<?xml version="1.0" encoding="UTF-8" ?>
<rdf:RDF xmlns:admin="http://webns.net/mvcb/" xmlns="http://purl.org/rss/1.0/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:prism="http://purl.org/rss/1.0/modules/prism/" xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:syn="http://purl.org/rss/1.0/modules/syndication/">
<channel rdf:about="https://biorxiv.org">
<admin:errorReportsTo rdf:resource="mailto:biorxiv@cshlpress.edu"/>
<title>bioRxiv Subject Collection: Neuroscience</title>
<link>https://biorxiv.org</link>
<description>
This feed contains articles for bioRxiv Subject Collection "Neuroscience"
</description>

<items>
<rdf:Seq>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721225v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721150v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721195v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721190v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721172v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721224v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721143v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721136v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721160v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721216v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.720989v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721238v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.28.721215v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721202v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721217v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.720701v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721133v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721107v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721106v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721075v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721094v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.720934v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.720696v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721086v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721041v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.28.721468v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721046v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.720597v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721024v1?rss=1"/>
<rdf:li rdf:resource="https://www.biorxiv.org/content/10.64898/2026.04.27.721014v1?rss=1"/>
</rdf:Seq>
</items>
<prism:eIssn/>
<prism:publicationName>bioRxiv</prism:publicationName>
<prism:issn/>

<image rdf:resource=""/>
</channel>
<image rdf:about="">
<title>bioRxiv</title>
<url>https://www.biorxiv.org/sites/default/files/bioRxiv_article.jpg</url>
<link>https://www.biorxiv.org</link>
</image>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721225v1?rss=1">
<title>
<![CDATA[
Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721225v1?rss=1
</link>
<description><![CDATA[
Background: Moyamoya disease (MMD) is a progressive cerebrovascular disorder characterized by steno-occlusive lesions and intimal hyperplasia. Although vascular smooth muscle cell (VSMC) phenotypic switching is implicated in its pathogenesis, the precise spatial interplay between extracellular matrix (ECM) remodeling and local metabolic alterations within the distinct vascular microenvironments remains unknown. Methods: Superficial temporal artery (STA) samples from patients with MMD and controls were analyzed by histology, immunofluorescence, spatial transcriptomics, spatial proteomics, and spatial metabolomics. Single cell RNA sequencing was used to profile the cellular landscape of STA tissues. To functionally validate the identified pathway, human brain vascular smooth muscle cells (HBVSMCs) were stimulated with fibronectin 1 (FN1), and patient derived induced pluripotent stem cell smooth muscle cells (iPSC-SMCs) were generated for migration and protein expression assays following ITGA5 silencing or focal adhesion kinase (FAK) inhibition. Results: MMD STA samples exhibited marked intimal hyperplasia with medial thinning and intimal accumulation of -SMA positive cells. Spatial transcriptomic and proteomic analyses identified an intimal remodeling program characterized by increased FN1, EFEMP1, fibronectin, ITGA5, and FAK, together with reduced MYH11. FN1 stimulation promoted smooth muscle cell migration, ECM associated protein expression, and FAK phosphorylation, whereas ITGA5 knockdown or FAK inhibition attenuated these effects. Patient derived MMD iPSC-SMCs showed similar abnormalities, including enhanced migration, increased FAK activation, reduced contractile markers, and increased ECM associated proteins. Spatial metabolomics and integrated multi-omics analyses further revealed that these changes were coupled to a metabolically depleted intimal niche enriched for reduced acyl-CoA related metabolites. Conclusions: Integrated spatial multi-omics identifies coupled ECM remodeling and metabolic alteration in the hyperplastic intima of MMD. Within this context, the FN1-ITGA5-FAK axis emerges as a plausible mediator of smooth muscle remodeling that warrants further validation.
]]></description>
<dc:creator><![CDATA[ He, S., Yu, X., Ahmed, T., Chang, Y., Zhou, Z., Liu, H., Xu, Y., Zhang, J., Xu, S., Du, L., Ye, X., Wang, R., Zhao, Y. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721225</dc:identifier>
<dc:title><![CDATA[Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721150v1?rss=1">
<title>
<![CDATA[
Macaque Area LIP Reflects Confidence-Dependent Changes in Decision Policy 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721150v1?rss=1
</link>
<description><![CDATA[
The process of forming a decision gives rise to an estimate of its quality or likelihood of success. This graded sense of confidence is important for guiding subsequent decisions, but a neural mechanism linking subjective confidence to formation of the next decision has not been identified. We trained rhesus monkeys to report a perceptual choice and simultaneous confidence judgment in a reaction-time (RT) motion discrimination task. Monkeys were more likely to repeat a rewarded choice when they reported low confidence on the previous trial, and showed greater changes in RT after a surprising outcome (low-confidence correct or high-confidence error). Neural activity in the lateral intraparietal area (LIP) encoded the previous trial's choice and confidence more strongly after a low-confidence correct trial, and the strength of history encoding was correlated with a trial-by-trial estimate of choice bias. Ramping dynamics of the decoded decision variable also depended systematically on the conjunction of confidence and reward on the previous trial, in a manner that reflected individual differences between animals. The findings suggest that LIP not only reflects the formation of the current decision but could participate in confidence-guided learning via adjustments of the subsequent decision process.
]]></description>
<dc:creator><![CDATA[ Tu, M. S., Vivar-Lazo, M., Fetsch, C. R. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721150</dc:identifier>
<dc:title><![CDATA[Macaque Area LIP Reflects Confidence-Dependent Changes in Decision Policy]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721195v1?rss=1">
<title>
<![CDATA[
Premotor cortex uses a compositional neural geometry to plan words 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721195v1?rss=1
</link>
<description><![CDATA[
Speech requires precise serial ordering of words and phonemes into novel combinations. To accomplish this, the brain is believed to flexibly prepare utterances before producing them, even allowing pronunciation of never-before spoken words. To discover how neural populations achieve this, intracortical activity from premotor cortex was recorded while two speech neuroprosthesis pilot clinical trial participants attempted to speak factorially-balanced phoneme sequences. During preparation, activity encoded not only the next-phoneme, but multiple upcoming phoneme positions spanning whole words. We found that word-level plans were formed by compositionally combining phoneme representations, a mechanism that may enable efficient planning of novel sequences. When utterances contained more than one word, premotor cortex activity was largely limited to the first word, suggesting that articulatory planning is segmented by higher-order features. Together, these results reveal a compositional, hierarchically-segemented planning geometry, potentially a universal neural strategy for sequence organization across higher levels of language.
]]></description>
<dc:creator><![CDATA[ Abramovich Krasa, B., Kunz, E. M., Kamdar, F., Avansino, D., Hahn, N. V., Singh, A., Card, N. S., Wairagkar, M., Iacobacci, C., Hochberg, L. R., Brandman, D. M., Stavisky, S. D., Henderson, J. M., Willett, F. R., Druckmann, S. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721195</dc:identifier>
<dc:title><![CDATA[Premotor cortex uses a compositional neural geometry to plan words]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721190v1?rss=1">
<title>
<![CDATA[
Sniffing Shapes Dopamine Signals for Reward Prediction 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721190v1?rss=1
</link>
<description><![CDATA[
Adaptive behaviors depend on predicting outcomes from sensory evidence. Dopamine neurons in the ventral tegmental area (VTA) broadcast reward-prediction signals that guide learning. Yet the principles functionally coordinating information flow from input regions to VTA are incompletely understood. In the olfactory system, the sniff cycle structures sampling and odor encoding. We therefore asked whether this rhythm also entrains the ventral striatum to VTA communication and if so, how this shapes the implementation of predictive coding in dopamine neurons. We recorded identified dopamine neurons throughout olfactory conditioning and found that their firing shifted systematically to the post-inspiratory phase of the sniff cycle with learning. This temporal realignment predicted a neuron's engagement in value encoding along the optimism-pessimism-spectrum of distributional reinforcement learning. This is associated with an enhanced phase-gated communication channel from the striatal olfactory tubercle to dopamine neurons, the strength of which predicts task performance. Thus, the sniffing rhythm provides a scaffold for information flow, revealing a phase-gating mechanism for the integration of outcome predicting sensory evidence to dopamine neurons during reinforcement learning.
]]></description>
<dc:creator><![CDATA[ Scheller, M. F., Luis, C., Kelsch, W. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721190</dc:identifier>
<dc:title><![CDATA[Sniffing Shapes Dopamine Signals for Reward Prediction]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721172v1?rss=1">
<title>
<![CDATA[
In Vivo Massively Parallel Reporter Assay Reveals Sequence Determinants of mRNA Localization in Astrocytes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721172v1?rss=1
</link>
<description><![CDATA[
RNA localization and local translation are essential mechanisms to fine-tune spatiotemporal gene expression in the nervous system. However, efficiently assessing the thousands of possible sequence determinants of RNA localization is a challenge, particularly for cell types that only reach morphological maturity in vivo. Here, we developed an in vivo Massively Parallel Reporter Assay (MPRA), termed Synaptoneurosomal (SN)-MPRA to enable identification of sequence determinants of mRNA localization and local translation, and applied this to astrocytes. We evaluated multiple models of RNA localization for two locally translated astrocyte mRNAs, Glt1 and Sparc, including increased transcript abundance, "zipcode" elements, and RNA secondary structure. Our results establish a high-throughput in vivo framework for identifying cis-regulatory sequences driving RNA localization and local translation, and suggest astrocytes use diverse mechanisms to regulate subcellular gene expression. More broadly, SN-MPRA offers a versatile platform to study RNA localization in vivo, where biological context and intercellular interactions are preserved.
]]></description>
<dc:creator><![CDATA[ Koester, S. K., Sakers, K., Rurak, G. M., Plassmeyer, S. P., McFarland White, K., Alves Ferreira Dias, S., Baird, P., Kornbluth, D. J., Dougherty, J. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721172</dc:identifier>
<dc:title><![CDATA[In Vivo Massively Parallel Reporter Assay Reveals Sequence Determinants of mRNA Localization in Astrocytes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721224v1?rss=1">
<title>
<![CDATA[
Modulation statistics allow robust prediction of speech recognition accuracy across many words, voices, and natural background sounds. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721224v1?rss=1
</link>
<description><![CDATA[
Although humans excel at speech recognition, recognition accuracy can vary widely due to differences in background environments as well as the speaker's voice quality, intonation, and pitch. Predicting when speech recognition will succeed or fail, however, remains an ongoing challenge in hearing research. Here we characterize recognition abilities across a wide range of natural conditions using digits spoken by many male and female talkers of multiple ages with 33 unique backgrounds. Across this diverse set of sounds, speech recognition is most strongly influenced by the spectrum and modulation statistics of the noise. Yet, articulatory features of the speech, including fundamental and formant frequencies, show categorically distinct modulatory effects on accuracy across age, gender, and words. We then show that a low-dimensional model of sound, based on computations in the auditory midbrain, accounts for participants' single-trial recognition behavior across voices, words and backgrounds. Thus, speech-in-noise perception across extremely diverse natural conditions depends largely on a simple set of spectrotemporal statistics likely encoded by central neural populations.
]]></description>
<dc:creator><![CDATA[ Clonan, A. C., Stevenson, I. H., Escabi, M. A. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721224</dc:identifier>
<dc:title><![CDATA[Modulation statistics allow robust prediction of speech recognition accuracy across many words, voices, and natural background sounds.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721143v1?rss=1">
<title>
<![CDATA[
Benchmarking spatial interpolation methods for brain maps 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721143v1?rss=1
</link>
<description><![CDATA[
The human brain is a unique biological space that hosts complex processes unfolding at multiple scales. To study these processes, an abundance of imaging technologies evolved over many decades to produce large-scale, dense mappings of structural and functional features. In parallel, a rich universe of techniques for cellular and molecular biology supplies us with fine-scale, highly specific and reliable measurements in sparse tissue samples. To represent cortical processes integratively across scales, spatial interpolation is necessary for bridging dense and sparse data. The absence of a field consensus for realistic interpolation of features over the whole brain prompts a comprehensive comparison of existing frameworks from the broader scientific literature. Here, we benchmark the performance of multiple deterministic (Inverse Distance Weighting, K-Nearest Neighbours, and Radial Basis Function) and stochastic (Spatially-Weighted Regression, Ordinary Kriging, and Regression Kriging) strategies first with simulated or empirical ground truths. We then demonstrate two use cases with textit{de novo} sparse brain data (intracranial EEG and microarray gene expression). In these experiments, we investigate how differences in data characteristics, such as spatial dependency structure and sampling distribution, impact the performance of different interpolation methods. Throughout the results, we consistently find that maps interpolated through spatially-informed stochastic frameworks such as Ordinary Kriging and Regression Kriging are more accurate and biologically realistic across geometric constraints, data modalities, and sampling conditions. This invites continued development of spatially-informed statistical frameworks for analyzing brain data and, more fundamentally, the biological processes that produce them.
]]></description>
<dc:creator><![CDATA[ Zhou, Y., Bazinet, V., Misic, B. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721143</dc:identifier>
<dc:title><![CDATA[Benchmarking spatial interpolation methods for brain maps]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721136v1?rss=1">
<title>
<![CDATA[
A motif for domain-specific analysis applets that are easy to learn, reuse, test, and to compose into pipelines: application to vision science 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721136v1?rss=1
</link>
<description><![CDATA[
Scientific progress depends on the analysis of primary data, yet the small, domain-specific programs that perform most scientific analyses are typically poorly documented, narrowly tested, and difficult to reuse outside the lab that created them. General-purpose pipeline tools address the problem of running steps in order but do not enforce documentation, testing, or standardized outputs. We describe a motif for building domain-specific analysis applets, which we call calculators, that constrains developer choices in order to produce code that is readable, tested, and reusable almost as a byproduct of following the template. Calculators operate on a typed, searchable database of documents, eliminating the need to explicitly wire inputs and outputs together; instead, each calculator searches the database for documents it can operate on and adds its results as new typed documents. Calculators must provide documentation in a standard location, self-tests that can be run and inspected interactively, adjustable input parameters, a single well-defined output document type, and a default plotting method. Sets of calculators compose naturally into pipelines whose outputs satisfy FAIR principles at every stage. We demonstrate the motif by implementing calculators for common analyses in vision science, including orientation and direction selectivity, contrast tuning, spatial and temporal frequency tuning, speed tuning, and Hartley reverse correlation. These calculators have been used in published work and are in active use across collaborating laboratories. We discuss the design principles of the motif, its advantages and limitations, and its applicability to domain-specific computation across neuroscience and beyond.
]]></description>
<dc:creator><![CDATA[ Lepsky, A. A., Severson, M. K., Wang, R., Cheng, X., Rodriguez, R. L., Gong, R., Van Hooser, S. D. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721136</dc:identifier>
<dc:title><![CDATA[A motif for domain-specific analysis applets that are easy to learn, reuse, test, and to compose into pipelines: application to vision science]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721160v1?rss=1">
<title>
<![CDATA[
An integrated RNA-centric imaging and omics approach reveals distinct properties and composition of neuronal RNA granules 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721160v1?rss=1
</link>
<description><![CDATA[
RNA granules are essential regulators of post-transcriptional gene expression, enabling mRNA transport, localization, and local translation in neurons. The localized transcriptome is diverse; however, how different mRNAs are organized into granules for efficient localization and translation remains unknown. Here, we combine real-time endogenous single RNA imaging with protein and RNA proximity labeling to investigate two distinct endogenous neuronal mRNA granule populations, Actb and Arc, in stimulated primary hippocampal neurons. Using orthogonal RNA labeling systems in a dual knock-in mouse model, we show that Actb and Arc mRNAs are packaged into spatially segregated granules with distinct trafficking dynamics, localization kinetics, and responses to synaptic stimulation. Actb granules displayed rapid and sustained localization, whereas Arc granules showed delayed, transient recruitment, consistent with their respective roles in structural and activity-dependent plasticity. Proximity labeling reveals that these granules are distinct in their mRNA composition, despite sharing core RNA-binding proteins, suggesting that shared cis-regulatory elements within mRNA 3'UTR regions drive selective co-packaging of mRNAs into unique granules. Together, these findings demonstrate that neuronal mRNAs are differentially sorted into molecularly and functionally distinct granules, providing a framework for understanding how precise spatio-temporal control of mRNA localization and translation is achieved across complex neuronal arbors.
]]></description>
<dc:creator><![CDATA[ Rogow, J. A., Doron-Mandel, E., Cutler, R., Nunez, L., Vazquez, R., Harris, L., Jovanovic, M., Singer, R. H., Das, S. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721160</dc:identifier>
<dc:title><![CDATA[An integrated RNA-centric imaging and omics approach reveals distinct properties and composition of neuronal RNA granules]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721216v1?rss=1">
<title>
<![CDATA[
Explicit knowledge gates expectation suppression in the motor system: Evidence from a TMS motor oddball paradigm 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721216v1?rss=1
</link>
<description><![CDATA[
Models of predictive processing propose that the brain continuously generates predictions about incoming sensory input, updating an internal model of the environment through prediction errors when those predictions are violated. A foundational assumption of these models is that prediction error generation occurs automatically, independently of conscious awareness. Evidence from auditory oddball studies in unconscious patients appears to support this view, though findings are complicated by stimulus-specific adaptation confounds that make it difficult to isolate genuine predictive effects. To investigate whether expectation suppression or prediction-based attenuation extends to the motor system and whether it operates automatically, we developed a novel motor oddball paradigm using brain stimulation. Transcranial magnetic stimulation (TMS) delivered over the primary motor cortex elicit motor-evoked potentials (MEPs) in peripheral muscles, providing an index of corticospinal excitability. By varying stimulation intensity in an oddball-like manner using repeating and deviating sequences, we manipulated the predictability of TMS pulses and compared MEP amplitudes for expected versus unexpected intensity-matched stimulation. Incorporating experimental designs to control for adaptation and an instruction manipulation to test the role of awareness, expected TMS reliably produced smaller MEPs than unexpected TMS. Critically, this attenuation was observed only in participants with explicit knowledge of the sequence structure. These findings extend expectation suppression effects to the motor system and support the domain-generality of prediction-based neural attenuation while challenging the assumption that predictive processing operates entirely automatically.
]]></description>
<dc:creator><![CDATA[ Cost-Chretien, M. E., Rideaux, R., Tran, D. M. D. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721216</dc:identifier>
<dc:title><![CDATA[Explicit knowledge gates expectation suppression in the motor system: Evidence from a TMS motor oddball paradigm]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.720989v1?rss=1">
<title>
<![CDATA[
Auditory Attention Implements Complementary but Independent Cortical Mechanisms of Enhancement and Suppression 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.720989v1?rss=1
</link>
<description><![CDATA[
In noisy environments, goal-directed behavior requires the brain to prioritize task-relevant sound and to suppress distraction. While mechanisms of proactive attention in the presence of foreknowledge about targets and distractors are well-characterized, the neural dynamics governing reactive auditory attention in the absence of foreknowledge remain less understood. To fill this gap, we recorded the electroencephalogram (EEG) from N = 34 participants performing an auditory search task. Participants identified an amplitude-modulated spoken target number amid distractor numbers of varying salience. Presenting stimuli from three spatial locations enabled isolation of lateralized electrophysiological responses to targets and distractors. We quantified selection of targets versus distractors by continuously tracking cursor movements of participants on a virtual response pad. Behaviorally, the target-directedness of cursor movements (i.e., towardness) increased for target repetitions (positive priming) and decreased when the target was a distractor from the previous trial (negative priming), indicating respective enhancement and suppression. Neurally, lateral targets evoked an N2ac component reflecting reactive enhancement. Importantly, we here demonstrate for the first time in an auditory attention task that distracting sounds evoke an auditory distractor positivity (PD) component. Target enhancement and distractor suppression were largely independent: their neural and behavioral markers were not significantly correlated and they originated from distinct cortical sources. Furthermore, shorter N2ac, but not PD, latencies related to higher towardness. By dissociating neural signatures and behavioral relevance of enhancement and suppression, our findings refine biased-competition models of attention, demonstrating that reactive selection relies on separable mechanisms rather than a single competitive gain process.
]]></description>
<dc:creator><![CDATA[ Schulz, M., Gundlach, C., Obleser, J., Woestmann, M. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.720989</dc:identifier>
<dc:title><![CDATA[Auditory Attention Implements Complementary but Independent Cortical Mechanisms of Enhancement and Suppression]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721238v1?rss=1">
<title>
<![CDATA[
Fast learning, memorization and generalization: A computational characterization of sparse to dense hippocampal-cortical codes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721238v1?rss=1
</link>
<description><![CDATA[
Classic findings from neuropsychology and animal studies established the hippocampus as a key substrate for rapid learning and episodic memory, with the dentate gyrus exhibiting extreme sparse coding. Sparse coding has long been hypothesized to enable fast learning through pattern separation, enabling rapid separation of highly similar inputs. However, prior computational work has largely focused on episodic memory or simplified linear tasks, leaving open how hippocampal sparsity affects learning speed and generalization in complex tasks. Here, we present a systematic investigation of sparse coding in deep neural networks varying the sparsity level and location (layer depth) and evaluated the functional consequences for learning and generalization. We found that learning performance is maximized at a balanced sparsity level of 5%, matching empirical estimates of the hippocampal sparse code. Dimensionality and representational similarity analyses revealed that sparse layers promoted orthogonalization of input representations, mirroring hippocampal pattern separation that enables fast learning. Furthermore, sparsity in early layers led to fast learning only on the training set and poor generalization to a held out test set, reflecting memorization, while sparsity in later layers consistently aided generalization, providing implications for theories of hippocampal-cortical learning. Our findings demonstrate the power and tradeoffs of the hippocampal sparse code, and show how hippocampal-cortical circuits possess the computational capacity to support both fast learning and generalization, depending on where sparsity is implemented. We offer a unifying perspective on how the hippocampus works as a fast, sparse memory system and the hippocampal-cortical pathway as a mechanism for generalizable learning.
]]></description>
<dc:creator><![CDATA[ Sasan, A., Mok, R. M. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721238</dc:identifier>
<dc:title><![CDATA[Fast learning, memorization and generalization: A computational characterization of sparse to dense hippocampal-cortical codes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.28.721215v1?rss=1">
<title>
<![CDATA[
Interactions between hippocampus and visceral organs in sleep and wakefulness 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.28.721215v1?rss=1
</link>
<description><![CDATA[
Exteroception is attenuated during sleep, while interoceptive signals may remain active. If so, they can trigger responses in their target areas, including the hippocampus, which is known to receive information from the internal organs and is susceptible to oversynchronization while triggered. We investigated whether the hippocampus is synchronized to various visceral events in sleep and wakefulness. Activity of hippocampal neurons and local field potentials (LFPs) was co-registered with respiration, heart rate and myoelectric signals of the stomach and duodenum in two adult female cats over multiple sleep-wake cycles. Visceral event-triggered and neuronal spike-triggered (bootstrapping-based) analyses were performed in wakefulness and slow wave sleep (SWS). Synchronization between visceral and hippocampal activities occurred in both wakefulness and SWS. However, hippocampal cells and LFPs showed preferences for one state only. Consistent with prior studies, we found the strongest link between high-amplitude respiratory events and hippocampal activity, with significantly higher occurrence during SWS. Both stomach and duodenal signals were also represented in hippocampal activity. Motility-associated duodenal myoelectric signals correlated with hippocampal activity more during wakefulness where gastrointestinal motility is more active, while synchronization between regular duodenal waves and the hippocampus was more frequent during SWS. We conclude that the interoceptive signals reach the hippocampus in both sleep and wakefulness and suggest that they have the potential to oversynchronize any ongoing synchronized slow-wave activities in the hippocampal network during SWS
]]></description>
<dc:creator><![CDATA[ Levichkina, E., Pigarev, I. N., Vidyasagar, T. R. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.28.721215</dc:identifier>
<dc:title><![CDATA[Interactions between hippocampus and visceral organs in sleep and wakefulness]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721202v1?rss=1">
<title>
<![CDATA[
Visual activity in primate superior colliculus requires geniculostriate input 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721202v1?rss=1
</link>
<description><![CDATA[
The superior colliculus (SC) is an ancient visual structure whose principle source of visual drive comes directly from the retina. In primates, however, the SC also receives geniculostriate input from primary visual cortex (V1) via the lateral geniculate nucleus (LGN), making it unclear which pathway normally drives visually evoked spiking. Here we tested whether visually evoked spiking in the primate SC depends on retinal signals routed through LGN and V1, rather than on direct retinal input alone. We recorded from macaque SC neurons before and during reversible inactivation of the ipsilateral LGN and found that LGN inactivation nearly abolished visually evoked spiking. This loss was not due to nonspecific suppression of SC, because saccade-related bursts were spared and was observed across SC layers. Magnocellular-biased stimuli, designed to reveal any potential direct retinal drive, failed to produce visually evoked spiking during LGN inactivation. Interhemispheric inhibition (i.e., a "Sprague effect") was ruled out, because contralateral SC silencing during LGN inactivation did not restore SC visual responses. Consistent with a geniculostriate input route to SC, V1 inactivation also reduced SC visual responses, with effects proportional to the overlap between the V1-induced scotoma and the stimulus representation. Together, these results show that visually evoked neural responses in primate SC depend on retinal signals routed through LGN and V1, and that direct retinotectal input is insufficient to drive SC spiking in the absence of geniculostriate input. These findings revise current models of visual drive to the primate SC and constrain theories of SC-dependent visual behavior.
]]></description>
<dc:creator><![CDATA[ Katz, L. N., Yu, G., Krauzlis, R. J. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721202</dc:identifier>
<dc:title><![CDATA[Visual activity in primate superior colliculus requires geniculostriate input]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721217v1?rss=1">
<title>
<![CDATA[
NEURA: An agentic system for autonomous neuroimaging workflows 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721217v1?rss=1
</link>
<description><![CDATA[
Neuroimaging is essential for studying the human brain; however, the deep interdisciplinary expertise required imposes a very high threshold, limiting its broader clinical and scientific applications. We introduce NEURA, a large language model (LLM)-powered agentic system for automated neuroimaging workflow planning and analysis. NEURA processes free-text research questions and multimodal neuroimaging datasets to generate evidence-grounded analysis plans, executable scripts, validated statistical results and structured reports, with traceable reasoning linked to intermediate artefacts and full execution records. Through extensive evaluations on a curated benchmark, NEURA achieved an 89.5% planning accuracy and substantially outperformed direct LLM queries, with average gains of 30.5% in planning accuracy, 25.6% in tool selection and 36.7% in tool ordering. In case studies of spinocerebellar ataxia type 3, NEURA autonomously identified cerebellar atrophy and abnormal diffusivity patterns consistent with established pathologies and expert manual analyses. Collectively, these results demonstrate that our work advances from pipeline automation to rigorous, scalable and interpretable neuroimaging research systems.
]]></description>
<dc:creator><![CDATA[ Xie, J., Wang, J., Wu, X., Liu, X., Mi, Y., Liu, Q., Xu, T., Liu, C., Chen, H., Guo, J. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721217</dc:identifier>
<dc:title><![CDATA[NEURA: An agentic system for autonomous neuroimaging workflows]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.720701v1?rss=1">
<title>
<![CDATA[
Multidimensional dynamics of object representations in the human visual system 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.720701v1?rss=1
</link>
<description><![CDATA[
Natural image representations are distributed across many dimensions of visual cortex activity, but little is known about how the multidimensional structure of these representations evolves over time following stimulus onset. Here we examined the temporal dynamics and latent dimensional structure of natural object representations in large-scale EEG and MEG data. We also compared these data with leading representational models derived from large-scale human similarity judgments and deep neural networks. Our findings reveal a rapid expansion of stimulus dimensionality in the brain, which peaks within 100 milliseconds and gradually decays over hundreds of milliseconds. The dynamics of these dimensionality changes tracked the decoding accuracy for both behavioral embeddings and neural network features, suggesting that dimensionality may be a general indicator of representational expressivity. Interestingly, the dimensionality of the neural representations could not be fully explained by leading behavior-based or neural network models. Follow-up experiments showed that the remaining neural variance carried additional perceptually relevant information not yet explained by leading models. Together, these findings reveal previously unrecognized complexity in measurements of dynamic human brain responses to natural objects.
]]></description>
<dc:creator><![CDATA[ Chen, Z., Isik, L., Bonner, M. F. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.720701</dc:identifier>
<dc:title><![CDATA[Multidimensional dynamics of object representations in the human visual system]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721133v1?rss=1">
<title>
<![CDATA[
Gut microbiota-derived indole-3-propionic acid preserves dorsal hippocampal catecholamines to prevent post-stroke cognitive impairment 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721133v1?rss=1
</link>
<description><![CDATA[
Background Gut dysbiosis has been increasingly implicated in post-stroke cognitive impairment (PSCI), yet the causal contribution and therapeutic potential of gut microbiota-derived metabolites remain unclear. This study aimed to identify key microbiota-derived metabolites involved in PSCI and to elucidate their underlying mechanisms. Results We found that both PSCI patients and middle cerebral artery occlusion (MCAO) mice exhibited distinct gut microbial alterations, characterized by a marked reduction in tryptophan-metabolizing bacteria and indole-3-propionic acid (IPA), a gut microbiota-derived tryptophan metabolite. Exogenous IPA administration alleviated PSCI-like phenotypes in MCAO mice. Mechanistically, IPA preserved tyrosine hydroxylase-positive (Th+) fibers and catecholamine levels in the dorsal hippocampus. Further analyses showed that IPA binds to the adaptor protein Ywhab, promotes ERK activation, and enhances neuronal survival, thereby counteracting neuronal apoptosis-associated inflammation and subsequent Th+ fiber degeneration. Conclusion These findings identify IPA as a gut microbiota-derived neuromodulator that mitigates PSCI by preserving dorsal hippocampal catecholaminergic transmission. IPA may therefore serve as a promising predictive biomarker and therapeutic candidate for PSCI.
]]></description>
<dc:creator><![CDATA[ Liu, Y., Zhang, H., Xia, F., Gao, X. X., Li, Z., Zhao, X., Wu, F., Li, M., Xu, K., Chen, M., Ren, Y., Hu, W., Yin, J., Zhou, H.-W., Zhang, D. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721133</dc:identifier>
<dc:title><![CDATA[Gut microbiota-derived indole-3-propionic acid preserves dorsal hippocampal catecholamines to prevent post-stroke cognitive impairment]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721107v1?rss=1">
<title>
<![CDATA[
Premovement suppression of corticospinal excitability is modulated by reaction time task requirements 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721107v1?rss=1
</link>
<description><![CDATA[
The amplitude of motor-evoked potentials (MEPs) elicited using transcranial magnetic stimulation (TMS) has been shown to decrease in the short interval prior to response initiation. The cause of this premovement MEP suppression is currently unclear and has been attributed to various processes such as preparation-related inhibition preventing the premature release of planned action or increasing signal-to-noise ratio to facilitate rapid response initiation. The present study explored whether the decrease in MEP amplitude is affected by the task requirements, using reaction time (RT) paradigms that differ in the timeline of preparation and initiation of a motor response. Participants completed simple RT (SRT), choice RT (CRT), and go/no-go (GNG) tasks, while TMS was applied at various times between the warning signal and go-signal. It was hypothesized that if MEP suppression relates to preparation level, the greatest suppression would be observed during the SRT and GNG tasks, as these paradigms encourage advance preparation and response inhibition. Conversely, if the reduction in corticospinal excitability is associated with facilitating response initiation processes, then suppression would be expected for all tasks, including the CRT paradigm in which preparation does not occur until presentation of the go-signal. Results showed MEP amplitudes decreased for all tasks as the go-signal approached; however, both the SRT and GNG had significantly greater MEP suppression 50 ms prior to, and coincident with the go-signal. These results indicate that the nature and origin of the suppression is likely multifactorial and relates to both preparatory and initiation-related processes, with the timeline and magnitude of suppression dependent on the nature of the task being executed.
]]></description>
<dc:creator><![CDATA[ Carlsen, A. N., Santangelo, C. M., Sadler, C. M., Maslovat, D. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721107</dc:identifier>
<dc:title><![CDATA[Premovement suppression of corticospinal excitability is modulated by reaction time task requirements]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721106v1?rss=1">
<title>
<![CDATA[
fMRI and MEG Fingerprints Diverge at the Individual Level 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721106v1?rss=1
</link>
<description><![CDATA[
Abstract: Functional connectivity (FC) profiles derived from fMRI and MEG offer complementary perspectives on large-scale brain organization, while showing reasonable correspondence at the population-average level. However, how their individual variability relates between these modalities remains unclear. Using the Cam-CAN dataset, we derived neural fingerprints from subject-level resting-state fMRI FC and MEG FC obtained from the same participants (N=543). Fingerprints derived from each modality separately showed robust within-subject, cross-session consistency and successfully predicted age and cognition, confirming that these features capture stable and behaviourally relevant individual traits. We then quantified shared individual variability between modalities using variance partitioning analyses and representational similarity measures. Two main findings emerged. First, despite strong similarity at the population-average level, correspondence between MEG and fMRI neural fingerprints at the subject level was low, as reflected in both cross-modal shared variance and the preservation of pairwise inter-subject similarity patterns, quantified by linear Centred Kernel Alignment (CKA). Second, structural fingerprints accounted for the majority of age-related variance in functional neural fingerprints, almost entirely explaining the age-related variance in, and shared between, fMRI and MEG. MEG functional fingerprints did have unique information not accounted for by structure when explaining variability in cognitive traits, but this was not shared with fMRI. Together, these findings demonstrate that there is a surprisingly lack of similarity in the way that subjects vary between fMRI and electrophysiology, especially when structural variability is accounted for.
]]></description>
<dc:creator><![CDATA[ Mo, B. Z., Smith, S., Woolrich, M. W. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721106</dc:identifier>
<dc:title><![CDATA[fMRI and MEG Fingerprints Diverge at the Individual Level]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721075v1?rss=1">
<title>
<![CDATA[
Divergent molecular and circuit mechanisms underlie light entrainment of retinal and suprachiasmatic nucleus circadian clocks 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721075v1?rss=1
</link>
<description><![CDATA[
The circadian system aligns behavior and physiology with the 24-hour environmental cycle through a distributed network of clocks including the master pacemaker in the suprachiasmatic nucleus (SCN) and an autonomous retinal clock critical for local retinal physiology and function. Although both clocks are entrained by light, they differ in their photoreceptor inputs and light sensitivity. The specific contributions and mechanisms by which distinct photoreceptor pathways drive their photoentrainment, however, remain incompletely understood. In this study, we conducted a comprehensive transcriptomic and integrative comparative analysis of retinal and SCN circadian light responses using mouse models lacking specific photoreceptors or key components of signaling pathways. Under photopic conditions, we found that each tissue displays distinct light-responsive transcriptional signatures across genotypes, yet both shared a conserved cluster of rod-driven immediate early-genes. Strikingly, the light-evoked transcriptional response was not sufficient to shift the phase of the SCN clock, in contrast to its robust phase-shifting effect on the retinal clock. Furthermore, by genetically disrupting rod/cone electrical coupling and pharmacologically isolating rod pathways, we identified the OFF-cone bipolar cell circuit as both necessary and sufficient to mediate light-induced phase resetting of the retinal clock. Together, these findings delineate the specialized retinal circuitry that underlies circadian entrainment and reveal a fundamental divergence between retinal and SCN mechanisms of photic timekeeping.
]]></description>
<dc:creator><![CDATA[ Jandot, A., Calligaro, H., Dianak-Shoori, A., Tartour, K., Sandu, C., Haddjeri, N., Ribelayga, C. P., Ananthasubramaniam, B., Padmanabhan, K., Felder-Schmittbuhl, M.-P., Dkhissi-Benyahya, O. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721075</dc:identifier>
<dc:title><![CDATA[Divergent molecular and circuit mechanisms underlie light entrainment of retinal and suprachiasmatic nucleus circadian clocks]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721094v1?rss=1">
<title>
<![CDATA[
Coherence from Context - Two-Point Neuron Models for Contextual Integration in Visual Information Processing 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721094v1?rss=1
</link>
<description><![CDATA[
The integration of contextual information is crucial for coherent perception and cognition. The morphology and conductance properties of cortical pyramidal cells suggest that they operate as "two-point neurons" (TPNs), asymmetrically combining driving sensory input at basal dendrites with modulating context at apical compartments. We present a mechanistic computational TPN model that captures the causal cell-internal apical-basal integration. The model is extended incorporating the interactions between pyramidal cells and local inhibitory interneuron circuits of PV, SOM, and VIP cells. The model rests on guiding principles of asymmetric feedforward-feedback integration, contextual feedback, and pooled inhibition to implement local competition and global cooperation supporting the selective amplification of coherent signals. We validate our approach against detailed multi-compartment pyramidal cell simulations reproducing key electrophysiological phenomena. We then extend it to interacting TPN populations with joint spatial and feature selectivity. In such networks, contextual signals propagate through structured lateral recurrence and top-down feedback, exhibiting contextual integration, coherence formation, and evidence propagation. To support larger-scale network simulations, we derive a reduced mathematical model that preserves the core computational principles of TPNs, while substantially reducing complexity. We demonstrate the model's applicability in biological vision, showing how it explains motion integration and incremental grouping--processes requiring dynamic resolution of perceptual ambiguity. Finally, we discuss how the proposed framework connects cellular and circuit-level mechanisms of pyramidal neurons to broader questions about cortical computation, the formation of representations for globally consistent perceptual states, and the potential for embedding TPN principles into artificial neural network architectures.
]]></description>
<dc:creator><![CDATA[ Schmid, D., Neumann, H. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721094</dc:identifier>
<dc:title><![CDATA[Coherence from Context - Two-Point Neuron Models for Contextual Integration in Visual Information Processing]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.720934v1?rss=1">
<title>
<![CDATA[
Poly(lactic-co-glycolic acid) immunomodulatory nanoparticles attenuate neuroinflammation and Alzheimer's disease-related pathology in 5xFAD mice 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.720934v1?rss=1
</link>
<description><![CDATA[
Alzheimer's disease is characterized by progressive cognitive decline, amyloid-{beta} deposition, neuroinflammation, and neurodegeneration, yet effective and well-tolerated therapies remain limited. Because dysregulated myeloid responses are increasingly recognized as important drivers of disease progression, we investigated the therapeutic potential of poly(lactic-co-glycolic acid) immunomodulatory nanoparticles in the 5xFAD mouse model of amyloid-driven neurodegeneration. Poly(lactic-co-glycolic acid) immunomodulatory nanoparticles and fluorescently labeled particles displayed the expected size range and negative surface charge. After intraperitoneal administration, fluorescent particles were preferentially associated with myeloid cells in the blood, spleen, and brain, with greater uptake by brain myeloid populations in 5xFAD mice than in wild-type controls. Therapeutic treatment of 6.5-month-old 5xFAD mice, a stage at which behavioral abnormalities are already established, resulted in significant improvement in elevated plus maze behavior and a more modest improvement in Barnes maze performance. Flow cytometric analysis performed 9 weeks after the final treatment demonstrated persistent changes in brain immune composition, with the most prominent effects observed in P2RY12+ microglial populations, particularly the CD11c+ subset, and comparatively limited sustained effects in CD11b+P2RY12- myeloid cells. These changes were accompanied by reduced expression of activation- and disease-associated markers and lower pro-inflammatory cytokine production within microglial populations. Histological analysis further showed reduced cortical amyloid plaque burden, decreased CD68 immunoreactivity, and reduced neurodegeneration in treated 5xFAD mice. Together, these findings show that systemically administered poly(lactic-co-glycolic acid) immunomodulatory nanoparticles produce durable behavioral, immunological, and pathological benefits in 5xFAD mice and support further investigation of this biodegradable myeloid-targeted platform as a therapeutic strategy for Alzheimer's disease.
]]></description>
<dc:creator><![CDATA[ Sanders, B., Korthauer, M., Singh Parihar, K., Ifergan, I. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.720934</dc:identifier>
<dc:title><![CDATA[Poly(lactic-co-glycolic acid) immunomodulatory nanoparticles attenuate neuroinflammation and Alzheimer's disease-related pathology in 5xFAD mice]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.720696v1?rss=1">
<title>
<![CDATA[
Complement Dysregulation During the Early Phases of Synucleinopathy 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.720696v1?rss=1
</link>
<description><![CDATA[
Parkinsons disease (PD) is characterized by progressive degeneration of nigrostriatal dopamine neurons and synucleinopathy, which is the accumulation of aggregated alpha-synuclein (a-syn). Increasing evidence implicates a-syn-associated neuroinflammation as a contributor to PD pathogenesis; however, immune mechanisms linking synucleinopathy to neurodegeneration remain incompletely defined. Activation of the complement cascade occurs in PD and other neurodegenerative disorders, but most studies report complement activation after overt neurodegeneration, making it difficult to conclude if complement is directly activated by pathological a-syn or secondarily following neurodegeneration. We used the rat a-syn preformed fibril (PFF) mode, in vitro complement assays and human postmortem PD tissue to test whether pathological a-syn directly activates complement prior to overt neurodegeneration. The a-syn PFF model exhibits a protracted pathological time course and distinct temporal separation between peak a-syn aggregation and nigrostriatal degeneration; thus we quantified complement expression, activation, and regulation during the aggregation phase. Synucleinopathy induced complement activation prior to nigrostriatal degeneration, including upregulation of components of both the classical (C1qa, C1r, C4b) and alternative (Cfd, Cfb) pathways, the anaphylatoxin (C3aR, C5aR) and phagocytic (CR3) complement receptors, and activation of complement C3. During early synucleinopathy, microglia upregulated C3 which significantly correlated with synucleinopathy burden across several brain regions, including the substantia nigra pars compacta (SNc) and cortex. Concurrently, complement regulatory proteins, including CD55, CD59, neuronal pentraxin-1 (Nptx1), and the neuronal pentraxin receptor were downregulated in the synucleinopathy-affected SNc. Importantly, increased levels of C1q and iC3b along with downregulation of CD55 and NPTX1 were also observed in human postmortem PD SNc, supporting the translational relevance of our findings. Mechanistically, we demonstrate that aggregated, but not monomeric, a-syn directly binds C1q and activates the complement cascade in a C1q-dependent manner. These data provide the first in vivo evidence that synucleinopathy triggers complement activation and dysregulation prior to neurodegeneration.
]]></description>
<dc:creator><![CDATA[ Khan, H., Gifford, M., Kordbacheh, A., Bury, A., Panoushek, S., Cole-Strauss, A., Kemp, C. J., Luk, K. C., Steece-Collier, K., Khun, N. C., Kanaan, N. M., Sortwell, C. E., Patterson, J. R., Benskey, M. J. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.720696</dc:identifier>
<dc:title><![CDATA[Complement Dysregulation During the Early Phases of Synucleinopathy]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721086v1?rss=1">
<title>
<![CDATA[
Towards Identifying a Molecular Activator of Spreading Depolarization Generated by the Ischemic Brain 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721086v1?rss=1
</link>
<description><![CDATA[
Spreading depolarizations (SDs) are waves of neuronal depolarization that propagate through gray matter following Na+/K+-ATPase (NKA) failure because of stroke, traumatic brain injury or sudden cardiac arrest. SDs expand the initial site of neuronal injury and worsen clinical outcomes. The molecular events underlying SD initiation and propagation are not well understood. In this rodent study, we hypothesized that gray matter stressed by oxygen/glucose deprivation (OGD) releases a compound(s) that promotes SD, which we term a spreading depolarization activator (SDa). We used rat brain slices incubated in artificial cerebrospinal fluid (aCSF) and subjected to OGD to release a putative SDa. The aCSF was collected either prior to (Pre-SD aCSF) or 10 min after initiation of OGD conditions (Post-SDOGD aCSF). These solutions were then separately superfused over a healthy, naive (non-stressed) brain slice. Post-SDOGD aCSF (with re-normalized O2 and glucose) evoked SD in 82.35% of the naive brain slices (n = 17) whereas Pre-SD aCSF evoked no SD in 10 naive slices. Then to investigate the NKA as a potential target of the SDa, we used a hemolysis assay, comparing the effects of Pre- or Post-SDOGD aCSF on red blood cell (RBC) lysis and compared it to the known hemolytic effect of the NKA-specific inhibitor, palytoxin. Post-SDOGD aCSF evoked neither swelling nor lysis of RBCs on its own. However, when a sub-threshold concentration (0.01 to 0.02 nM) of the specific NKA inhibitor palytoxin (PLTX) was added, a striking priming effect was observed, whereby Post-SDOGD aCSF evoked a highly significant increase in both RBC swelling and then hemolysis, compared to Pre-SD aCSF. High pressure liquid chromatography (HPLC) experiments show a several-fold increase in released molecules post-SD vs pre-SD. This was also true for SD evoked by mild heating (Ht). Overall, this study provides support for SDa release capable of inducing SD-associated swelling in brain slices and, when combined with a trace amount of PLTX, swelling/hemolysis of RBCs caused by NKA inhibition. A greater understanding of the molecular events underlying SD should identify novel targets to reduce recurrent SD-evoked neuronal injury under ischemic conditions.
]]></description>
<dc:creator><![CDATA[ Lowry, C. A., Hellas, J. A., Ollen-Bittle, N., Gagolewicz, P. J., Bennett, B. M., Andrew, R. D. D. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721086</dc:identifier>
<dc:title><![CDATA[Towards Identifying a Molecular Activator of Spreading Depolarization Generated by the Ischemic Brain]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721041v1?rss=1">
<title>
<![CDATA[
Volumetric functional ultrasound imaging in macaques 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721041v1?rss=1
</link>
<description><![CDATA[
Linking circuit-level activity to larger-scale functional organizations requires methods combining high spatial resolution, broad coverage, and single-trial sensitivity. We present volumetric functional ultrasound imaging (3D-fUS) in behaving macaques, a method fulfilling these criteria. 3D-fUS enables the imaging of brain activity within a ~1 cm3 cortical volume at high spatiotemporal resolution (100 x 150 x 150 m3 at 1.67 Hz). Its sensitivity was sufficient to detect visually evoked responses on single trials and in single voxels, substantially reducing experimental time. To enable model-based analyses analogous to fMRI, we estimated a canonical hemodynamic response function (fUS-HRF), which was consistent across subjects, areas, and visual stimuli and could be approximated by a gamma function. Compared to a canonical fMRI-HRF, the fUS-HRF exhibited faster dynamics, enabling shorter and more closely spaced stimulus presentations. Together, these results establish 3D-fUS as a fast, volumetric, and circuit-relevant imaging method for efficiently studying distributed cortical dynamics in primates.
]]></description>
<dc:creator><![CDATA[ Fitzgerald, N. E., Montaldo, G., Froesel, M., Urban, A., Vanduffel, W. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721041</dc:identifier>
<dc:title><![CDATA[Volumetric functional ultrasound imaging in macaques]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.28.721468v1?rss=1">
<title>
<![CDATA[
Structural and Immunological Alterations at the Human Cribriform Plate in Streptococcus pyogenes Meningitis: A Case Study 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.28.721468v1?rss=1
</link>
<description><![CDATA[
Streptococcus pyogenes or group A Streptococcus (GAS) meningitis is a rare but deadly infection with a high mortality. Its mechanisms of invasion are unknown, but it has been proposed to enter either through the cribriform plate olfactory nerve bundles or the blood brain barrier. Knowledge of how GAS impacts the cribriform plate olfactory nerves can help us better understand GAS pathogenesis and invasion, as well as how it impacts the olfactory nerve bundles. Here we present the case of a 39-year-old otherwise healthy man who presented to the local emergency department with altered mental status and expired the following day. Neuropathologic examination revealed bacterial leptomeningitis; blood and cerebrospinal fluid cultures both grew Streptococcus pyogenes. Examination of the cribriform plate was notable for perineural accumulation of GAS around certain olfactory nerve bundles. The accumulation around nerves seems to be random and not correlated to size. Nerves that are impacted by GAS as well as nerves that are not impacted display similar levels of gliosis markers GFAP and podoplanin. Neuropeptide Y, a neuropeptide that implicated in neuro-proliferation and hunger was found to colocalize with CD68 positive immune cells within the nasal epithelium, leading to speculations of its involvement in the inflammatory profile during this case of GAS meningitis. Cribriform plate skull channels had undergone width expansion within the patient, pointing towards local bone marrows involvement during infections. These findings are essential to better understanding the human cribriform plate's role in CNS immune response and drainage.
]]></description>
<dc:creator><![CDATA[ Port, J. M., Brooks, E. G., Helgager, J., Laaker, C. J., Herbath, M., Sandor, M., Fabry, Z. ]]></dc:creator>
<dc:date>2026-04-30</dc:date>
<dc:identifier>doi:10.64898/2026.04.28.721468</dc:identifier>
<dc:title><![CDATA[Structural and Immunological Alterations at the Human Cribriform Plate in Streptococcus pyogenes Meningitis: A Case Study]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-30</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721046v1?rss=1">
<title>
<![CDATA[
Associations between the environment, brain, mental health, and cognition across adolescence 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721046v1?rss=1
</link>
<description><![CDATA[
Adolescence is a critical period for the development of the brain, cognition, and mental health, which are shaped by a wide range of environmental factors. In the present study, we analysed the Adolescent Brain and Cognitive Development (ABCD) dataset to examine how a range of proximal (e.g., socioeconomic status, familial circumstances) and distal (e.g., neighbourhood conditions, access to healthcare and education) environmental factors are associated with changes in centile-based measures of brain structure, and whether these brain differences subsequently mediate variations in cognition and mental health. We analysed these associations both at baseline (N = 6,911; 3,605 M, 3,606 F; mean age = 9.93) and longitudinally across three timepoints (N = 1,628; 879 M, 749 F; ages 8-15). At baseline, a more advantaged proximal and distal environment was associated with larger volumes across the whole brain relative to age- and sex-matched peers, which, in turn, mediated better mental health outcomes and cognitive performance. In the longitudinal analysis, the childhood environment predicted changes in brain structure across adolescence, and these structural changes predicted changes in mental health and cognition. The childhood environment also predicted cognitive but not mental health changes across adolescence, suggesting that these associations may already be established early in adolescence. These findings provide insight into how environmental and neural factors shape adolescent mental health and cognition, with potential implications for early intervention strategies aimed at promoting positive developmental outcomes.
]]></description>
<dc:creator><![CDATA[ Khan, Y. T., Seidlitz, J. T., Dorfschmidt, L., Tsompanidis, A., Allison, C., Lifespan Brain Chart Consortium,, Barzilay, R., Alexander-Bloch, A., Baron-Cohen, S., Blakemore, S.-J., Bethlehem, R. A. I. ]]></dc:creator>
<dc:date>2026-04-29</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721046</dc:identifier>
<dc:title><![CDATA[Associations between the environment, brain, mental health, and cognition across adolescence]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-29</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.720597v1?rss=1">
<title>
<![CDATA[
Untangling mechanisms for cerebellar neural specification using human pluripotent stem cell-derived organoids 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.720597v1?rss=1
</link>
<description><![CDATA[
The cerebellum is one of the most complex structures of the brain composed of a high diversity of GABAergic and glutamatergic neurons. Whereas cerebellar biogenesis has been extensively studied in the mouse, an in-depth characterization of genes and pathways involved in cerebellar specification and maturation in the humans remains overlooked. Here, we used human pluripotent stem cells (hPSC)-derived cerebellar organoids (CRBOs) to study the temporal biogenesis of neuronal subtypes. Our results show that CRBOs acquire caudal neural tube identity at an early stage followed by a time-dependent expression of mature cerebellar neuronal markers in vitro, mimicking human neurodevelopment. CRBOs show the generation of both cerebellar excitatory and inhibitory neurons and the expression of glial cell markers, suggesting the generation of a high variety of cerebellar cell types in vitro. Further, in vitro CRBOs show expression of cerebellar disease associated genes, such as those related to ataxia. Our results establish CRBOs as a valuable platform to explore the mechanisms of human cerebellar development and related disorders.
]]></description>
<dc:creator><![CDATA[ Helgueta Romero, S., Bonafina, A., Olivie, N., Coumans, B., Nguyen, L., Espuny Camacho, I. ]]></dc:creator>
<dc:date>2026-04-29</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.720597</dc:identifier>
<dc:title><![CDATA[Untangling mechanisms for cerebellar neural specification using human pluripotent stem cell-derived organoids]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-29</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721024v1?rss=1">
<title>
<![CDATA[
Neuromuscular impairments alter energetic cost landscape curvature and stride speed variability in post-stroke locomotion 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721024v1?rss=1
</link>
<description><![CDATA[
Neuromuscular impairments induce compensatory effects which alter the dynamics of human movement, but the mechanism linking specific impairments to post-stroke locomotion remains poorly understood. Here, we combine a predictive neuromusculoskeletal simulation framework with experimental gait observations in stroke survivors to test how two hemiparetic impairments, reduced muscle strength and increased baseline muscle activity, reshape the energetic cost landscape. We then evaluate whether impairment-dependent changes in the cost landscape curvature are associated with stride speed variability, which is experimentally observed to be higher after stroke. Using neuromusculoskeletal simulations, we show that increased paretic muscle activity reduces local curvature near the cost-minimized speed more than reduced paretic muscle strength and find that this predicts increases in stride speed variability observed in hemiparetic locomotion. These results support a mechanistic hypothesis that flatter cost landscapes reduce the relative cost of suboptimal behavior and, therefore, may contribute to increased motor variability after stroke.
]]></description>
<dc:creator><![CDATA[ Smith, M., Namburi, P., Seethapathi, N., Anthony, B. ]]></dc:creator>
<dc:date>2026-04-29</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721024</dc:identifier>
<dc:title><![CDATA[Neuromuscular impairments alter energetic cost landscape curvature and stride speed variability in post-stroke locomotion]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-29</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.04.27.721014v1?rss=1">
<title>
<![CDATA[
L-serine diet restores impaired adult neurogenesis in the hippocampus of 3xTg-AD mice 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.04.27.721014v1?rss=1
</link>
<description><![CDATA[
Altered adult neurogenesis is reported in Alzheimer disease (AD) in humans and rodent models, though the mechanisms remain unclear. L-serine, a non-essential amino acid that plays a critical role in cell proliferation and survival, is produced by neuroepithelial cells and radial glia in the developing brain, as well as by astrocytes and neural precursors in the adult brain. Its production is altered in AD, particularly in the hippocampus. We sought to determine whether a deficiency of L-serine availability contributes to the reduced adult neurogenesis in AD. We confirm that phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme of the L-serine biosynthetic pathway, is expressed by neural stem cells (NSCs) of the mouse dentate gyrus (DG). We further report PHGDH expression in cells with somata located in the subgranular zone (SGZ) of the human DG and displaying the typical radial morphology associated with NSCs in rodents. We observed a significant decrease in the number of proliferating cells (proliferating cell nuclear antigen, PCNA) as well as immature neurons (doublecortin, DCX) in the DG of 12-month-old 3xTg-AD mice compared to their age-matched controls. Importantly, chronic dietary supplementation with a L-serine-enriched diet for 8 months significantly increased plasma L- and D-serine levels and partially rescued adult neurogenesis deficits in 3xTg-AD mice, while having no significant impact on the progression of amyloidosis. Our results suggest that chronic metabolic impairment in L-serine production, and the resulting shortage of D-serine, likely contributes to reduced survival of newborn neurons in the DG of 3xTg-AD mice.
]]></description>
<dc:creator><![CDATA[ Than-Trong, E., Torres, L., Gaudin, M., Jan, C., Ghettas, A., Amadio, A., Oliet, S., Panatier, A., Bonvento, G. ]]></dc:creator>
<dc:date>2026-04-29</dc:date>
<dc:identifier>doi:10.64898/2026.04.27.721014</dc:identifier>
<dc:title><![CDATA[L-serine diet restores impaired adult neurogenesis in the hippocampus of 3xTg-AD mice]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-04-29</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
