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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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<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751829v1?rss=1">
<title>
<![CDATA[
Chronic lower limb pain is not associated with a loss of inhibitory neurons in the human lumbar spinal dorsal horn 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751829v1?rss=1
</link>
<description><![CDATA[
The spinal dorsal horn is the primary processing site of nociceptive sensory input from the periphery. Excitatory spinal interneurons releasing glutamate can amplify this information before it is sent to the brain, whereas inhibitory neurons releasing GABA and/or glycine can suppress the outflow of nociceptive signals. An imbalance favoring excitation is thought to underlie certain aspects of chronic pain. Although rodent studies have identified spinal mechanisms underlying hyperalgesia and allodynia, little is known about the anatomical changes associated with chronic pain in the human spinal cord, a gap in knowledge we sought to address in this study. Using immunohistochemistry and in situ hybridization on lumbar spinal cord tissue recovered from organ donors, we characterized neuronal size and density across the human dorsal horn and confirmed the presence of the human equivalent of the lateral spinal nucleus in many individuals. Chronic lower limb pain was not associated with changes in neuronal density in the dorsal horn. Likewise, the ratio of excitatory (SLC17A6+) to inhibitory (PAX2+) neurons remained consistent across laminae for age, sex and chronic pain state, providing no evidence for selective loss of inhibitory neurons with chronic pain in humans. We found no differences in the size or density of the postsynaptic markers Homer1 and gephyrin between groups, suggesting glutamatergic and GABAergic postsynaptic sites remain structurally stable. These findings provide a thorough evaluation of cellular anatomy of the human dorsal horn and form a foundation for future studies investigating neuronal changes that may contribute to chronic pain in humans.
]]></description>
<dc:creator><![CDATA[ Davis, O. C., Brandon, J. M., Natarajan, K., He, L., Khan, Z., Selvakumaran, N., Babar, M., Alfayadh, A., Shiers, S. I., Yousuf, M. S. C., Vines, E., Horton, P., Cervantes, A., Khan, T., Funk, G., Todd, A., Dussor, G., Price, T. J. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751829</dc:identifier>
<dc:title><![CDATA[Chronic lower limb pain is not associated with a loss of inhibitory neurons in the human lumbar spinal dorsal horn]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.17.752361v1?rss=1">
<title>
<![CDATA[
Low-dose ketamine tilts the cortical excitation--inhibition balance irrespective of systemic physiological response 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.17.752361v1?rss=1
</link>
<description><![CDATA[
Non-invasive proxies of cortical excitation--inhibition (E:I) balance, are increasingly used to understand human neural dynamics; especially so the aperiodic (1/f) electroencephalographic (EEG) exponent. Ketamine, an NMDA-receptor antagonist, is thought to shift this balance toward excitation. Propofol, a GABAA-receptor agonist, should behave oppositely. Here we show that these pharmacological manipulations at low doses tilt the noninvasive read-out of E:I balance as predicted, and we demonstrate this effect to be robust against potential mediation by the ketamine-related systemic cardiovascular response. In a single-blind, placebo-controlled crossover study, 25 healthy adults received low, subanesthetic doses of ketamine, propofol, or placebo by target-controlled infusion during resting-state EEG. We further analyzed electrocardiogram (ECG) and dissociating ratings. Ketamine flattened the aperiodic exponent (i.e., a shift toward excitation) and raised heart rate and blood pressure; propofol exerted its effects in the opposite direction, while both agents reduced alpha oscillatory power. Critically, the cardiovascular response did not mediate the cortical E:I shift. Controlling for heart rate left the ketamine effect not only intact but numerically stronger, suggesting that E:I balance findings might even be underestimated when ignoring the systemic physiological response.
]]></description>
<dc:creator><![CDATA[ Kunze, J., Student, J. P., Tune, S., Oster, H., Schmidt, S., Ihmsen, H., Tzabazis, A., Lorenz, B., Nau, C., Obleser, J. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.17.752361</dc:identifier>
<dc:title><![CDATA[Low-dose ketamine tilts the cortical excitation--inhibition balance irrespective of systemic physiological response]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.17.752481v1?rss=1">
<title>
<![CDATA[
Face ensembles reshape the neural other-race effect 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.17.752481v1?rss=1
</link>
<description><![CDATA[
The other-race effect (ORE), poorer recognition of other-race (OR) than same-race (SR) faces, is established for individual faces, but its neural expression during group viewing remains unclear. Twenty-two East Asian adults viewed East Asian and White faces in different formats: individually and in six-face ensembles during EEG recording. Behavioral testing confirmed an SR advantage. Decoding and generative reconstruction characterized neural discriminability, geometry, dynamics, sensor-level information, and recoverable content. Single SR faces were more discriminable, more dispersed in face space, and reconstructed more accurately. Ensembles preserved racial-composition information but reduced the cumulative SR-OR decoding difference and showed instead an early OR advantage. Reconstructions supported identification of individual faces and ensemble summaries, with an overall SR advantage but no reliable race-by-format interaction. Independent judgments revealed race- and format-dependent shifts in reconstructed age, valence, and arousal. These findings reveal a neural ORE whose expression depends on viewing context and representational measure.
]]></description>
<dc:creator><![CDATA[ Shoura, M., Jiang, H. N., Azeem, Z., Iancu, O., Sama, M. A., Cant, J. S., Nestor, A. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.17.752481</dc:identifier>
<dc:title><![CDATA[Face ensembles reshape the neural other-race effect]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.16.752209v1?rss=1">
<title>
<![CDATA[
Field-Based Characterization of Temporal Interference Stimulation: Beyond the Target-Centric Perspective 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.16.752209v1?rss=1
</link>
<description><![CDATA[
Temporal interference (TI) stimulation is a promising non invasive technique for deep brain neuromodulation, yet accurately characterizing its complex and spatially distributed electric fields remains a fundamental challenge. This study proposes a novel computational framework that integrates topological analysis with mesh-aware metrics to overcome the limitations of conventional global field descriptors. The method introduces three interconnected components: (1) connected component , which extracts spatially continuous field regions above thresholds; (2) discrete ellipsoid modeling, which quantifies the geometric centroid, directional spread, and anisotropy of each region; and (3) Local Moran's I to identify robust spatial clusters while suppressing numerical noise. Applied to TI simulations using individualized tetrahedral head models, the framework demonstrates that the few largest connected components above an elevated intensity threshold collectively provide a more accurate representation of the stimulation targets. The approach provides highly interpretable visual outputs that directly map field topology to brain anatomy, including layered component maps, discrete ellipsoids, and spatially weighted clustering landscapes. By offering a topologically coherent, noise robust, and visually intuitive analytical toolbox, this work advances the precision and interpretability of TI field assessment, supporting more reliable target localization, focality quantification, and parameter exploration in translational neuromodulation research.
]]></description>
<dc:creator><![CDATA[ Chen, T., Huo, C., Shao, G., Cao, Z., Li, C., Liu, J., Li, Z. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.16.752209</dc:identifier>
<dc:title><![CDATA[Field-Based Characterization of Temporal Interference Stimulation: Beyond the Target-Centric Perspective]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751814v1?rss=1">
<title>
<![CDATA[
Action potential waveforms are state-dependent 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751814v1?rss=1
</link>
<description><![CDATA[
Action potentials are brief electrical impulses that form the mechanistic basis for how neurons communicate. While it is well known that the shape of action potentials can differ across neurons, one fundamental assumption is that the complex voltage waveforms of action potentials within a given neuron are reducible to binary spikes. This assumption has constrained our conception of possible neural codes to those amenable to binary signaling, such as rate, temporal, and population codes. Here, we show that action potential waveform variability is not random, but is, instead, state dependent. To show this, we parameterize action potential waveforms in a set of very high temporal resolution (200 kHz) intracellular action potential recordings. We show that an action potential is not a digital '1', but is instead a rich signal whose fine-scale features influence the shape and timing of the next action potential and whose waveform is systematically biased by input drive. We then show that intracellular action potential waveforms can vary as a function of the extracellular local field potential, but do so heterogeneously, as a function of the field potential amplitude and standard deviation. Our results have profound implications for systems and computational neuroscience, especially regarding the development of next-generation, biologically-inspired artificial neural networks that incorporate waveform dynamics. Non-binary action potentials point to a broader landscape of possible neural codes, whereby neurons communicate not just via binary spikes, but through their state-dependent waveform features.
]]></description>
<dc:creator><![CDATA[ Martin-Burgos, B., Juavinett, A., Riviere, P. D., Hammonds, R., Voytek, B. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751814</dc:identifier>
<dc:title><![CDATA[Action potential waveforms are state-dependent]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751722v1?rss=1">
<title>
<![CDATA[
Sex-stratified fixel-based analysis reveals reduced frontal fibre density in males with first-episode of psychosis 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751722v1?rss=1
</link>
<description><![CDATA[
Background: Schizophrenia has been conceptualised as a disorder of brain disconnectivity, with white matter abnormalities contributing to altered neural communication. However, fibre-specific white matter alterations in early illness and their potential sex-related differences remain insufficiently characterised. We applied fixel-based analysis to investigate sex-stratified white matter microstructural alterations in first-episode schizophrenia (FES). Methods: Diffusion MRI data from individuals with FES and healthy controls were stratified by biological sex. The male cohort included 79 patients and 29 controls, and the female cohort included 48 patients and 46 controls. Fixel-based analysis was performed separately in males and females to assess fibre density, fibre-bundle cross-section, and their combined measure. Head motion was included as a covariate in the fixel-based analyses. A descriptive follow-up voxel-scale analysis extracted mean fibre density from a binary mask derived from significant male fixels and applied the same region to the female cohort. Results: Males with first-episode schizophrenia showed significantly reduced fibre density compared with male controls, primarily in bilateral frontal white matter and a thin segment of the anterior corpus callosum. The voxel-scale follow-up confirmed lower mean fibre density in males within the significant fixel-derived mask. In contrast, females showed no significant group differences in any fixel-based metric or within the male-derived region. Conclusions: Early white matter microstructural alterations were detected in males with FES but not in females. These findings highlight a differential pattern emerging from sex-stratified analyses and support further investigation of sex-related differences in white matter alterations during the early stages of schizophrenia.
]]></description>
<dc:creator><![CDATA[ Sanchez, S. M., Schmidt, H., Skoch, A., Hugdahl, K., Spaniel, F., Hlinka, J. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751722</dc:identifier>
<dc:title><![CDATA[Sex-stratified fixel-based analysis reveals reduced frontal fibre density in males with first-episode of psychosis]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751857v1?rss=1">
<title>
<![CDATA[
A convergent behavioral-neural profile of parental dysregulation and the link between parent-child brain-state similarity and child negative affect 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751857v1?rss=1
</link>
<description><![CDATA[
Parent-child neural similarity is often interpreted as a marker of attunement, but its developmental significance may not be uniformly positive across family environments. We tested whether the parent's own emotional and regulatory profile, measured both behaviorally and neurally, moderates the developmental significance of parent-child neural similarity. Applying a hidden Markov model (HMM-MAR; K = 6 states) to whole-brain fMRI timeseries from 32 parent-youth dyads who separately watched the same emotional film, we derived per-dyad measures of brain-state similarity. Parent-child dyads showed greater brain-state similarity than parent-shuffle null pairs (d = -0.55, p = .004), indicating dyad-specific alignment beyond responses shared across viewers of the same film. Parent self-reported internalizing showed only a weak direct relation to child negative affect (r = .31, p = .085). However, the association between neural similarity and child negative affect depended on parent internalizing (b = 5.62, p = .018; R^2): stronger parent-child similarity predicted higher child negative affect when parents reported higher, but not lower, internalizing. A parallel interaction emerged when parent internalizing was replaced by a neural index of the parent's own state dynamics (parent neural-state unpredictability, Htrans; b = 5.95, p = .004), indicating that the effect reflects the parent's broader regulatory profile rather than a single measurement modality. Both interactions were clearest in the primary model and only partially robust across model orders and parcellations. These findings suggest that dyadic neural similarity should be interpreted in context: resembling a parent with a dysregulated profile may confer risk rather than protection.
]]></description>
<dc:creator><![CDATA[ Li, Q., Chen, Y.-Y., Zhou, Z., Qu, Y., Kim-Spoon, J., Lee, T.-H. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751857</dc:identifier>
<dc:title><![CDATA[A convergent behavioral-neural profile of parental dysregulation and the link between parent-child brain-state similarity and child negative affect]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751835v1?rss=1">
<title>
<![CDATA[
Regulation of protein kinase pathways in primary neuron model of anti-NMDA receptor encephalitis. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751835v1?rss=1
</link>
<description><![CDATA[
The most common form of autoimmune encephalitis is associated with antibodies that target N-methyl-D-aspartic acid receptors (NMDARs). NMDARs play a pivotal role in neurotransmission and synaptic plasticity. Mounting evidence has shown that antibody targeting of the NMDAR GluN1 subunit, as in anti-NMDAR encephalitis, leads to NMDAR cross-linking and receptor internalization. However, the underlying signaling pathways affected by antibodies targeting NMDARs remain to be explored. We previously demonstrated that a human GluN1 monoclonal antibody 5F5 (GluN1 mAb 5F5) rapidly localizes to and regulates synaptic NMDAR function at native synapses of primary hippocampal neurons. Here, we sought to explore signaling targets of GluN1 mAb 5F5 in primary cortical neurons of either sex using subcellular fractionation, Western blotting, and label-free quantitative phosphoproteomics by mass spectrometry. We find that human GluN1 mAb 5F5 does not change NMDAR abundance or surface levels of GluN1 on primary cortical neurons at 2 hr. Despite this, we observe that GluN1 mAb 5F5 alters the phosphoproteome in synaptoneurosomes and regulates numerous synapse-related biological processes and protein kinase activities. Bioinformatic analyses suggest that these phosphoproteomic changes are positively correlated with NMDAR activation and negatively correlated with NMDAR inhibition. Together, these data suggest that GluN1 mAb 5F5 alters intracellular kinase signaling pathways in primary cortical neurons, likely by activating the NMDAR. These studies may help to identify novel therapeutic strategies for anti-NMDAR encephalitis and other antibody-mediated encephalitides targeting cell surface antigens.
]]></description>
<dc:creator><![CDATA[ Joo, Y., Ciryam, P., Zhang, T., Huang, W., Dean, C. A., Lawrence, A. P., Vu, T. H., Gooya, N., Dessain, S. K., Kane, M. A., Benavides, D. R. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751835</dc:identifier>
<dc:title><![CDATA[Regulation of protein kinase pathways in primary neuron model of anti-NMDA receptor encephalitis.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751847v1?rss=1">
<title>
<![CDATA[
Machine learning on subcortical brain features: A study of sample size efficiency for neurodegenerative disease classification 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751847v1?rss=1
</link>
<description><![CDATA[
Subcortical brain alterations are a key feature of dementia disease progression. Machine learning (ML) has been applied widely to MRI-based brain features in dementia, where performance depends on the model choice, training data size, and input feature characteristics. Most studies compare ML models using a single training sample size. Here, we evaluate the sample-size efficiency of ML models based on subcortical gross volume and vertex-wise shape features for dementia stage classification using 2,511 samples in the Alzheimer's Disease Neuroimaging Initiative (ADNI). Learning curves were generated for dementia vs. cognitively normal controls (CN), dementia vs. mild cognitive impairment (MCI), and MCI vs. CN across increasing training sample sizes. Classification performance improved when increasing sample size for all models, with late- fusion models consistently achieving the highest performance, and Logit-TVL1 outperforming the other shape-based models. Learning curve analysis showed that classification performance was driven by the training sample size and the magnitude of anatomical group differences, and can be used to optimize future model selection tasks in dementia and other brain disorders.
]]></description>
<dc:creator><![CDATA[ Im, Y., Kang, M. J. Y., Gutman, B. A., Thomopoulos, S. I., Thompson, P. M., Ching, C. R. K., for the Alzheimers Disease Neuroimaging Initiative ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751847</dc:identifier>
<dc:title><![CDATA[Machine learning on subcortical brain features: A study of sample size efficiency for neurodegenerative disease classification]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751842v1?rss=1">
<title>
<![CDATA[
The impact of alpha synuclein overexpression on nigrostriatal transmission 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751842v1?rss=1
</link>
<description><![CDATA[
Accumulation of wild type synuclein in dopamine neurons of the Substantia Nigra pars compacta is a pathological hallmark of Parkinson's disease (PD), which commonly precedes neurodegeneration. Yet how synuclein accumulation affects nigrostriatal neurotransmission early in the progression of PD remains poorly understood. In addition to axonal dopamine release, SNc neurons also co-release GABA and glutamate from striatal axon terminals and release dopamine from their somatodendritic region. However, the selective vulnerability of these distinct functions to increased synuclein remains largely unexplored. Here, we selectively overexpressed wild type human synuclein in SNc dopamine neurons to examine impacts on nigrostriatal and somatodendritic transmission and correlated these changes to impairments in locomotion. We found that dopamine release in the dorsolateral striatum was robustly reduced, while transmission to postsynaptic medium spiny neurons remained intact. Glutamate co-release from dopamine terminals onto both medium spiny neurons and cholinergic interneurons was selectively impaired, while GABA co-release was unaffected. Conversely, somatodendritic dopamine release within the SNc was completely abolished by synuclein overexpression. Together, these findings identify selective deficits in nigrostriatal neurotransmission associated with wild type synuclein accumulation prior to overt degeneration and raise the possibility of compensatory adaptations shaping the early functional consequences of synuclein pathology in PD.
]]></description>
<dc:creator><![CDATA[ Bergum, N., Yee, A., Edwards, R., Ford, C. P. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751842</dc:identifier>
<dc:title><![CDATA[The impact of alpha synuclein overexpression on nigrostriatal transmission]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.19.752823v1?rss=1">
<title>
<![CDATA[
Localized SARS-CoV-2 Infection Triggers a Tissue-Wide Antiviral Response and Functional Impairment of Olfactory Sensory Neurons 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.19.752823v1?rss=1
</link>
<description><![CDATA[
Olfactory dysfunction is a hallmark of COVID-19, yet the mechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes widespread sensory impairment remain incompletely understood. We compared the olfactory epithelial tropism of multiple SARS-CoV-2 variants in a mouse model and observed that Alpha and Beta variants exhibited the greatest infectivity for the olfactory epithelium (OE), whereas Omicron rarely infected this tissue despite comparable pulmonary viral titers. We further defined the effects of SARS-CoV-2 on olfactory sensory neurons (OSNs) using immunohistochemistry, single-cell RNA sequencing, spatial gene expression characterization, and functional odor stimulation. The localized infection of sustentacular cells triggered a tissue-wide interferon-stimulated antiviral response that extended beyond infected regions for Alpha and Beta but was largely absent following Omicron infection. Mature OSNs transiently adopted an interferon-responsive state before exhibiting persistent downregulation of odorant signal transduction, mitochondrial, and activity-dependent gene pathways. Consistent with these transcriptional changes, odor stimulation failed to elicit normal activity-dependent gene expression during SARS-CoV-2 infection, indicating impaired neuronal function without widespread neuronal loss. Progressive accumulation of macrophages further indicated sustained inflammatory remodeling of the OE. Together, these findings demonstrate that SARS-CoV-2 infection initiates tissue-wide antiviral signaling in the OE that persistently disrupts OSN function, providing a mechanistic framework for COVID-19-associated anosmia.
]]></description>
<dc:creator><![CDATA[ Liu, J., Akhtar, M. S., Liu, H., Kim, Y., Ramirez, B. M., Weidner, A. L., Chan, A., Collins, M., Rothenburg, S., Coffey, L. L., Gong, Q. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.19.752823</dc:identifier>
<dc:title><![CDATA[Localized SARS-CoV-2 Infection Triggers a Tissue-Wide Antiviral Response and Functional Impairment of Olfactory Sensory Neurons]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751810v1?rss=1">
<title>
<![CDATA[
Task Engagement Gates Interareal Communication Geometry in the Mouse Thalamocortical-Midbrain Visual Circuit 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751810v1?rss=1
</link>
<description><![CDATA[
Visual processing unfolds across hierarchically organized brain circuits. Existing theories largely explain changes in population geometry through local shifts in gain, firing-rate statistics, or recurrent dynamics, yet do not account for how interareal coordination interacts with local population geometry to constrain downstream population states. We used task engagement, compared to a passive condition, to probe this coordination in Neuropixels recordings spanning the mouse visual thalamocortical-midbrain circuit. Engagement reduced network activity, response participation, and dimensionality across the hierarchy. To account for this circuit-level organization, we developed a theoretical framework in which afferent population geometry interacts with local recurrent dynamics to constrain the accessible dynamics of downstream populations. Across the thalamocortical stages, population-wide afferent statistics predicted downstream activity and dimensionality. At the cortex--midbrain interface, engagement instead reorganized interareal communication geometry. Together, these results identify interareal input geometry as a key constraint on neural population dynamics and uncover a general principle by which behavioral engagement constrains neural state spaces across distributed visual circuits.
]]></description>
<dc:creator><![CDATA[ Amalberti, L., Hauer, M., Bennett, C., Olsen, S. R., Dahmen, D., Recanatesi, S. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751810</dc:identifier>
<dc:title><![CDATA[Task Engagement Gates Interareal Communication Geometry in the Mouse Thalamocortical-Midbrain Visual Circuit]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751608v1?rss=1">
<title>
<![CDATA[
Focused Ultrasound Neuromodulation of the Central Lateral Thalamus in a Non-Human Primate Model of Disorders of Consciousness 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751608v1?rss=1
</link>
<description><![CDATA[
Objectives: Disorders of consciousness (DOC) affect an estimated 200,000 patients in the United States. Effective treatment options have remained elusive. Focused ultrasound neuromodulation (FUS) of brain regions controlling consciousness, such as the central lateral thalamus (CLT), has emerged as a promising non-invasive treatment. However, prior studies have been limited by broad effective stimulation volumes, missing control conditions, and limited target validation. This study investigated the effects of FUS of the CLT in a non-human primate model of DOC with robust control conditions and more robust targeting than previous experiments. Materials and Methods: Two male rhesus macaques underwent 1-hour propofol anesthesia sessions as a model of DOC. Bilateral CLT targets were sonicated using a stereotactically mounted 256-element phased-array focused ultrasound system. Focused and unfocused (random phases) paradigms were tested in both animals, and a spotlighting (sonicating multiple targets) paradigm was tested in one animal. Arousal was monitored via EEG beta power, pulse oximetry, breathing rate, and movement, and compared between sonication and control sessions for each paradigm. Results: Paired Wilcoxon signed-rank tests showed no significant differences for any of the four measures across the three paradigms (all pFDR [&ge;] 0.30). The largest observed effect was increased body movement under the unfocused paradigm (rrb = +0.58), though this did not reach statistical significance. Animals remained physiologically stable throughout sessions and recovery periods, with no clinically significant changes in heart rate, breathing rate, blood oxygen saturation, or other safety concerns. Conclusions: Under the tested parameters, FUS of the CLT did not produce measurable changes in arousal. The absence of adverse physiological effects supports the safety of this FUS paradigm. The largest effect occurring under spatially distributed sonication, consistent with prior evidence that broader stimulation volumes produce stronger arousal responses, suggests that distributed network stimulation may warrant investigation as an alternative to focal targeting. Future studies should investigate this possibility and should include robust control conditions to properly quantify effects.
]]></description>
<dc:creator><![CDATA[ Lybbert, C., Garrett, C., Webb, T. D., Tsunoda, K., Begum, R., Kubanek, J. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751608</dc:identifier>
<dc:title><![CDATA[Focused Ultrasound Neuromodulation of the Central Lateral Thalamus in a Non-Human Primate Model of Disorders of Consciousness]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751776v1?rss=1">
<title>
<![CDATA[
Dorsal ocelli set the luminance-dependent operating state of the bumblebee visual system 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751776v1?rss=1
</link>
<description><![CDATA[
Despite long-standing hypotheses that insect dorsal ocelli modulate compound-eye processing to support flight stabilization, dim-light navigation, and locomotor speed, the neurophysiological basis of these functions remains unclear. Combining behavioural assays with multi-site local field potential recordings in bumblebees, we tested how ocellar input affects compound-eye processing. Ocellar occlusion impaired orientation precision at dusk, supporting a role for ocelli in dim-light navigation. Under bright daytime skies, occlusion did not affect orientation but reduced flight speed, consistent with a role in locomotor control under high illumination. Neurophysiologically, ocellar occlusion disrupted luminance-dependent scaling across the visual system, most prominently in the medulla. In intact bees, broadband neural power scaled inversely with luminance, decreasing under bright and increasing under dim conditions. When ocellar input was blocked, this relationship reversed, leaving visual-system activity in a high-power, dark-like state even under bright illumination. Ocellar modulation was particularly evident in the green-sensitive pathway, implicated in optic-flow processing and flight-speed regulation, providing a neural correlate of the behavioural speed reduction while UV-sensitive responses remained largely invariant following ocellar occlusion. These findings reconcile disparate views of ocellar function and identify ocelli as regulators of the neural dynamic range supporting orientation in low light and movement control in bright conditions.
]]></description>
<dc:creator><![CDATA[ Restrepo, C. E., Araujo, P., Mikulovic, S., Bauer, P., Baird, E. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751776</dc:identifier>
<dc:title><![CDATA[Dorsal ocelli set the luminance-dependent operating state of the bumblebee visual system]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751760v1?rss=1">
<title>
<![CDATA[
Head-level lesion-symptom mapping of picture naming in vision-language models 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751760v1?rss=1
</link>
<description><![CDATA[
Researchers in artificial intelligence increasingly intervene on language models to study how their functions are organized, silencing weights and attention components in ways reminiscent of the brain lesions long used to map language in post-stroke aphasia. Under this program of mechanistic interpretability, a common move is to ablate an attention head and read the resulting drop in a behavior as evidence that the head implements it. How much that move can establish about where a behavior is computed remains unclear, because a head whose removal disrupts a behavior is necessary for it but need not be the site where it is computed. We examined this question for the picture naming task, taking the loss of naming (anomia) that defines aphasia as the behavior of interest. Across six vision-language models, spanning three language backbones and a range of parameter scales, we ablated each attention head in turn during single-word picture naming and measured accuracy before and after. The degree of localization varied widely across models. In LLaVA-1.6-Vicuna-13B, a single early head (layer 0, head 20) was necessary: removing it alone reduced naming accuracy from 0.99 to 0.006. The same head was not sufficient, because retaining it while ablating the other 1{,}599 heads also produced 0% accuracy. Two Mistral-backbone models (LLaVA-Mistral-7B and Idefics2-8B) had no critical head. An early-layer dependence was present in every model but varied in strength, whereas dependence on any single head ranged from dominant to absent. Within Qwen2.5-VL, a dominant head was present in the 7B model but not the 3B model, indicating that this concentration emerged with scale rather than being fixed across a model family, and it was not explained by attention type. These results show that ablating the head whose removal disrupts naming does not establish that the head computes the behavior, that the result generalizes across models, or that the behavior localizes to a head at all.
]]></description>
<dc:creator><![CDATA[ Nemati, S., Newman-Norlund, R. D., Ahmadi, S., Guan, X., Warren, K., Yang, Y., Nelakuditi, S., Rorden, C., Bonilha, L., Fridriksson, J. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751760</dc:identifier>
<dc:title><![CDATA[Head-level lesion-symptom mapping of picture naming in vision-language models]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751684v1?rss=1">
<title>
<![CDATA[
A dopaminergic visuomotor gateway to the zebrafish optic tectum 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751684v1?rss=1
</link>
<description><![CDATA[
Dopamine (DA) is widely known as a neuromodulator essential for reward, motivation and learning, yet it also modifies rapid sensorimotor transformations. Understanding how dopaminergic neurons process sensory input and motor-related signals is therefore critical for elucidating their role in sensorimotor control. In vertebrates, a conserved visual center under dopaminergic influence is the superior colliculus, or optic tectum in fish. Here, using anatomical and molecular analyses in larval zebrafish, we identify a defined cluster of pretectal DA (PrDA) neurons whose axons densely innervate the tectum, predominantly in its deep neuropil. Combining functional Ca2+ imaging with visual stimulation and motor recordings, we show that PrDA neurons respond reliably to visual stimulation. However, most PrDA neurons exhibit pronounced activity also during spontaneous locomotion, and enhanced activity when visual stimuli and motor output co-occur, indicating that PrDA neurons integrate convergent input from visual and motor centers. Furthermore, spontaneous PrDA neuron activity was synchronized and the synchrony was even stronger when visual or motor activity contributed to their activation. Notably, as visual stimuli differed in their efficacy to drive swim activity, motor-associated responsiveness of PrDA neurons produced apparent direction selectivity to stimulus motion when motor activity was not accounted for. This apparent neural response bias disappeared once motor activity was taken into account. Together, these findings suggest that PrDA neurons provide rapid, visuomotor-related dopaminergic modulation of tectal circuits that transform visual information into context-dependent motor commands, a principle that may extend to homologous mammalian midbrain circuits.
]]></description>
<dc:creator><![CDATA[ Brehm, N., Chakraborty, S., Bollmann, J. H. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751684</dc:identifier>
<dc:title><![CDATA[A dopaminergic visuomotor gateway to the zebrafish optic tectum]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751773v1?rss=1">
<title>
<![CDATA[
Transient excitability and synaptic consolidation support stable memory despite neural drift 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751773v1?rss=1
</link>
<description><![CDATA[
Long-term memories remain behaviorally stable despite turnover in the neuronal populations that encode them. This representational drift differs across brain regions: hippocampal representations can reconfigure within hours, whereas cortical ensembles remain comparatively stable over days to weeks. This asymmetry poses a challenge for systems consolidation, in which hippocampal activity is thought to instruct the formation of persistent cortical memory traces. We developed a two-region recurrent network model of the hippocampus (HPC) and anterior cingulate cortex (ACC) incorporating region-specific synaptic plasticity, excitability-dependent neuronal allocation, hippocampal-to-cortical coupling, and activity-dependent intrinsic plasticity. When the regions evolved independently, faster synaptic turnover in HPC produced pronounced drift, whereas persistent ACC connectivity preserved a more stable cortical ensemble. In the intact circuit, hippocampal input recruited ACC neurons but also propagated hippocampal variability into cortex, destabilizing the emerging cortical engram and impairing memory expression. A transient increase in the intrinsic excitability of recruited ACC neurons counteracted this instability by promoting repeated reactivation during an early consolidation window, stabilizing cortical ensemble membership without preventing hippocampal drift. Simulated erasure of learning-induced potentiation further reproduced the early dependence of memory on hippocampal, but not ACC, plasticity. Together, these results support a sequential mechanism in which hippocampal recruitment, transient cortical intrinsic plasticity, and persistent cortical synaptic plasticity transform a dynamic hippocampal representation into a stable cortical memory trace.
]]></description>
<dc:creator><![CDATA[ Wagle, S., Clopath, C. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751773</dc:identifier>
<dc:title><![CDATA[Transient excitability and synaptic consolidation support stable memory despite neural drift]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751737v1?rss=1">
<title>
<![CDATA[
Prefrontal control of hippocampal map reorganization during sleep 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751737v1?rss=1
</link>
<description><![CDATA[
During wakefulness, exposure to novel experiences induces hippocampal remapping, in which place cell ensembles reorganize to form distinct representations of new information. Classical models of systems consolidation posit that subsequent sleep stabilizes these wake-formed representations and supports their gradual transfer to medial prefrontal cortex (mPFC) networks primarily via bottom-up hippocampal reactivations. Using miniscope Ca2+ imaging of CA1 place cells, we monitored hippocampal activity as mice explored a familiar environment followed by a similar novel one. As expected, place cells remapped in the novel context. However, a single episode of post-encoding sleep selectively reversed remapping dynamics by promoting the reinstatement of familiar place cell representations in the novel environment, an effect that was absent in the wake condition. This neural reinstatement was accompanied by behavioral indicators of familiarity, including reduced exploration and rearing. Chemogenetic inactivation of the mPFC during post-encoding sleep abolished this generalization effect, and instead preserved the novel hippocampal map. Thus, our results extend current models by showing that sleep not only consolidates wake-established hippocampal patterns, but actively shapes hippocampal maps via prefrontal control, thereby supporting memory generalization.
]]></description>
<dc:creator><![CDATA[ Huang, R., Nakano, M., Clopath, C., Born, J., Bartsch, T., Both, M., Blanco-Hernandez, E., Burgalossi, A. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751737</dc:identifier>
<dc:title><![CDATA[Prefrontal control of hippocampal map reorganization during sleep]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751573v1?rss=1">
<title>
<![CDATA[
Learning to play with spikes: characterizing, predicting, and engineering unsupervised plasticity rules for spiking reservoir computing 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751573v1?rss=1
</link>
<description><![CDATA[
Spiking reservoir computing, and reservoir computing more generally, is a powerful and efficient framework for neuromorphic and biological applications, in which a fixed random reservoir drives a trained readout. Its performance depends critically on the reservoir initialization, so that enriching the reservoir with adaptive, unsupervised plasticity rules offers a natural solution to this limitation. However, it is unclear which rules work, or why, and how to find the best-suited rules for specific tasks without exhaustive and expensive search. Here, we learn how to play the Atari game Pong in a plastic spiking reservoir network. We systematically characterize a large family of local plasticity rules that were meta-learned in prior work. We then show that their performance is predictable and structured: high-scoring rules are characterized by strong differentiation between neurons encoding the ball trajectory and the background, with stable weight dynamics, and consistent readout alignment across time. These mechanistic signatures are not task-specific and transfer to a delayed-match recognition task. Rule performance can be estimated from rule parameters alone. Finally, conditioning simulation-based inference (SBI) on high scores allows us to sample directly from promising regions of the rule space, to discover rules that exceed the performance of those found in the prior distribution and reveal stable, high-performing configurations. Together, these results offer competitive performance against classical reservoir computing while providing a transparent, interpretable account of what makes a plasticity rule useful for neuromorphic hardware and biological computing.
]]></description>
<dc:creator><![CDATA[ Kania, M., Confavreux, B., Vogels, T. P. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751573</dc:identifier>
<dc:title><![CDATA[Learning to play with spikes: characterizing, predicting, and engineering unsupervised plasticity rules for spiking reservoir computing]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751783v1?rss=1">
<title>
<![CDATA[
Number, order and time influence how the brain integrates distinct experiences 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751783v1?rss=1
</link>
<description><![CDATA[
How does the brain integrate experiences that are separated in time? The present study addressed this question using sensory preconditioning protocols in rats. In these protocols, rats integrate an A-B association (e.g., tone-light) formed in stage 1 with a B-shock association (e.g., light-shock) formed in stage 2 to generate fear responses (freezing) when tested with A alone in stage 3. Here we show that the mechanism of integration depends on the number, order and timing of events across the two stages of training. When the events are novel (low number of exposures) and the interval between stages 1 and 2 is short (24 hours), the A-B and B-shock associations are integrated through formation of a mediated A-shock association during stage 2. By contrast, when the events are more familiar (greater number of exposures), ordered in a particular way, and the interval between stages 1 and 2 is long (14-days), the A-B and B-shock associations are integrated through their chaining at the time of testing with A alone. Thus, number, order and time determine how distinct experiences are integrated in the brain. These findings are discussed with respect to theories of integration and information processing in the medial temporal lobe.
]]></description>
<dc:creator><![CDATA[ Thomas, A. B., Wong, F. S., Killcross, S., Westbrook, R. F., Holmes, N. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751783</dc:identifier>
<dc:title><![CDATA[Number, order and time influence how the brain integrates distinct experiences]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751758v1?rss=1">
<title>
<![CDATA[
Human see, human do? Viewing tool pictures evokes tool-use action information in hand-selective occipitotemporal cortex 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751758v1?rss=1
</link>
<description><![CDATA[
Amongst all the objects we encounter, tools are unique because they are tightly linked to predictable actions. Neuroimaging studies have reported selective responses in occipitotemporal and parietal cortices when viewing pictures of tools or hands. Whether these responses contain information about specific tool-use actions (e.g., rotation for keys), and whether such information shares a neural format with action execution, remains unclear. Here, we used fMRI and multivoxel pattern analysis to ask whether specific actions associated with viewed tools could be decoded and whether action-specific information generalised across viewing and acting. Participants (N=18; 11 females) viewed tool pictures and, in separate runs, pantomimed tool-use actions in response to tool names. Familiar tools differed in their associated action (rotate or squeeze) but were matched for grip type. Viewing tool pictures elicited tool-use action information in lateral occipitotemporal cortex (LOTC), parietal cortex, and even somatosensory cortex. Notably, hand-selective LOTC was the only region in which action decoding exceeded tool-identity decoding during both viewing and pantomime, suggesting sensitivity to learned relationships between objects and characteristic hand actions. However, neither region-of-interest nor whole-brain searchlight analyses yielded reliable cross-task decoding. Thus, although overlapping cortical regions contained information about tool-use actions during perception and production, we found no evidence that this information was represented in a shared multivoxel format. These findings suggest that seeing familiar tools evokes distributed information about their associated actions and sensory consequences, but that such information may be expressed in task-dependent formats rather than simply reinstating the neural patterns engaged during action production.
]]></description>
<dc:creator><![CDATA[ Warman, A., Tonin, D., Smith, F., Rossit, S. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751758</dc:identifier>
<dc:title><![CDATA[Human see, human do? Viewing tool pictures evokes tool-use action information in hand-selective occipitotemporal cortex]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.19.752867v1?rss=1">
<title>
<![CDATA[
Stable Network Motifs with Divergent Engagement Across Memory Outcomes 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.19.752867v1?rss=1
</link>
<description><![CDATA[
Visual recognition memory depends on coordinated interactions across distributed medial temporal, prefrontal, and limbic networks, yet the sub-second large-scale network dynamics distinguishing successful from unsuccessful recognition remain poorly understood. Here we used intracranial EEG recordings from seven patients (4 female, 3 male) with medically refractory epilepsy performing a new-old visual recognition memory task to characterize time-resolved directed functional connectivity and dynamic network organization. Directed effective connectivity was estimated using bivariate Granger causality in a sliding-window framework, and dynamic community structure was identified using the Louvain modularity algorithm. Successful recognition (Hits) was associated with a qualitatively distinct network configuration: low modularity (Q = 0.05 vs. 0.09-0.15 in other conditions), a cross-hemispheric community structure integrating left medial temporal lobe (MTL) with right prefrontal cortex, and sustained network integration throughout the post-stimulus period. Right-hemisphere nodes within this cross-hemispheric community showed stronger within-community directed connectivity than left-hemisphere nodes (mean asymmetry index = 0.33, p < 0.001), consistent with right prefrontal dominance in driving network integration during successful retrieval. In contrast, Correct Rejections were characterized by early transient network segregation (onset 32 ms) dominated by right-hemisphere activity. Hub regions were non-overlapping across conditions--left-lateralized during Hits, right-lateralized during Correct Rejections. These findings imply that successful visual recognition is distinguished not by stronger connectivity per se, but by a reorganization of large-scale network topology that transiently integrates left MTL with right prefrontal cortex into a unified functional community.
]]></description>
<dc:creator><![CDATA[ Kumar, A., Tyner, K., Moseley, R., Svalina, M., Geller, A. S., Rutishauser, U., Kramer, D. R., Thompson, J. A. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.19.752867</dc:identifier>
<dc:title><![CDATA[Stable Network Motifs with Divergent Engagement Across Memory Outcomes]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751719v1?rss=1">
<title>
<![CDATA[
Tracing high transductive cohort AUC to same-site supervision in a site-aware population GNN for multisite fMRI 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751719v1?rss=1
</link>
<description><![CDATA[
Population-graph models can exploit cohort-level context, which complicates the interpretation of high multisite neuroimaging performance. We asked which information pathways account for a previously reported high transductive cohort AUC in multisite autism fMRI. Under a frozen cohort (canonical ABIDE-I, 871 subjects, 20 sites) and a fixed evaluation protocol, we applied controlled graph, feature, supervision, and architecture interventions to a clean-room re-implementation, replicated across two preprocessing pipelines (C-PAC and NIAK). Cohort out-of-fold AUC was approximately 0.94 and depended on site-linked edges: a site-only graph matched the full model (0.948 vs. 0.941). The gain required same-site supervision (masking it reduced AUC to 0.480), was not explained by the supervision budget, and, among architecture-matched heads, was observed only with the evaluated sex-heterogeneous dual-channel head, whereas a canonical topology-only Parisot-GCN did not show the same pattern. Under leave-one-site-out evaluation, performance fell to near-chance AUC (0.522 for C-PAC and 0.532 for NIAK), whereas an imaging-only reference remained at 0.653 and 0.588, respectively. The high cohort AUC therefore depends on same-site supervision through the evaluated transductive graph under this protocol, whereas it does not translate to unseen-site discrimination.
]]></description>
<dc:creator><![CDATA[ Wan, K., Chen, Z., Liu, G., Yu, B., Zhang, Q., Zhang, F., Zhong, N., Kuai, H. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751719</dc:identifier>
<dc:title><![CDATA[Tracing high transductive cohort AUC to same-site supervision in a site-aware population GNN for multisite fMRI]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751647v1?rss=1">
<title>
<![CDATA[
Spike-history gating of plateau potentials enables closed-loop rewriting of CA1 representations 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751647v1?rss=1
</link>
<description><![CDATA[
Behavioral time scale synaptic plasticity (BTSP) allows hippocampal CA1 neurons to form or shift place fields after a single plasticity-inducing plateau potential, but what determines when individual neurons become eligible for another plasticity event remains unclear. Here we propose that recent somatic spike history provides a cell-specific gate for plateau initiation, making neurons sensitive to rising activity after relative silence while suppressing repeated plasticity during sustained firing. In a two-compartment spiking model of CA1, this gate interacts with entorhinal input to create a feedback loop in which existing representations bias subsequent plateau locations. The resulting dynamics produce gradual place-field drift, reward-associated overrepresentation, recovery of environment-specific representations after remapping, and cross-day reinstatement. Our model further predicts that stronger residual activity biases subsequent plateaus toward previous field locations, a relationship we identify by reanalyzing experimental data. Thus, the expression of neural representations can help determine when and where they are subsequently rewritten.
]]></description>
<dc:creator><![CDATA[ Kurth, A. C., Asabuki, T. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751647</dc:identifier>
<dc:title><![CDATA[Spike-history gating of plateau potentials enables closed-loop rewriting of CA1 representations]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751678v1?rss=1">
<title>
<![CDATA[
Diffusion MRI Tractography Predicts Electrophysiological Connectivity and Explains Spectral Signatures of Evoked Potentials in the Human Brain 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751678v1?rss=1
</link>
<description><![CDATA[
White matter fiber bundles are the structural conduits of information flow in the human brain and thereby mediate the spatial trajectories and timings of the electrophysiological signaling. Here, we combined diffusion magnetic resonance imaging (dMRI) and stereoelectroencephalography (SEEG) recordings in neurosurgical patients to develop an integrated framework for predicting and interpreting causal electrophysiological connectivity patterns between pairs of brain regions. We used repeated single-pulse electrical stimulation in 40 participants implanted with a total of 5794 intracranial electrodes throughout the human brain, encompassing both cortical and multiple thalamic nuclei. A nonlinear, time-frequency manifold learning approach was used to define electrophysiological connectivity, which was then compared with subject-specific and atlas-based structural connectivity. Across 150,000 electrode pairs, we found that the presence of a structural connection predicted causal electrophysiological connectivity with a probability of ~0.95; and its absence predicted the lack of the direct electrophysiological connectivity with a probability of ~0.8. We also show evidence of indirect/polysynaptic pathways supported by both modalities and reported neural features from time-frequency decomposition that distinguished between direct and indirect signaling. We demonstrated that an early phase-locked broadband component (10-70 ms) marked direct structural pathways, whereas delayed and slower components reflected indirect propagation. Notably, we reported that thalamic involvement within an indirect pathway results in increased latency (> 200 ms) and enhanced late oscillatory behavior, despite increased conduction velocity measures along thalamo-cortical pathways. Therefore, our multimodal framework maps human brain connectivity, bridging structural architecture, causal electrophysiological dynamics, and network-level communication.
]]></description>
<dc:creator><![CDATA[ Shailja, S., Lyu, D., Chau Loo Kung, G., Mortazavi, L., Dai, E., Zeineh, M. M., Buch, V. P., Deisseroth, K., Parvizi, J., McNab, J. A. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751678</dc:identifier>
<dc:title><![CDATA[Diffusion MRI Tractography Predicts Electrophysiological Connectivity and Explains Spectral Signatures of Evoked Potentials in the Human Brain]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.15.751731v1?rss=1">
<title>
<![CDATA[
Hunger and sleep recruit distinct brain systems to form spatial memory 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.15.751731v1?rss=1
</link>
<description><![CDATA[
By demonstrating that hunger consolidates spatial memory via a non-hippocampal mechanism that critically involves the retrosplenial cortex, we identify a mode of memory formation that is distinct from well-known hippocampus-dependent memory formation during sleep. Food-deprived rats encoded object locations and, during a subsequent 2-h consolidation phase, either received food and slept (Sleep-Fed) or stayed awake (Wake-Fed), or remained hungry and stayed awake (Wake-Hungry). At later retrieval testing, both Wake-Hungry and Sleep-Fed rats exhibited robust spatial memory, whereas Wake-Fed rats did not. Blocking neuropeptide-Y (NPY) signaling during the consolidation phase abolished hunger-consolidated memory. Unlike sleep-dependent consolidation, hunger-consolidated memory did not require the hippocampus during consolidation or retrieval, and not even during encoding. In contrast, inhibiting retrosplenial cortex during retrieval abolished hunger-consolidated memory but spared memory formed during sleep. Thus, recruitment of brain systems to form spatial memory is tuned to specific brain states, and fundamentally differs between sleep and hunger.
]]></description>
<dc:creator><![CDATA[ Tosadori, E., Bou, J., Dimitrov, S., Ocampo-Garces, A., Valdes, J., Inostroza, M., Born, J., Sawangjit, A. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.15.751731</dc:identifier>
<dc:title><![CDATA[Hunger and sleep recruit distinct brain systems to form spatial memory]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.14.751532v1?rss=1">
<title>
<![CDATA[
Refinement and Retrospective Shift of the CA1 Place Code during Food-Carrying Decisions 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.14.751532v1?rss=1
</link>
<description><![CDATA[
Food carrying is an adaptive component of foraging that integrates resource evaluation with home-directed navigation, providing a naturalistic model for investigating how the brain organizes goal-directed behaviour. Despite extensive work on hippocampal coding during navigation and homing, how CA1 representations are reorganized when animals spontaneously transport acquired food home remains largely unexplored. We recorded dorsal CA1 population activity using one-photon calcium imaging with a V4 Miniscope while mice performed a self-paced foraging task in which food could be consumed at the acquisition site followed by a homeward return or carried to the home for consumption. Mice preferentially carried larger pellets, indicating that transport behaviour was sensitive to resource value. CA1 spatial coding differed systematically across behavioural outcomes. During carry-homeward runs, spatial representations were sparser, conveyed more spatial information, and showed greater trial-to-trial stability than during eat-inward runs, indicating a more precise and reliable place code during home-directed transport. Place fields also shifted forward during carrying, consistent with a retrospective bias toward recently traversed locations. By linking a self-generated food-handling decision to coordinated changes in the precision, stability, and temporal organization of CA1 activity, these findings extend hippocampal spatial-coding frameworks from trained navigation to ecologically grounded foraging behaviour.
]]></description>
<dc:creator><![CDATA[ Rezaei, Z., Whishaw, I. Q., Sutherland, R. J., Chang, H., Mohajerani, M. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.14.751532</dc:identifier>
<dc:title><![CDATA[Refinement and Retrospective Shift of the CA1 Place Code during Food-Carrying Decisions]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.18.752602v1?rss=1">
<title>
<![CDATA[
The Influence of Early Life Stress on the Development of Neural Representations during Mentalizing 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.18.752602v1?rss=1
</link>
<description><![CDATA[
Early life stress (ELS) is associated with altered social cognition, but the neurodevelopmental mechanisms of this association remain understudied. In the present longitudinal study spanning 20-years, eighty-nine young adults performed the Reading the Mind in the Eyes Test (RMET) with a matched control condition during fMRI. Two ELS indices were inspected separately: a prospective cumulative risk score based on caregiver wellbeing during pregnancy and first year of life, and a retrospective self-report of adverse experiences by the participants in late adolescence. Neural outcomes were characterized by univariate activation, representational similarity analysis (RSA), and inter-subject RSA. Inter-subject RSA tested two pairwise approaches to intersubject similarity in ELS: absolute pairwise difference, and pairwise average. Prospective ELS was associated with better RMET performance, and one region survived correction across 360 cortical regions tested in RSA and IS-RSA: left anterior inferior frontal sulcus. The IS-RSA effect was pairwise average: low-exposure participants shared a more typical neural representational geometry, while high-exposure participants demonstrated increasing neural representational idiosyncrasy. Additionally, higher prospective ELS was associated with weaker RMET-versus-control separation within the same region. Retrospective ELS yielded no behavioral nor neural associations. The present study offers novel findings relating to neural representations of mentalizing using the RMET, alongside their neurodevelopmental susceptibility to ELS. The present study additionally highlights implications relating to the differentiation of mentalizing from lexical-semantic and semantic-control demands for future research.
]]></description>
<dc:creator><![CDATA[ Ilomäki, M., Lindblom, J., Flykt, M., Vänskä, M., Wikman, P. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.18.752602</dc:identifier>
<dc:title><![CDATA[The Influence of Early Life Stress on the Development of Neural Representations during Mentalizing]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.14.748905v1?rss=1">
<title>
<![CDATA[
Confidence Read from Others Movements Guides Collective Decisions 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.14.748905v1?rss=1
</link>
<description><![CDATA[
A central challenge in decision-making is deciding when to trust ones own judgement and when to rely on others. Because subjective confidence correlates with objective accuracy, a sensible strategy is to follow the choice made with higher confidence. Crucially, however, this strategy depends on accessing others confidence. Here, we show that humans spontaneously  read out confidence from others movements and use this information to guide collective decisions. Dyads performed a collective perceptual decision-making task. In each trial, one participant--the arbitrator--first made an individual decision by reaching toward one of two targets, then observed their partner doing the same, and finally made the collective decision on behalf of the dyad, confirming or revising their initial choice. When own confidence was low or high, arbitrators relied on simple heuristics--revising their choice when uncertain and confirming it when certain. At intermediate confidence levels, however, they extracted confidence from their partner's movement kinematics to guide revision. Computational simulations demonstrated that integrating the partners encoded confidence improved collective accuracy. Our findings highlight the importance of bodily motion for the social transmission of confidence information in collective decision-making.
]]></description>
<dc:creator><![CDATA[ Schmitz, L., Montobbio, N., Memeo, M., Sabri, O., Bahrami, B., Cavallo, A., Panzeri, S., Becchio, C. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.14.748905</dc:identifier>
<dc:title><![CDATA[Confidence Read from Others Movements Guides Collective Decisions]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.09.16.752084v1?rss=1">
<title>
<![CDATA[
A discrete Connexin26+ neural crest lineage emerges in mid-life and mediates enhanced central brainstem responses to elevated CO2 levels for deep breathing. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.09.16.752084v1?rss=1
</link>
<description><![CDATA[
The precise control of breathing is fundamental to vertebrate survival. Increased PCO2 in blood and brain parenchyma causes an increase in both the frequency and volume of lung ventilation. We have previously demonstrated that CO2 directly binds to connexin26 (Cx26) hemichannels causing them to open and allow release ATP. We now document the role of Cx26 as a direct physiological CO2 sensor in vivo. Here we describe a unique Cx26+ neural crest cell lineage that populates the ventral brainstem in the vicinity of the PreBoetz nucleus/caudal CO2 chemosensory area during middle age and dies again in old age. Ablating Cx26 genetically specifically within this population of about 20 cells by two independent neural crest Cre-driver lines leads to a loss of local ATP release in the posterior chemosensory area as well as a 40% reduction in elevated tidal volume responses specifically in middle age, as measured by whole-body plethysmography. These in vivo effects change over a life-time: they directly mirror the arrival, wiring in middle age and later death of this cell population in old age. This is a first known example of a middle age change in cranial neural crest lineage composition and highlights the significant power of very few cells for global metabolism. Such lineage-dependent middle-age dynamics also impacts upon the evolution of eusociality: altricial naked pups of our common amniote/synapsid ancestors were heated by by the breath of their (middle-aged) carers, sensing elevated CO2 levels in hypercapnic burrows. Such mechanistic exaptation enabled small amniotes to sense and survive the lethal global CO2 spikes during the Permo-Triassic and other extinction events.
]]></description>
<dc:creator><![CDATA[ Zhang, X., Zhang, J., Lapage, J. M. J., Gourine, A. V., Dale, N., Koentges, G. ]]></dc:creator>
<dc:date>2026-09-21</dc:date>
<dc:identifier>doi:10.64898/2026.09.16.752084</dc:identifier>
<dc:title><![CDATA[A discrete Connexin26+ neural crest lineage emerges in mid-life and mediates enhanced central brainstem responses to elevated CO2 levels for deep breathing.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-09-21</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
