensory information undermines successful navigation in Egyptian fruit bats, Rousettus aegyptiacus, a species that has access to vision and echolocation to traverse natural environments. Bats flew over repeated trials to a perch at a fixed location in the light, allowing them to navigate using both vision and echolocation. The experiment was then repeated in the dark to exclude the bats use of vision. The perch was subsequently displaced by either 15 or 30 cm in one of six different directions (up, down, left, right, front, back). Echolocation behavior was recorded using a 25-channel microphone array, while flight paths were tracked using 13 motion capture cameras. The directional aim of echolocation clicks served as a metric for the bats spatial attention to locations in their environment. In the light, bats modified their flight paths to successfully land on a perch that was moved 15 cm but surprisingly, often failed to land on it when displaced by 30 cm. In the dark, bats often failed to land on the perch after it was moved by only 15 cm. Landing failures suggest that learned spatial priors invoked inattentional blindness to changes in the environment, which interfered with successful navigation. In both the light and dark, when bats failed to land on the perch at its new location, they directed their attention toward the original perch position. Performance differences in the light and dark suggest that the bats attentional spotlight may be narrower when it relies on echolocation than vision. To our knowledge, these findings provide the first evidence of inattentional blindness in a flying echolocating animal, demonstrating that spatial priors can dominate sensory processing during navigation.

animal behavior and cognition↗

Foundry-fabricated dual-color nanophotonic neural probes for photostimulation and electrophysiological recording

SignificanceCompact tools capable of delivering multicolor optogenetic stimulation to deep tissue targets with sufficient span, spatiotemporal resolution, and optical power remain challenging to realize. Here, we demonstrate foundry-fabricated nanophotonic neural probes for blue and red photostimulation and electrophysiological recording, which use a combination of spatial multiplexing and on-shank wavelength-demultiplexing to increase the number of on-shank emitters. AimWe demonstrate Si photonic neural probes with 26 photonic channels and 26 recording sites, which were fabricated on 200-mm diameter wafers at a commercial Si photonics foundry. Each photonic channel consists of an on-shank demultiplexer and separate grating coupler emitters for blue and red light, for a total of 52 emitters. ApproachWe evaluate neural probe functionality through bench measurements and in vivo experiments by photostimulating through 16 of the available 26 emitter pairs. ResultsWe report neural probe electrode impedances, optical transmission, and beam profiles. We validated a packaged neural probe in optogenetic experiments with mice sensitive to blue or red photostimulation. ConclusionsOur foundry-fabricated nanophotonic neural probe demonstrates dense dual-color emitter integration on a single shank for targeted photostimulation. Given its two emission wavelengths, high emitter density, and long site span, this probe will facilitate experiments involving bidirectional circuit manipulations across both shallow and deep structures simultaneously.

neuroscience↗