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<title>bioRxiv Subject Collection: Neuroscience</title>
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This feed contains articles for bioRxiv Subject Collection "Neuroscience"
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<title>bioRxiv</title>
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<link>https://www.biorxiv.org</link>
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<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710206v1?rss=1">
<title>
<![CDATA[
Mouse strain and network-level activity differences underlie social decision-making 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710206v1?rss=1
</link>
<description><![CDATA[
Adaptive social behavior requires balancing self-interest with the welfare of others, a core axiom of social decision-making that determines whether actions are selfish or prosocial. Although the medial prefrontal cortex (mPFC) has been implicated in prosocial behavior, the broader cortical-subcortical networks that arbitrate between selfish and prosocial actions remain poorly understood. Moreover, most studies of social decision-making (at both the single-region and circuit levels) have focused on inbred C57BL/6 mice, leaving unclear whether similar neural mechanisms operate across genetically diverse populations. Here, we combined a social decision-making task with c-Fos mapping to examine activity across distributed cortical and subcortical regions in inbred C57BL/6 and outbred CD1 male mice during prosocial and selfish choices. We found that CD1 mice exhibited a stronger bias toward selfish behavior, whereas C57BL/6 mice were more prosocial. This behavioral divergence was associated with elevated c-Fos activity in the mPFC and nucleus accumbens core (NAcC) in CD1 mice compared with C57BL/6 mice, and mPFC activity positively correlated with selfish choice bias. At the network level, social decision-making selectively recruited coordinated activity among the distinct mPFC subregions, ventral tegmental area (VTA), and NAcC. Importantly, prosocial and selfish individuals recruited distinct prefrontal-subcortical network configurations during social decision-making. Together, these findings identify distributed cortical-subcortical network dynamics underlying social choice bias and reveal strain-dependent differences in the neural architecture supporting prosocial and selfish behavior.
]]></description>
<dc:creator><![CDATA[ Illescas-Huerta, E., Villamizar, A., Cum, M., Padilla-Coreano, N. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710206</dc:identifier>
<dc:title><![CDATA[Mouse strain and network-level activity differences underlie social decision-making]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.09.710050v1?rss=1">
<title>
<![CDATA[
Astrocyte-neuron mitochondrial transfer via mitoEVs supports neuronal energy metabolism and is impaired in early Alzheimer's disease 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.09.710050v1?rss=1
</link>
<description><![CDATA[
Background: Mitochondrial dysfunction is an early and central feature of Alzheimer's disease (AD). In particular, intercellular mitochondrial transfer has emerged as a mechanism of neuronal support in brain injury and neurodegeneration. However, pathways governing astrocyte-to-neuron transfer and its role in AD pathogenesis remain unknown. Methods: Using the AppNL-G-F knock-in AD model, we combined high-resolution 4D live-cell imaging with quantitative fluorescence-based reporters to assess synaptic function and mitochondrial network dynamics in neurons and astrocytes. Direct and extracellular vesicle (EV)-restricted neuron-astrocyte co-culture systems were used to investigate bidirectional mitochondrial transfer. We performed the first in-depth structural, proteomic, and functional characterization of astrocyte-derived mitochondrial extracellular vesicles (mitoEVs) using cryo-electron microscopy, quantitative mass spectrometry, and bioenergetic analyses to define their cargo composition and metabolic effects. Results: We identified cell-type-specific mitochondrial remodeling in early AD, with compartmentalized synaptic energy deficits in neurons and hyperdynamic, less interconnected, yet metabolically preserved networks in astrocytes, preceding global bioenergetic decline. Bidirectional mitochondrial transfer between astrocytes and neurons, also at axonal terminals, was mediated by specialized mitoEVs but significantly reduced in the AppNL-G-F model. Comprehensive proteomic and functional profiling revealed that WT astrocyte-derived mitoEVs are enriched in inner membrane and matrix proteins, supporting oxidative phosphorylation, lipid and amino acid metabolism, and redox homeostasis. In contrast, AppNL-G-F mitoEVs are selectively depleted of respiratory and fatty acid oxidation components and exhibit impaired respiration with reduced Complex IV activity. Functionally, WT mitoEVs promote mobilization of abnormal accumulation of lipid droplets in AppNL-G-F neurons, restore fatty acid oxidation, and increase neuronal bioenergetics, including at the synapses. In contrast, disease-derived mitoEVs fail to engage these pathways. Conclusions: Together, these findings identify mitoEV-mediated mitochondrial transfer as a glia-to-neuron metabolic pathway compromised in early AD and reveal a coordinated role for oxidative phosphorylation and fatty acid oxidation in supporting synaptic energy homeostasis.
]]></description>
<dc:creator><![CDATA[ Voorbraeck, L., Alarcon-Gil, J., Giraud, R., Pozzobon, F., Pereira, M. J., Guo, S., Cao, Z., Distefano, K., Mohammad, D. K., Wiklander, O. P. B., Mijalkov, M., Pereira, J. B., Mamand, D. R., Ankarcrona, M., Naia, L. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.09.710050</dc:identifier>
<dc:title><![CDATA[Astrocyte-neuron mitochondrial transfer via mitoEVs supports neuronal energy metabolism and is impaired in early Alzheimer's disease]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.07.710303v1?rss=1">
<title>
<![CDATA[
Functional Connectivity Changes in Major Depressive Disorder 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.07.710303v1?rss=1
</link>
<description><![CDATA[
Major depressive disorder (MDD) is associated with brain-wide network disruptions. This study investigates a large resting-state functional magnetic resonance imaging dataset (N = 519) to analyze static and dynamic functional network connectivity (FNC). Using independent component analysis, our analysis revealed hyperconnectivity within sensorimotor and temporal subdomains, hypoconnectivity from higher cognitive networks, and hyperconnectivity from the default mode and sensorimotor domains in MDD. A novel frequency-sensitive dynamic approach identified disruptions in the temporal synchrony of brain states engaging the default mode-paralimbic, sensorimotor, and frontal regions, as well as the subcortical limbic, frontal, and salience regions. Overall, the findings highlight the utility of combining static and dynamic approaches in large neuroimaging datasets to elucidate the neural underpinnings of MDD pathology.
]]></description>
<dc:creator><![CDATA[ Sridhar, M., Wiafe, S.-L., Baker, B., Calhoun, V. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.07.710303</dc:identifier>
<dc:title><![CDATA[Functional Connectivity Changes in Major Depressive Disorder]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.07.710036v1?rss=1">
<title>
<![CDATA[
Rebound Relays and Inhibitory Vetoes Stabilize Sparse Sequential Activity in HVC 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.07.710036v1?rss=1
</link>
<description><![CDATA[
Brains build behavior by chaining actions and perceptions into precisely timed sequences, an ability central to speech, skilled movement, and memory, yet the circuit logic that propagates sequences remains unclear. Songbird HVC captures this problem: premotor HVCRA neurons burst once per motif, while basal ganglia-projecting HVCX neurons burst 2-4 times across the same motif. We developed a biophysically grounded HVC network as linked microcircuits encoding sub-syllabic segments. The model highlights inhibition not merely as suppressive but actively structuring sequence propagation and fidelity. Tonic inhibitory epochs prime HVCX by deinactivating T-type Ca2+ channels and recruiting I_h, so that release elicits precisely timed rebound bursts that recruit the next HVCRA ensemble. A complementary phasic inhibitory veto suppresses off-time activation, preventing pathological restarts while preserving HVCRA single-burst sparseness. More broadly, inhibitory timing can serve as the brain's internal "clocked handshake", converting suppression into forward drive to advance sequences while enforcing error-corrected precision.
]]></description>
<dc:creator><![CDATA[ Bou Diab, Z., Daou, A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.07.710036</dc:identifier>
<dc:title><![CDATA[Rebound Relays and Inhibitory Vetoes Stabilize Sparse Sequential Activity in HVC]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.07.705326v1?rss=1">
<title>
<![CDATA[
A Vector Navigation and Inference Architecture can Construct Universal Cognitive Maps for Abstract Reasoning 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.07.705326v1?rss=1
</link>
<description><![CDATA[
The idea of cognitive maps in the hippocampal formation has its origins in decades of spatial cognition research. However, increasing evidence points to cognitive maps also supporting non-spatial tasks. It appears that the hippocampal-entorhinal system can map any combination of systematically varying stimulus dimensions onto the same neural manifolds that support spatial representations - grid cells. Here I propose a model that shows how spatial navigation architectures can iteratively construct universal cognitive maps. The model is neurally plausible and exhibits noise-tolerance that implies specific behavioral predictions. The mapping process accommodates discontinuous stimulus spaces and the model can be used to support several types of abstract reasoning, including analogy making, subspace construction, and perspective taking. Importantly, these capabilities are supported by the same neural processes that are used to build a map. Thus, the combination of mechanisms at play suggests how spatial navigation architectures can function as domain-general substrates of cognition.
]]></description>
<dc:creator><![CDATA[ Bicanski, A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.07.705326</dc:identifier>
<dc:title><![CDATA[A Vector Navigation and Inference Architecture can Construct Universal Cognitive Maps for Abstract Reasoning]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.08.710351v1?rss=1">
<title>
<![CDATA[
Dorsoventral gradient of theta sweeps in medial entorhinal cortex 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.08.710351v1?rss=1
</link>
<description><![CDATA[
During random foraging, the positional signal decoded from entorhinal grid cells exhibits left-right theta sweeps, alternating from one side of the heading direction to the other across successive theta cycles. Here, we report that theta sweeps are topographically organised along the dorsoventral axis of the medial entorhinal cortex, with the angular deviation from heading direction increasing gradually from dorsal (smaller scale) to ventral (larger scale) modules. This gradient coexists with a corresponding dorsoventral increase in angular deviation decoded from theta-modulated directional cells, which drive grid-cell theta sweeps. These phenomena parallel a broadening of head direction tuning and increasing occurrence of theta cycle skipping in single cell firing along the dorsoventral axis. Computational modelling demonstrates that these patterns are consistent with continuous attractor dynamics and a dorsoventral gradient in firing rate adaptation. These results highlight how theta sweeps can simultaneously represent multiple potential future locations and reveal a clear neural mechanism underlying this process.
]]></description>
<dc:creator><![CDATA[ Ji, Z., Zhang, H., Stonis, R., Burgess, N. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.08.710351</dc:identifier>
<dc:title><![CDATA[Dorsoventral gradient of theta sweeps in medial entorhinal cortex]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710072v1?rss=1">
<title>
<![CDATA[
Neural investigation of idea selection during creative thinking reveals value-based mechanisms 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710072v1?rss=1
</link>
<description><![CDATA[
Creative thinking enables humans to innovate and solve problems, via the generation of candidate ideas, their evaluation and the selection of the most promising one. While recent studies have demonstrated that idea evaluation relies on the assignment of subjective values (the assessment of how much one likes an idea, or valuation), the selection mechanism remains unknown. Using behavioral experiments and fMRI, we tested whether the selection step of creative thinking is driven by the same value comparison circuits that guide economic decisions. Participants performed creative idea production, rating, and choice tasks. We found behavioral evidence of value-based comparison during both isolated choice and overall creative idea production, in a manner that predicts creative abilities. Critically, we demonstrate that creative idea selection involves the brain valuation system and the dorsal anterior cingulate cortex: during creative thinking, these neural circuits compare candidate idea values, mirroring economic choice. Our findings reveal that idea selection is mediated by the brain's generic valuation system, rather than specialized creative machinery, unifying theories of decision-making and creativity.
]]></description>
<dc:creator><![CDATA[ Moreno-Rodriguez, S., Beranger, B., VOLLE, E., Lopez-Persem, A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710072</dc:identifier>
<dc:title><![CDATA[Neural investigation of idea selection during creative thinking reveals value-based mechanisms]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710130v1?rss=1">
<title>
<![CDATA[
A flexible quality metric for electrophysiological recordings across brain regions and species 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710130v1?rss=1
</link>
<description><![CDATA[
The increasing size of electrophysiological datasets has heightened the need for quality metrics that automatically reject neurons whose activity was recorded with low sensitivity or specificity. One key approach estimates artifactual contamination by assuming that each neuron has a refractory period (RP), a brief time interval following each action potential when further activity cannot occur. However, existing methods cannot be applied without prior knowledge of the neurons' RP durations, limiting their usefulness in datasets that include neurons from brain regions or species in which RP durations have not been systematically characterized. Here, we find that neurons in some brain regions (thalamus) and species (macaque) have shorter RP durations than commonly assumed, and we introduce a new metric, the Sliding Refractory Period metric, which is robust to variation in a neuron's RP duration without tuning. We validate the method using simulations, demonstrating that it improves acceptance of uncontaminated spike trains with short or long RP durations while still rejecting contaminated ones. Moreover, by incorporating Poisson statistics into the calculation, the method also improves on prior work by allowing the user to approximately control the false acceptance rate. Our new metric improves quantification of contamination in electrophysiological recordings and enables application of a single tuning-free quality metric to data recorded from diverse brain regions and species.
]]></description>
<dc:creator><![CDATA[ Roth, N., Chapuis, G., Winter, O., Laboratory, I. B., Ressmeyer, R. A., Bun, L. M., Canfield, R. A., Horwitz, G. H., Steinmetz, N. A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710130</dc:identifier>
<dc:title><![CDATA[A flexible quality metric for electrophysiological recordings across brain regions and species]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710089v1?rss=1">
<title>
<![CDATA[
Arousal elicits a brain-wide hemodynamic wave independent of locus coeruleus noradrenergic tone 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710089v1?rss=1
</link>
<description><![CDATA[
Arousal fluctuations during wakefulness have a major impact on physiology and behavior, including perception and task performance. Arousal is also known to be a strong modulator of neural activity, but the brain-wide spatiotemporal structure of this modulation is not fully characterized. We used functional ultrasound imaging to record brain-wide hemodynamics - a proxy for neural activity - in head-fixed mice during spontaneous and sensory-evoked arousal fluctuations, tracked via pupil diameter. Both conditions recruited a common brain-wide hemodynamic wave that followed a subcortex-to-cortex gradient. We then tested whether noradrenaline, widely associated with arousal, was necessary or sufficient to drive this wave. Sustained bidirectional optogenetic manipulations of locus coeruleus activity affected brain-wide vascular signal amplitude but, surprisingly, left arousal-linked dynamics largely intact. Together, these results identify a common spatiotemporal motif of arousal that appears independent of noradrenergic tone.
]]></description>
<dc:creator><![CDATA[ Martinez de Paz, J. M., Mayer, J. L., Wanken, P., Rodrigues Apgaua, B., Ablitip, A., Behera, L., Mace, E. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710089</dc:identifier>
<dc:title><![CDATA[Arousal elicits a brain-wide hemodynamic wave independent of locus coeruleus noradrenergic tone]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.709427v1?rss=1">
<title>
<![CDATA[
RhoGEF12 regulates endosomal SORL1-retromer and its inhibition is therapeutic in human neuronal models of Alzheimer's disease 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.709427v1?rss=1
</link>
<description><![CDATA[
The interaction of the endosomal sorting protein SORL1 with the retromer complex at endosomal membranes controls a recycling pathway whose dysfunction is pathogenic in Alzheimer's disease (AD) and is linked to other neurodegenerative disorders. To search for novel therapeutic targets, we hypothesize that endosomal SORL1-retromer might be regulated by SORL1's cytoplasmic tail. We begin by completing an in vitro analysis of the tail and show that its phosphorylation by ROCK2 (Rho-associated kinase 2) reduces SORL1's affinity to retromer. Since RhoGEF12 (Rho guanine nucleotide exchange factor 12) is an upstream activator of ROCK2 that is upregulated in AD, we used a RhoGEF12 pharmacological inhibitor to mechanistically and therapeutically validate the findings in neuronal cultures. First, in mouse neurons we confirm that the inhibitor increases endosomal SORL1-retromer. Next, we turned to human iPSC-derived neurons to show that the inhibitor reduces A{beta}40 and A{beta}42, an indicator of pathway upregulation, in a SORL1-dependent manner. Finally, we validate its therapeutic potential by applying the RhoGEF12 inhibitor to human iPSC-derived neurons expressing AD-associated mutations in either APP or SORL1. Collectively, our results identify a novel and therapeutically amenable mechanism that regulates endosomal SORL1-retromer and preclinically validate RhoGEF12 as a therapeutic target for AD and potentially other neurodegenerative disorders.
]]></description>
<dc:creator><![CDATA[ Qureshi, Y. H., Williams, C. A., Hajdu, I., Kannan, S., Govindarajan, A., Vegh, B., Petsko, G. A., Young, J. E., Zavodszky, P., Small, S. A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.709427</dc:identifier>
<dc:title><![CDATA[RhoGEF12 regulates endosomal SORL1-retromer and its inhibition is therapeutic in human neuronal models of Alzheimer's disease]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.08.710364v1?rss=1">
<title>
<![CDATA[
Cell-type specific astrocyte activation is driven by cortical top-down modulation 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.08.710364v1?rss=1
</link>
<description><![CDATA[
Cortical projections to cortical and subcortical targets provide top-down modulation that shapes neuronal performance, including gain control and excitation-inhibition balance. However, the contribution of astrocytes to this process remains poorly understood. In the olfactory bulb, the first relay station of odor information processing, bottom-up input is transmitted from olfactory sensory neurons to mitral/tufted (M/T) cells, which project to the olfactory cortex. Context- and state-dependent top-down modulation arises from feedback projections originating in the anterior piriform cortex (aPC) that target granule cells (GCs). We examined how astrocytes respond to bottom-up and top-down neuronal activity using confocal Ca2+ imaging, cell-type-specific optogenetics, electrical stimulation, and single-cell electrophysiology. We found that Ca2+ signals in astrocytes are selectively triggered by action potential-dependent ATP release from GCs while M/T cells failed to elicit significant astrocytic responses. Although synaptic input from M/T cells depolarized GCs, it was insufficient to induce action potential firing and subsequent astrocyte activation. By contrast, glutamatergic top-down input from the aPC evoked sustained GC firing, leading to ATP-dependent Ca2+ signaling in astrocytes. Our results reveal an unappreciated level of complexity in neuron-astrocyte communication, highlighting its cell-type specificity as well as its context- and state-dependence.
]]></description>
<dc:creator><![CDATA[ Beiersdorfer, A., Losse, K., Bostel, J., Popp, J. S., Rotermund, N., Schulz, K., Droste, D., Gee, C. E., Hirnet, D., Lohr, C. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.08.710364</dc:identifier>
<dc:title><![CDATA[Cell-type specific astrocyte activation is driven by cortical top-down modulation]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.709690v1?rss=1">
<title>
<![CDATA[
Genetic insights on the mechanisms of human cortical folding 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.709690v1?rss=1
</link>
<description><![CDATA[
The unique and intricate pattern of human cortical folding is rooted in fetal neurodevelopmental processes and can now be comprehensively quantified by new neuroimaging-derived measures of sulcal complexity. Here, we provide the first genetic maps of human sulcal complexity. Beginning with large effects of rare variants, we survey nine different neurogenetic syndromes (n=615), detecting visible changes in sulcal complexity on a shared axis of sulcal change coupled to the prenatal timing of sulcation. Turning to common genetic variants, we use genome-wide association studies of complexity scores for 40 sulci in the UK Biobank (n~29,000) to (i) resolve variable heritability across sulci, (ii) reveal both local and remote shared genetic effects with cortical morphology, and (iii) identify complexity-associated genes and their embedding in brain maps of prenatal gene expression. These reference genetic maps uncover multiple new mechanistic pathways for cortical morphogenesis in health and disease.
]]></description>
<dc:creator><![CDATA[ Snyder, W. E., Shafee, R., Liu, S., Levitis, E., Duan, K., Kumar, K. E., Schleifer, C. H., Boen, R., Ching, C. R., Han, J. C., Lee, N., Mulle, J. G., Shultz, S., Jacquemont, S., Bearden, C. E., Vertes, P. E., Bullmore, E. T., Raznahan, A. ]]></dc:creator>
<dc:date>2026-03-09</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.709690</dc:identifier>
<dc:title><![CDATA[Genetic insights on the mechanisms of human cortical folding]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-09</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709450v1?rss=1">
<title>
<![CDATA[
Zebrafish knockout models of atxn1a, atxn1b, and atxn1l reveal distinct and shared phenotypic and transcriptomic alterations 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709450v1?rss=1
</link>
<description><![CDATA[
Spinocerebellar ataxia type 1 (SCA1) is a progressive neurodegenerative disorder caused by polyglutamine expansion in ATXN1, yet the normal physiological roles of ATXN1 and its paralog ATXN1L remain incompletely understood. To define these roles, we generated the first zebrafish knockouts (KOs) of the three ataxin-1 family genes, atxn1a, atxn1b, and atxn1l, using CRISPR/Cas9. These mutants reveal distinct and shared developmental, behavioral, and transcriptomic alterations. All KOs showed reduced early survival and mild larval growth deficits, indicating essential developmental functions. Behavioral assays revealed distinct paralog-specific effects: atxn1a KO larvae exhibited a unique light-dependent locomotor deficit, whereas atxn1b and atxn1l KOs displayed global hypoactivity. Adult behavioral assessment revealed a gradient of phenotypic severity: atxn1a KOs displayed the earliest and most pronounced alterations in vertical tank exploration and the greatest impairment in swim tunnel performance, followed by atxn1b and then atxn1l mutants. To define molecular mechanisms underlying these phenotypes, we performed RNA seq at 5 days post fertilization and identified unique and shared differentially expressed genes across the three KO lines. Shared transcriptomic signatures highlighted suppression of leukotriene biosynthetic pathways and diminished innate immune pathways; suggesting that ATXN1 family genes influence neuroimmune signaling during early development. Weighted gene co expression network analysis identified distinct KO associated gene modules, including a phototransduction enriched module strongly correlated with atxn1a KO status, offering a mechanistic link to its light dependent locomotor phenotype. Together, these findings establish a comprehensive assessment of zebrafish models that reveal both shared core functions and specialized roles of ATXN1 family genes in development, neuroimmune regulation, sensorimotor behavior, and retinal signaling.
]]></description>
<dc:creator><![CDATA[ Karim, A., Keerthisinghe, P., Sarasamma, S., Ciaburri, N. A., Giraldez, M. G., Naidoo, K., Orengo, J. P. ]]></dc:creator>
<dc:date>2026-03-08</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709450</dc:identifier>
<dc:title><![CDATA[Zebrafish knockout models of atxn1a, atxn1b, and atxn1l reveal distinct and shared phenotypic and transcriptomic alterations]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710094v1?rss=1">
<title>
<![CDATA[
MDMA enhances prefrontal plasticity and representational drift during fear extinction 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710094v1?rss=1
</link>
<description><![CDATA[
Fear extinction requires dynamic updating of cortical representations, yet the neural mechanisms underlying successful extinction remain poorly understood. Some psychoactive substances induce structural plasticity in medial prefrontal cortex (mPFC), possibly underlying their therapeutic potential. Here we investigated whether MDMA, which enhances fear extinction, induces prefrontal structural and functional plasticity, and measured its effects on ensemble representations during extinction. Longitudinal two-photon microscopy revealed that MDMA increased spine density and spinogenesis across prefrontal subregions. Miniscope Ca imaging in infralimbic cortex (IL) during fear extinction revealed that IL became more correlated with the suppression of freezing behavior, consistent with a strengthening of its role in extinction. Longitudinal cell registration demonstrated accelerated representational drift across days in MDMA-treated mice; this effect was strongest in a functionally defined subpopulation of neurons that showed suppression of activity to conditioned cues. These findings demonstrate that MDMA facilitates structural and functional neuroplasticity, potentially underlying its enhancement of extinction learning.
]]></description>
<dc:creator><![CDATA[ Geva, N., Jefferson, S. J., Krishnamurthy, E., Anderson, T. L., Rondeau, J., Wehrle, P. H., Rosado, A. F., Pittenger, C., Krystal, J. H., Kaye, A. P. ]]></dc:creator>
<dc:date>2026-03-08</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710094</dc:identifier>
<dc:title><![CDATA[MDMA enhances prefrontal plasticity and representational drift during fear extinction]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-08</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709716v1?rss=1">
<title>
<![CDATA[
Do Symptoms Matter? Investigating Symptom-Based Lesion Network Mapping. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709716v1?rss=1
</link>
<description><![CDATA[
Lesion network mapping (LNM) is an approach to map focal brain lesions to a common brain network through the use of a reference connectome dataset. Van den Heuvel and colleagues recently showed that results produced by LNM lack disease specificity. Here, we expand on symptom-based LNM (sLNM), a variant designed to focus on symptom-specificity, statistical rigor, and clinical utility. We show that sLNM maps from unrelated disorders nonetheless converge toward a common output, confirming a lack of disease specificity similar to LNM. Given this lack of disease specificity, it is puzzling why studies have shown clinical efficacy of sLNM-guided treatment. Our findings suggest that sLNM results converge to the first principal gradient, which describes the brain's sensorimotor-association organizational axis that has been linked to development and pathology. Therefore, sLNM maps may be clinically useful because they reflect this fundamental brain organizational axis rather than disease-specific networks. Taken together with the results from van den Heuvel et al, these insights open an important opportunity for integrating findings from sLNM with findings on the sensorimotor-association brain axis.
]]></description>
<dc:creator><![CDATA[ Treeratana, S., Kasemsantitham, A.-A., Jarukasemkit, S., Phusuwan, W., Chokesuwattanaskul, A., Sriswasdi, S., Chunharas, C., Bijsterbosch, J. D. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709716</dc:identifier>
<dc:title><![CDATA[Do Symptoms Matter? Investigating Symptom-Based Lesion Network Mapping.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709765v1?rss=1">
<title>
<![CDATA[
A PRISMA-guided systematic review of musculoskeletal modelling approaches in lower-limb cycling biomechanics 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709765v1?rss=1
</link>
<description><![CDATA[
Cycling is commonly employed in sports performance, rehabilitation, and clinical contexts, while musculoskeletal (MSK) simulations enable the investigation of internal biomechanics that cannot be measured experimentally. Despite growing use, the application, validation, and standardisation of MSK simulations in cycling remain unclear. This review aimed to systematically characterise the application, validation strategies, modelling assumptions, and reporting practices of musculoskeletal simulations in lower-limb cycling biomechanics. Searches were performed in Scopus, PubMed, IEEE Xplore, and Web of Science on 1 August 2024, covering studies from January 2010 to July 2024. Peer-reviewed English-language journal articles applying MSK simulations to lower-limb cycling were included; inverse kinematics-only was excluded. No protocol was registered, and no formal risk-of-bias assessment was conducted, as there were no intervention effects and no quantitative synthesis. Twenty-eight studies met the inclusion criteria. Most of them investigated bicycle-rider configuration, neuromuscular coordination, or electrical stimulation control, with participant cohorts overwhelmingly composed of young men and minimal female representation~(272 total). Model reporting was often incomplete, with wide variation in anatomical scope, inconsistent descriptions of degrees of freedom, and limited sharing of models or code. Use of experimental data was uneven across studies: while all incorporated kinematic measurements, only two-thirds included kinetic data, and only one study reported physiological measures. Model validation was generally based on literature values. Seventy-eight per cent of studies used optimisation, mainly with effort-based cost functions, and parameter variations were exploratory rather than systematic. The evidence base is limited by small, predominantly male cohorts, inconsistent reporting standards, and limited physiological validation. These results consolidate current practices and highlight the need for more transparent and open reporting, sex-balanced and clinically diverse participant representation, stronger validation, and more rigorous sensitivity analysis to enhance reproducibility and practical relevance. This review was funded by AGAUR (Spain), CAPES (Brazil) and FAP-DF (Brazil).
]]></description>
<dc:creator><![CDATA[ C. de Sousa, A. C., Peres, A. B., Font-Llagunes, J. M., Baptista, R. d. S., Pamies-Vila, R. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709765</dc:identifier>
<dc:title><![CDATA[A PRISMA-guided systematic review of musculoskeletal modelling approaches in lower-limb cycling biomechanics]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709759v1?rss=1">
<title>
<![CDATA[
From Head to Toe: Efficient Somatosensory Mapping with Fast Stimulation and Multivariate Pattern Analysis 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709759v1?rss=1
</link>
<description><![CDATA[
Background: Somatosensory evoked potentials (SEPs) measured with electroencephalography (EEG) are widely used to study cortical responses to touch but most research has limited the focus on few body parts, typically a finger, and applied time-consuming testing protocols. Multivariate pattern analysis (MVPA) provides a complementary approach that may increase sensitivity and allow faster stimulation, yet its relationship to classical SEP analysis in somatosensory research remains largely unexplored. Methods: Fifteen participants received vibrotactile stimulation on the finger, hand, cheek, and foot while EEG was recorded. We compared a traditional 'slow' stimulation protocol (800-1200 ms inter-stimulus intervals) with a 'fast' protocol (300-500 ms). We compared temporal and topographical aspects between SEP and MVPA. Results: Both stimulation protocols produced highly similar SEP components (P100, N140, P200), topographies, and classification results, while the fast protocol reduced testing time by about 60%. SEPs revealed systematic body-part differences, with earlier components for cheek stimulation and delayed responses for the foot. Multivariate classification distinguished body parts with accuracies up to ~50-55% (chance: 25%), peaking around 100 ms after stimulus onset. Classifier weight maps closely matched SEP topographies over centroparietal electrodes, indicating that classification relied on physiologically meaningful somatosensory signals. Classification accuracy peaked around 100 ms after stimulus onset, coinciding with the SEP P100 component, but declined gradually thereafter, suggesting that early somatosensory responses contain particularly informative multivariate patterns that generalize over time. Conclusions: Faster stimulation protocols substantially increase efficiency without compromising interpretability. Combining classical SEP analysis with multivariate classification provides complementary insights and offers a powerful framework for mapping somatosensory representations across the body.
]]></description>
<dc:creator><![CDATA[ Fuchs, X., Schubert, J., Heed, T. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709759</dc:identifier>
<dc:title><![CDATA[From Head to Toe: Efficient Somatosensory Mapping with Fast Stimulation and Multivariate Pattern Analysis]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709070v1?rss=1">
<title>
<![CDATA[
Neural sensing of surface traction modulates proprioceptive activity and locomotion in Caenorhabditis elegans 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709070v1?rss=1
</link>
<description><![CDATA[
Locomotion - whether walking, running, or crawling - depends on the precise coordination of forces between the body and its surroundings. Two critical factors in this process are the force that resists the relative motion between two bodies, and mechanosensation, the body's ability to sense and respond to mechanical forces. Together, they allow organisms to move efficiently, adapt to varying environments, and maintain balance. Here we show that the `gentle touch' receptor neurons (TRNs) in the Caenorhabditis elegans body wall are sensitive to dynamic surface traction. Using a combination of calcium recordings and traction force microscopy in freely moving animals, microfluidics, and whole connectome computer simulations, we show that MEC-4 DEG/ENaC ion channel activity depends on the crawling velocity and friction force. Mutations disrupting MEC-4 activity and body wall mechanoreceptor function produce lethargic worms with impaired proprioceptive regulation, suggesting functional coupling between surface mechanoreceptors and proprioceptors. Our data reveal a new role for classical touch receptors in locomotion and critically define the mechanical modality sensed by skin mechanosensors.
]]></description>
<dc:creator><![CDATA[ Pidde, A., Porta-de-la-Riva, M., Agazzi, C., Martinez-Fernandez, C., Lorrach, A., Bijalwan, A., Sanfeliu-Cerdan, N., Calatayud-Sanchez, A., Torralab-Sales, E., Das, R., Munoz, J. J., Krieg, M. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709070</dc:identifier>
<dc:title><![CDATA[Neural sensing of surface traction modulates proprioceptive activity and locomotion in Caenorhabditis elegans]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.707373v1?rss=1">
<title>
<![CDATA[
Tracing the invisible: Quantifying mirroring and embodied attunement in dyadic and triadic Dance Movement Therapy 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.707373v1?rss=1
</link>
<description><![CDATA[
Background: Mirroring is a foundational method used in Dance Movement Therapy (DMT), assumed to foster empathy and therapeutic attunement, yet its embodied dynamics remain insufficiently studied. In this paper, we provide the first quantitative exploration of client/therapist mirroring across dyadic and triadic formats, examining how synchrony unfolded during a structured mirroring exercise in which participants alternated between leading and following roles. Methodology: Using optical motion capture and time series modelling, we quantified movement coordination in dyadic (female client/therapist; male client/therapist) and triadic (therapist with both clients) interactions. Results: In dyadic tasks, the female client/therapist interaction was marked by tight temporal alignment, significant synchrony, robust predictive accuracy, and clear client to therapist influence, consistent with kinaesthetic empathy and affect-sensitive entrainment. By contrast, the male client/therapist dyad exhibited weaker and more delayed temporal coupling, alongside reduced phase synchronisation and fewer directional dependencies, despite comparable levels of interpersonal proximity. In the triadic task, temporal entrainment attenuated: therapist movement had few matching qualities to clients movement, yet recurrent synchrony with both clients persisted, suggesting a strategic shift from fine-grained entrainment to stable postural scaffolding under divided attention. Discussion: These findings demonstrated that mirroring is not a uniform technique, but a family of embodied coordination modes flexibly recruited according to relational context and client expressivity. They align with theories of embodied simulation and affect attunement, implicating rapid motor resonance in dyadic entrainment and interoceptive/affective scaffolding in triadic stability. Clinically, the results underscore the need for training in flexible embodied strategies, split attention, and equitable allocation of attunement in group work. More broadly, they open a translational agenda linking kinematic synchrony to neural, interoceptive, and autonomic mechanisms, positioning mirroring as both an experiential hallmark and a measurable mechanism of change in embodied psychotherapy.
]]></description>
<dc:creator><![CDATA[ MAKRIS, S., Langley, B., Page, R., Perris, E., Karkou, V., Cazzato, V. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.707373</dc:identifier>
<dc:title><![CDATA[Tracing the invisible: Quantifying mirroring and embodied attunement in dyadic and triadic Dance Movement Therapy]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709724v1?rss=1">
<title>
<![CDATA[
Ultrastructural preservation of a whole large mammal brain with a protocol compatible with human physician-assisted death 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709724v1?rss=1
</link>
<description><![CDATA[
Building a high-fidelity computational model of the whole human brain will require preservation of the ultrastructure at the level of the entire organ, post-mortem. For such a model to reflect as closely as possible the brain in the living state, artifacts that arise during both the agonal phase and the postmortem interval will need to be minimized. This is potentially feasible if a terminally-ill patient donates their brain for research following physician-assisted death. In this paper, we modify a protocol for aldehyde-stabilized cryopreservation to make it compatible with physician-assisted death. We use pigs as a model, which resemble humans in cardiovascular and brain anatomy. Aldehyde-stabilized cryopreservation was designed to provide superior structural preservation of brains of any size, across all anatomical scales, compatible with diverse analytical assays and long-term storage without ultrastructural degradation. We demonstrate, with light microscopy and volume electron microscopy, that our brain preservation protocol results in connectomically traceable whole brains and propose an economically feasible storage modality that is expected to maintain stability of ultrastructure and macromolecules in the brain even for thousands of years. Most importantly, we establish that 14 min is the approximate length of the perfusability window--the time after the cardiac arrest during which blood washout needs to be initiated so that the brain ultrastructure is preserved.
]]></description>
<dc:creator><![CDATA[ Song, A., LaVergne, A., Wrobel, B. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709724</dc:identifier>
<dc:title><![CDATA[Ultrastructural preservation of a whole large mammal brain with a protocol compatible with human physician-assisted death]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709020v1?rss=1">
<title>
<![CDATA[
Neurocognitive deficits in controlling aversive memory among insomnia disorders 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709020v1?rss=1
</link>
<description><![CDATA[
Background. Insomnia disorder is a common sleep disturbance characterized by adverse daytime cognitive and emotional impairments, such as repetitive negative thinking and increased psychological distress. Memory control, a key self-regulatory ability to control or inhibit unwanted thoughts and memories, plays an essential role in supporting cognitive functions and emotional well-being. Here, we delineate the neurocognitive mechanisms underlying memory control among individuals with insomnia. Methods. 41 participants meeting DSM-5 criteria for insomnia disorder and 40 healthy sleepers completed an emotional Think/No-Think task, during which participants either retrieved (Think) or suppressed the retrieval (No-Think) of aversive memories in response to memory cues while electroencephalograms were recorded. Results. Linear mixed model analyses with age and depression scores as covariates showed that participants with insomnia exhibited impaired memory control abilities, as evidenced by reduced suppression-induced forgetting in memory recall when compared to healthy sleepers. Electrophysiologically, healthy sleepers showed enhanced right prefrontal theta power in retrieval suppression than in retrieval, indicating elevated needs of inhibitory control during memory control. In sharp contrast, this difference was absent among those with insomnia. Notably, the greater the severity of insomnia symptoms, the smaller the retrieval vs. retrieval suppression theta power differences across participants, linking inefficient top-down control of unwanted memories with low sleep qualities. Conclusion. Individuals with insomnia showed impaired memory control of aversive memories and aberrant electrophysiological activities during retrieval suppression. Future research shall investigate the causal relationship between memory control abilities and insomnia symptoms.
]]></description>
<dc:creator><![CDATA[ Zuo, X., Lin, X., Yao, Z., Chen, D., Liu, J., Guo, S., Yue, W. Y. W., Yang, Y., Wang, W., Feng, H., Zhang, J., Anderson, M., Li, S. X., Hu, X. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709020</dc:identifier>
<dc:title><![CDATA[Neurocognitive deficits in controlling aversive memory among insomnia disorders]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709693v1?rss=1">
<title>
<![CDATA[
Modeling Multi-Modal Brain Connectomes for Brain Disorder Diagnosis via Graph Diffusion Optimal Transport Network 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709693v1?rss=1
</link>
<description><![CDATA[
Network analysis of human brain connectivity provides a fundamental framework for identifying the neurobiological mechanisms that cause cognitive variations and neurological disorders. However, existing diagnostic models often treat structural connectivity (SC) as a fixed or optimal topological scaffold for functional connectivity (FC). This consequently overlooks the higher-order dependencies between brain regions that are critical for characterizing pathological alterations. Moreover, the distinct spatial organizations of SC and FC complicate their direct integration, as naive alignment methods may distort the inherent nonlinear patterns of brain connectivity. To address these limitations, we propose the Graph Diffusion Optimal Transport Network (GDOT-Net), which models disease-related topological evolution and achieves precise alignment between SC and FC. Unlike existing diffusion studies, the proposed model introduces an evolvable brain connectome modeling approach to infer the complex topological structure of brain networks, unveiling higher-order connectivity patterns linked to specific neuropsychiatric disorders. Furthermore, GDOT-Net incorporates a Pattern-Specific Alignment mechanism, leveraging optimal transport to align structural and functional topological representations in a geometry-aware manner. To capture nonlinear topological relationships between brain regions, a Neural Graph Aggregator Module was developed, which adaptively learns complex node interaction patterns in brain networks. By leveraging this module, GDOT-Net generates highly discriminative representations that form a robust basis for the precision diagnosis of brain disorders. Experiments on REST-meta-MDD and ADNI demonstrate that GDOT-Net surpasses SOTA methods in uncovering structural-functional misalignments and disorder-specific subnetworks. The source code is publicly available at this Link.
]]></description>
<dc:creator><![CDATA[ Sheng, X., Liu, J., Liang, J., Zhang, Y., Mondal, S., Li, Y., Zhang, T., Liu, B., Song, J., Cai, H. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709693</dc:identifier>
<dc:title><![CDATA[Modeling Multi-Modal Brain Connectomes for Brain Disorder Diagnosis via Graph Diffusion Optimal Transport Network]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709732v1?rss=1">
<title>
<![CDATA[
Positive Affect Modulates Early Valuation and Conflict Processing in Social Decision-Making 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709732v1?rss=1
</link>
<description><![CDATA[
Social decision making relies on dynamic affect cognition interactions across distributed brain networks, yet how incidental positive affect modulates these mechanisms at a millisecond timescale remains unclear. This study investigated the impact of music-induced positive emotion on the neural dynamics of decision-making in the Ultimatum Game. Fifty six participants were assigned to either a happy music group or an active control (rain sound) group. Fifty six participants were assigned to either a happy music group or an active control (rain sound) group, while electroencephalography was recorded to capture rapid neural dynamics. Behaviorally, happy music accelerated reaction times (RTs) and decoupled the ERP RT correlations observed in the control condition. Neurally, positive affect amplified event-related potential amplitudes during early conflict detection (220 to 280 ms) and late valuation (520 to 560 ms) stages. Multivariate pattern analysis further revealed that happy music enhanced the neural separability and temporal stability of decision states (accept vs. reject). Moreover, using support vector regression based on functional network features, we found that decision acceptance rates were predicted with significantly higher accuracy in the happy music group (R = 0.60) compared to controls (R = 0.41). Crucially, feature weight analysis indicated a topological shift in decision strategy: while the control group relied on frontal central edges (implicating executive control), the happy music group was characterized by central temporal connections (suggesting integrative processing). Collectively, these findings provide novel evidence that incidental emotion intervenes at the millisecond timescale to bias social choices, offering a dynamic network based account of the affect cognition interaction.
]]></description>
<dc:creator><![CDATA[ Liu, Z., Liu, Y., Li, W., Cui, R., Liu, X. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709732</dc:identifier>
<dc:title><![CDATA[Positive Affect Modulates Early Valuation and Conflict Processing in Social Decision-Making]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709591v1?rss=1">
<title>
<![CDATA[
Early Binding of Anti-Amyloid Antibodies to CAA Drives Complement Activation, Inflammation and ARIA in Mice 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709591v1?rss=1
</link>
<description><![CDATA[
Anti-amyloid antibody treatment for Alzheimers disease is linked to Amyloid-Related Imaging Abnormalities (ARIA), including vasogenic edema (ARIA-E) and microhemorrhages (ARIA-H), especially in ApoE {epsilon} 4/4 carriers. To investigate mechanisms underlying ARIA, we examined the binding and temporal vascular effects of immunization with 3D6, the precursor to the anti-amyloid antibody bapineuzumab, in two aged Alzheimers disease amyloid mouse models. Acutely, 3D6 bound to cerebral amyloid angiopathy (CAA), resulting in C1q binding and classical complement activation. Weekly short-term immunization over 7 weeks resulted in elevated CAA- and plaque-associated complement deposition, red blood cell extravasation and microhemorrhages, and was accompanied by significant transcriptomic changes in genes related to complement, inflammation, vascular dysfunction, and endothelial lipid responses. Longer-term dosing over 13-15 weeks further increased complement deposition and was associated with blood-brain barrier disruption, MMP-9 upregulation, and microhemorrhages, accompanied by reduced amyloid burden and modest CAA clearance. C3 levels correlated with microhemorrhage severity. Perivascular macrophages co-localized with complement-decorated CAA in 3D6-treated mice. These findings implicate complement activation as an early key driver of ARIA and suggest that therapeutic targeting of complement may reduce ARIA risk.
]]></description>
<dc:creator><![CDATA[ Bathini, P., Schilling, S., Rahfeld, J. U., Holtzman, D. M., Sado, T. C., Lemere, C. A. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709591</dc:identifier>
<dc:title><![CDATA[Early Binding of Anti-Amyloid Antibodies to CAA Drives Complement Activation, Inflammation and ARIA in Mice]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709708v1?rss=1">
<title>
<![CDATA[
Enteric sensory neurons for nutrient detection and gut motility 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709708v1?rss=1
</link>
<description><![CDATA[
The enteric nervous system (ENS) orchestrates gastrointestinal reflexes and brain-gut communication via molecularly diverse neurons. Among these, intrinsic primary afferent neurons (IPANs) are essential for detecting luminal nutrients and irritants, yet their molecular identities, sensory properties, and functions remain poorly resolved. Here, we establish a segment-resolved single-cell atlas of the murine ENS, including a comprehensive characterization of the gastric ENS. This resource defines a refined taxonomy of enteric neurons and glia and enabled the development of a genetic toolkit for molecularly defined IPANs. Using chemogenetics and calcium imaging, we discovered that myenteric neurons detect a wide range of nutrients, irritants, and cytokines. Nutrient detection depends on a functional connection between chemosensory epithelial cells and enteric neurons mediated by 5-HT-HTR3 axis. Through optogenetic analysis, we demonstrated segment-specific regulation of gut motility by different IPANs. Our work establishes a genetic and physiological framework for enteric-specific sensory mechanisms.
]]></description>
<dc:creator><![CDATA[ Li, K., Mou, J., Sun, X., Chen, Y., Fu, L., Wang, Z., Wei, Y., Wang, M., Guo, P., Lin, X., Wang, L., Duan, S., Liberles, S., Ni, J. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709708</dc:identifier>
<dc:title><![CDATA[Enteric sensory neurons for nutrient detection and gut motility]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709667v1?rss=1">
<title>
<![CDATA[
Can grid cells produce hexadirectional signals? 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709667v1?rss=1
</link>
<description><![CDATA[
Hexadirectional analysis is widely used to infer population-level grid cell activity in humans, yet this signature has not been reproduced in rodent electrophysiology, where grid cells are best characterized. Moreover, it remains unclear how grid cell populations could generate such a signal. We address this issue theoretically and empirically by evaluating three prevailing hypotheses and the null model, while critically examining the analysis framework itself. We show that the standard approach is insensitive to grid firing per se. Instead, hexadirectional modulation emerges in firing variance, which we find in ratemaps of single-cell, MEC recordings of freely moving rats. Empirically, conjunctive grid-by-head-direction tuning does not produce hexadirectional signals, whereas specific nonlinear transformations can. We argue that false positive inferences can occur and suggest approaches for improved robustness and confidence. This work has critical implications for studies on hexadirectional signals and sheds light on the neural basis of fMRI.
]]></description>
<dc:creator><![CDATA[ Almog, N. Z., Navarro Schroeder, T., Doan, T. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709667</dc:identifier>
<dc:title><![CDATA[Can grid cells produce hexadirectional signals?]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.05.709791v1?rss=1">
<title>
<![CDATA[
A Novel Rapidly Manufacturable Flexible Subdural Electrode Array for Intraoperative Mapping of Cortical Activity 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.05.709791v1?rss=1
</link>
<description><![CDATA[
Flexible and biocompatible neurointerfaces are crucial elements for intraoperative monitoring and chronic neural recordings. However, existing fabrication methods often involve complex cleanroom processes, limiting rapid prototyping and customization. In this study, we present a fast, low-cost method for manufacturing a flexible subdural electrode array based on polydimethylsiloxane (PDMS) and gold conductive layer. The fabrication process utilizes a laser cutter for both mask generation and direct patterning of metal traces on a PDMS substrate, achieving a resolution of up to 30 m. A detachable interface was developed for reliable connectivity during testing. The electrochemical and mechanical properties of the array were characterized, demonstrating Ohmic behavior and stable conductivity after 50 cycles of mechanical bending, with a degradation of less than 10%. Electrochemical impedance spectroscopy (EIS) confirmed the viability of the electrodes for recording physiological signals. The functionality of the array was validated in vivo by performing simultaneous recordings of local field potentials (LFPs) and electrocorticography (ECoG) in the rat somatosensory cortex. The signals from the flexible subdural array showed a statistically significant (p < 0.001 ) median cross-correlation of 0.35 with LFPs recorded at a depth of 600-800 m by industrial electrode. We demonstrate here a robust and accessible approach for producing functional neural interfaces, suitable for rapid iteration and customization in research and clinical applications.
]]></description>
<dc:creator><![CDATA[ Mamleev, A. R., Suchkov, D. S., Malyshev, E. I., Vorobyov, A. A., Sitdikova, V. R., Silaeva, V. M., Logashkin, A. E., Kireev, A. K., Sorokina, M. A., Mitin, D. M., Mukhin, I. S., Belousov, V. V. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.05.709791</dc:identifier>
<dc:title><![CDATA[A Novel Rapidly Manufacturable Flexible Subdural Electrode Array for Intraoperative Mapping of Cortical Activity]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.04.709652v1?rss=1">
<title>
<![CDATA[
Xylazine's k-opioid agonist activity is not shared with other FDA-approved alpha2-adrenergic agonists 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.04.709652v1?rss=1
</link>
<description><![CDATA[
Xylazine is a a2-adrenergic agonist typically used in as a sedative and analgesic in veterinary medicine. For some years, xylazine has been reported as an additive to fentanyl on the illicit drug market and has been associated with severe side-effects including severe ulcerations and potential amputations at the sites of injection along with an increased risk of respiratory depression and death. We recently reported that xylazine has modest k-opioid agonist activity in vitro and in vivo and asked if other alpha2-adrenergic agonists had similar off-target activities. To test this hypothesis, we profiled US FDA-approved alpha2-adrenergic agonists at 320 G protein coupled receptors (GPCRs) to identify potentially deleterious and/or beneficial off-targets. Although all other tested alpha2-adrenergic agonists were devoid of k opioid agonist activity, each had a distinct pattern of activity at various GPCRs and differential patterns of signaling bias at alpha2-receptor subtypes. These findings suggest potential molecular targets for both side-effects and therapeutic activities among known alpha2-adrenergic agonists.
]]></description>
<dc:creator><![CDATA[ Huang, X.-P., Krumm, B. E., Bedard, M. L., McElligott, Z. A., Roth, B. L. ]]></dc:creator>
<dc:date>2026-03-07</dc:date>
<dc:identifier>doi:10.64898/2026.03.04.709652</dc:identifier>
<dc:title><![CDATA[Xylazine's k-opioid agonist activity is not shared with other FDA-approved alpha2-adrenergic agonists]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-07</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.710026v1?rss=1">
<title>
<![CDATA[
Distinct beta burst motifs exhibit opposing error relationships during motor adaptation 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.710026v1?rss=1
</link>
<description><![CDATA[
Beta-band activity (13-30 Hz) is a hallmark of human movement, yet a unifying account of its functional role remains unresolved. Although typically described as a sustained oscillation, beta activity is increasingly recognised to consist of transient bursts. More recently, beta bursts have been shown to exhibit heterogeneous waveforms. Here, we ask whether variability in burst shape corresponds to separable computational roles during motor adaptation. Using high-precision MEG, we recorded neural activity while participants performed a visuomotor rotation task under either implicit (sensorimotor adaptation) or explicit (strategic re-aiming) learning conditions. Conventional metrics, beta power and burst rate, showed context-dependent modulation during preparation but provided limited insight into trial-by-trial behaviour. In contrast, sorting bursts according to their waveforms revealed a repertoire of burst types with dissociable temporal dynamics and context-dependent modulation. Crucially, during post-movement evaluation, distinct burst subtypes showed opposing and temporally specific relationships with behavioural error: one subtype decreased with increasing error, whereas others increased. Together, these findings indicate that beta activity comprises separable transient events with specific computational roles, and that accounting for waveform diversity is essential for understanding how cortical beta supports adaptive behaviour.
]]></description>
<dc:creator><![CDATA[ Moreau, Q., Szul, M. J., Daligaut, S., Schwartz, D. P., Bonaiuto, J. J. ]]></dc:creator>
<dc:date>2026-03-06</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.710026</dc:identifier>
<dc:title><![CDATA[Distinct beta burst motifs exhibit opposing error relationships during motor adaptation]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-06</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.03.06.709780v1?rss=1">
<title>
<![CDATA[
Decoding Phonetic Features: Somatotopic and Sensorimotor Representations in Native and Non-native Consonant Perception 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.03.06.709780v1?rss=1
</link>
<description><![CDATA[
Speech perception relies on the integration of auditory and articulatory information, yet the precise role of motor regions remains debated. Cross-linguistic approaches and challenging listening situations can help fill this gap. We combined behavioral measures and fMRI with multivariate pattern analyses to investigate cortical representations of native French and non-native Mandarin consonant perception under clear and noisy conditions. Cross-modal classification analysis showed that articulatory features of degraded native labial and dental consonants are mapped somatotopically in right lip and tongue motor areas, regions also activated during consonant production. These representations may support phoneme categorization by compensating for degraded input. Representational similarity analysis further revealed that a network encompassing bilateral temporal and frontal motor regions encodes phonetic features of native and non-native consonants, including place and manner of articulation. Our findings highlight that speech perception relies on embodied sensorimotor representations, which contribute to decoding phonetic features both within and across languages.
]]></description>
<dc:creator><![CDATA[ Tseng, T., Thibault, S., Krzonowski, J., Canault, M., Roy, A., Brozzoli, C., Boulenger, V. ]]></dc:creator>
<dc:date>2026-03-06</dc:date>
<dc:identifier>doi:10.64898/2026.03.06.709780</dc:identifier>
<dc:title><![CDATA[Decoding Phonetic Features: Somatotopic and Sensorimotor Representations in Native and Non-native Consonant Perception]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-03-06</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
