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Rxivist combines preprints from bioRxiv with data from Twitter to help you find the papers being discussed in your field. Currently indexing 83,641 bioRxiv papers from 360,338 authors.

Most downloaded bioRxiv papers, all time

in category neuroscience

14,595 results found. For more information, click each entry to expand.

10481: Constitutive ghrelin receptor activity modulates AMPA receptor traffic and supports memory formation
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Posted to bioRxiv 05 Feb 2020

Constitutive ghrelin receptor activity modulates AMPA receptor traffic and supports memory formation
237 downloads neuroscience

Luís F. Ribeiro, Tatiana Catarino, Mário Carvalho, Sandra D. Santos, Luísa Cortes, Patricio O. Opazo, Lyn Rosenbrier Ribeiro, Daniel Choquet, José A. Esteban, João Peça, Ana Luísa Carvalho

The ability of animals to store and retrieve food caches in the wild requires the integration of biological signals of hunger, satiety and memory. The role of ghrelin in regulating feeding and memory makes ghrelin receptors an important target to shape the required cellular and molecular responses. We investigated the effects of the high ligand-independent activity of the ghrelin receptor on the physiology of excitatory synapses. Blocking this type of activity produced a decrease in the synaptic content of AMPA receptors in hippocampal neurons and a reduction in GluA1 phosphorylation at Ser845. Impaired constitutive activity from the ghrelin receptor increased surface diffusion of AMPA receptors and impaired AMPA receptor synaptic delivery mediated by chemical long-term potentiation. These observations support a role for the constitutive activity of the ghrelin receptor in regulating AMPA receptor trafficking under basal conditions and synaptic plasticity. Accordingly, we found that blocking the ghrelin receptor constitutive activity impairs spatial and recognition memory.

10482: Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice
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Posted to bioRxiv 21 Nov 2018

Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice
237 downloads neuroscience

Anna S. Warden, Moatasem M. Azzam, Adriana DaCosta, Sonia Mason, Yuri A. Blednov, Robert O. Messing, R. Dayne Mayfield, R. Adron Harris

Many genes differentially expressed in brain tissue from human alcoholics and animals that have consumed large amounts of alcohol are components of the innate immune toll-like receptor (TLR) pathway. TLRs initiate inflammatory responses via two branches: (1) MyD88-dependent or (2) TRIF-dependent. All TLRs signal through MyD88 except TLR3. Prior work demonstrated a direct role for MyD88-dependent signaling in regulation of alcohol consumption. However, the role of TLR3 as a potential regulator of excessive alcohol drinking has not previously been investigated. To test the possibility TLR3 activation regulates alcohol consumption, we injected mice with the TLR3 agonist polyinosinic:polycytidylic acid (poly(I:C)) and tested alcohol consumption in an every-other-day two-bottle choice test. Poly(I:C) produced a persistent increase in alcohol intake that developed over several days. Repeated poly(I:C) and ethanol exposure altered innate immune transcript abundance; increased levels of TRIF-dependent pathway components correlated with increased alcohol consumption. Administration of poly(I:C) before exposure to alcohol did not alter alcohol intake, suggesting that poly(I:C) and ethanol must be present together to change drinking behavior. To determine which branch of TLR signaling mediates poly(I:C)-induced changes in drinking behavior, we tested either mice lacking MyD88 or mice administered a TLR3/dsRNA complex inhibitor. MyD88 null mutants showed poly(I:C)-induced increases in alcohol intake. In contrast, mice pretreated with a TLR3/dsRNA complex inhibitor reduced their alcohol intake, suggesting poly(I:C)-induced escalations in alcohol intake function are, at least partially, dependent on TLR3. Together, these results strongly suggest that TLR3-dependent signaling drives excessive alcohol drinking behavior.

10483: Changes in alpha activity reveal that social opinion modulates attention allocation during face processing
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Posted to bioRxiv 21 Sep 2017

Changes in alpha activity reveal that social opinion modulates attention allocation during face processing
237 downloads neuroscience

Evelien Heyselaar, Ali Mazaheri, Peter Hagoort, Katrien Segaert

Participants' performance differs when conducting a task in the presence of a secondary individual, moreover the opinion the participant has of this individual also plays a role. Using EEG, we investigated how previous interactions with, and evaluations of, an avatar in virtual reality subsequently influenced attentional allocation to the face of that avatar. We focused on changes in the alpha activity as an index of attentional allocation. We found that the onset of an avatar's face whom the participant had developed a rapport with induced greater alpha suppression. This suggests greater attentional resources allocated to the interacted-with avatars. The evaluative ratings of the avatar induced a U-shaped change in alpha suppression, such that participants paid most attention when the avatar was rated as average. These results suggest that attentional allocation is thus an important element of how behaviour is altered in the presence of a secondary individual.

10484: Neurofeedback linked suppression of subthalamic beta oscillations speeds up movement initialisation in Parkinsonian Patients
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Posted to bioRxiv 01 Jul 2019

Neurofeedback linked suppression of subthalamic beta oscillations speeds up movement initialisation in Parkinsonian Patients
236 downloads neuroscience

Shenghong He, Abteen Mostofi, Emilie Syed, Flavie Torrecillos, Gerd Tinkhauser, Petra Fischer, Alek Pogsyan, Harutomo Hasegawa, Yuanqing Li, Keyoumars Ashkan, Erlick Pereira, Huiling Tan

Enhanced beta oscillations (13-30 Hz) in the subthalamic nucleus (STN) have been associated with clinical impairment in Parkinson’s disease (PD), such as rigidity and slowing of movement, with the suppression of STN beta activity through medication or deep brain stimulation correlating with improvement in these symptoms. Recent studies have also emphasized the importance of the time dynamics of the STN beta oscillations in the pathology of PD. An increased probability of prolonged beta bursts, defined as periods when beta band power exceeds a certain threshold, was more closely related to motor symptoms than average power; and the occurrence of beta bursts just before a go cue slows cued movements. Here we adopted a sequential neurofeedback-behaviour task paradigm to investigate whether patients with PD can learn to suppress pathological beta oscillations recorded from STN with neurofeedback training and whether the training improves the motor performance. Results from twelve patients showed that, compared with the control condition, the neurofeedback training led to reduced incidence and duration of beta bursts in the STN local field potential (LFP) and also reduced the synchrony between the STN LFP and cortical activities measured through EEG in the beta frequency band. The changes were accompanied by a reduced reaction time in cued movements. These results suggest that volitional suppression of beta bursts facilitated by neurofeedback training could help improve movement initialisation in Parkinson’s disease. Significance Statement Our study suggests that a neurofeedback paradigm which focuses on the time dynamics of the target neural signal can facilitate volitional suppression of pathological beta oscillations in the STN in Parkinson’s disease. Neurofeedback training was accompanied by reduced reaction time in cued movements, but associated with increased tremor in tremulous patients. The results strengthen the link between subthalamic beta oscillations and motor impairment, and also suggest that different symptom-specific neural signals could be targeted to improve neuromodulation strategies, either through brain stimulation or neurofeedback training, for patients with tremor and bradykinesia-rigidity.

10485: Dynamics of visual contextual interactions is altered in Parkinson's disease
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Posted to bioRxiv 14 Feb 2019

Dynamics of visual contextual interactions is altered in Parkinson's disease
236 downloads neuroscience

M. Isabel Vanegas, Annabelle Blangero, James E Galvin, Alessandro Di Rocco, Angelo Quartarone, M Felice Ghilardi, Simon P. Kelly

Over the last decades, psychophysical and electrophysiological studies in patients and animal models of Parkinson's disease (PD), have consistently revealed a number of visual abnormalities. In particular, specific alterations of contrast sensitivity curves, electroretinogram (ERG), and visual evoked potentials (VEP), have been attributed to dopaminergic retinal depletion. However, fundamental mechanisms of cortical visual processing, such as normalization or "gain-control" computations, have not yet been examined in PD patients. Here we measured electrophysiological indices of gain control in both space (surround suppression) and time (sensory adaptation) in PD patients based on steady-state VEP (ssVEP). Compared to controls, patients exhibited a significantly higher initial ssVEP amplitude that quickly decayed over time, and greater relative suppression of ssVEP amplitude as a function of surrounding stimulus contrast. Meanwhile, EEG frequency spectra were broadly elevated in patients relative to controls. Thus, contrary to what might be expected given the reduced contrast sensitivity often reported in PD, visual neural responses are not weaker; rather, they are initially larger but undergo an exaggerated degree of spatial and temporal gain control and are embedded within a greater background noise level. We conclude that compensatory cortical mechanisms may play a role in determining dysfunctional center-surround interactions at the retinal level.

10486: Macromolecular and electrical coupling between inner hair cells in the rodent cochlea
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Posted to bioRxiv 17 Dec 2019

Macromolecular and electrical coupling between inner hair cells in the rodent cochlea
236 downloads neuroscience

Philippe Jean, Tommi Anttonen, Susann Michanski, Antonio Miguel Garcia de Diego, Anna Maria Steyer, Andreas Neef, David Oestreicher, Jana Kroll, Christos Nardis, Tina Pangrsic, Wiebke Moebius, Jonathan Ashmore, Carolin Wichmann, Tobias Moser

Inner hair cells (IHCs) are the primary receptors for hearing. They are housed in the cochlea and convey sound information to the brain via synapses with the auditory nerve. IHCs have been thought to be electrically and metabolically independent from each other. We report that, upon developmental maturation, 30% of the IHCs are electrochemically coupled in mini-syncytia. This coupling permits transfer of fluorescently-labeled metabolites and macromolecular tracers. The membrane capacitance, Ca2+-current, and resting current increase with the number of dyecoupled IHCs. Dual voltage clamp experiments substantiate low resistance electrical coupling. Pharmacology and tracer permeability rule out coupling by gap junctions and purinoceptors. 3Delectron-microscopy indicates instead that IHCs are coupled by membrane fusion sites. Consequently, depolarization of one IHC triggers presynaptic Ca2+-influx at active zones in the entire mini-syncytium. Based on our findings and modeling, we propose that IHC-mini-syncytia enhance sensitivity and reliability of cochlear sound encoding. ### Competing Interest Statement The authors have declared no competing interest.

10487: Ultra-widefield fluorescein angiography findings in patients with multiple retinal holes.
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Posted to bioRxiv 14 Mar 2019

Ultra-widefield fluorescein angiography findings in patients with multiple retinal holes.
236 downloads neuroscience

Jiwon Baek, Byungju Jung, Hyunggu Kwon, Sohee Jeon

Purpose: To evaluate the ultra-widefield fluorescein angiography (UWFA) findings in patients with multiple retinal holes. Methods: Seventy-five eyes, each with more than two retinal holes, underwent a comprehensive ophthalmologic examination, including UWFA, along with 77 age-matched control eyes with no retinal holes. The UWFA was scored according to a system suggested by the Angiography Scoring for Uveitis Working Group (ASUWG). UWFA findings from the patients with retinal holes were compared with those of the control group without retinal holes. Factors associated with a high ASUWG score were also evaluated. Results: Patients with multiple retinal holes showed a significantly higher prevalence of retinal vascular staining/leakage, capillary leakage at the posterior pole, and capillary leakage at the periphery when compared to the control group (p<0.001, for each of them). Univariate analysis revealed that logMAR BCVA (r=0.271, p=0.027), spherical equivalent (r= -0.275, p=0.021), and number of retinal holes (r=0.271, p=0.027) were associated with a higher ASUWG score. After adjustments for age, gender, and logMAR BCVA, multivariate regression analysis revealed that the spherical equivalent was independently associated with a higher ASUWG score (r2=0.161, p=0.001). Conclusions: Patients with multiple retinal holes showed profound peripheral vascular leakages on UWFA findings, suggesting the presence of chronic retinal traction induced by equatorial scleral elongation.

10488: Cation-chloride cotransporters and the polarity of GABA signaling in mouse hippocampal parvalbumin interneurons
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Posted to bioRxiv 30 Oct 2019

Cation-chloride cotransporters and the polarity of GABA signaling in mouse hippocampal parvalbumin interneurons
236 downloads neuroscience

Yo Otsu, Florian Donneger, Eric J Schwartz, Jean Christophe Poncer

Transmembrane chloride gradients govern the efficacy and polarity of GABA signaling in neurons and are usually maintained by the activity of cation chloride cotransporters, such as KCC2 and NKCC1. Whereas their role is well established in cortical principal neurons, it remains poorly documented in GABAergic interneurons. We used complementary electrophysiological approaches to compare the effects of GABAAR activation in adult mouse hippocampal parvalbumin interneurons (PV INs) and pyramidal cells (PCs). Loose cell attached, tight-seal and gramicidin-perforated patch recordings all show GABAAR-mediated transmission is slightly depolarizing and yet inhibitory in both PV INs and PCs. Focal GABA uncaging in whole-cell recordings reveal that KCC2 and NKCC1 are functional in both PV INs and PCs but differentially contribute to transmembrane chloride gradients in their soma and dendrites. Blocking KCC2 function depolarizes the reversal potential of GABAAR-mediated currents in PV INs and PCs, often beyond firing threshold, showing KCC2 is essential to maintain the inhibitory effect of GABAARs. Finally, we show that repetitive 10 Hz activation of GABAARs in both PV INs and PCs leads to a progressive decline of the postsynaptic response independently of the ion flux direction or KCC2 function. This suggests intraneuronal chloride buildup may not predominantly contribute to activity-dependent plasticity of GABAergic synapses in this frequency range. Altogether our data demonstrate similar mechanisms of chloride regulation in mouse hippocampal PV INs and PCs and suggest KCC2 downregulation in the pathology may affect the valence of GABA signaling in both cell types.

10489: A Model for Navigation in Unknown Environments Based on a Reservoir of Hippocampal Sequences
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Posted to bioRxiv 19 Dec 2019

A Model for Navigation in Unknown Environments Based on a Reservoir of Hippocampal Sequences
236 downloads neuroscience

Christian Leibold

Hippocampal place cell populations are activated in sequences on multiple time scales during active behavior, resting and sleep states, suggesting that these sequences are the genuine dynamical motifs of the hippocampal circuit. Recently, prewired hippocampal place cell sequences have even been reported to correlate to future behaviors, but so far there is no explanation of what could be the computational benefits of such a mapping between intrinsic dynamical structure and external sensory inputs. Here, I propose a computational model in which a set of predefined internal sequences is used as a dynamical reservoir to construct a spatial map of a large unknown maze based on only a small number of salient landmarks. The model is based on a new variant of temporal difference learning and implements a simultaneous localization and mapping algorithm. As a result sequences during intermittent replay periods can be decoded as spatial trajectories and improve navigation performance, which supports the functional interpretation of replay to consolidate memories of motor actions.

10490: Neuronal population correlates of target selection and distractor filtering
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Posted to bioRxiv 20 Sep 2018

Neuronal population correlates of target selection and distractor filtering
236 downloads neuroscience

E. Astrand, Claire Wardak, Suliann Ben Hamed

Frontal Eye Field (FEF) single-cell neuronal activity discriminates between relevant and irrelevant visual stimuli and its magnitude has been shown to predict conscious perception. How this is reflected at the population level in terms of spatial codes is unknown. We recorded neuronal population activity in the FEF while monkeys were performing a forced choice cued detection task with identical target and distractor stimuli. Using machine learning techniques, we quantified information about the spatial estimate of targets and distracters in the FEF population activity and we analyzed how these relate to the report of perception. We found that the FEF population activity provides a precise estimate of the spatial location of perception. This estimate does not necessarily match the actual physical world. Importantly, the closer this prefrontal population estimate is to the veridical spatial information, the higher the probability that the stimulus was reported as perceived. This was observed both when the reported stimulus was a target (i.e. correct detection trials) or a distractor (i.e. false alarm trials). Overall, we thus show that how and what we perceive of our environments depends on the precision with which this environment is coded by prefrontal neuronal populations.

10491: Chronic stress exacerbates acute stress-induced neuronal activation in the anterior cingulate cortex and ventral hippocampus that correlates with behavioral deficits in mice
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Posted to bioRxiv 20 Feb 2020

Chronic stress exacerbates acute stress-induced neuronal activation in the anterior cingulate cortex and ventral hippocampus that correlates with behavioral deficits in mice
236 downloads neuroscience

Corey Fee, Thomas Prevot, Keith Misquitta, Mounira Banasr, Etienne Sibille

Altered activity of corticolimbic brain regions is a hallmark of stress-related illnesses, including mood disorders, neurodegenerative diseases, and substance abuse disorders. Acute stress adaptively recruits brain region-specific functions for coping, while sustained activation under chronic stress may overwhelm feedback mechanisms and lead to pathological cellular and behavioral responses. The neural mechanisms underlying dysregulated stress response and how they contribute to behavioral deficits are poorly characterized. Here, we tested whether prior exposure to chronic restraint stress (CRS) or unpredictable chronic mild stress (UCMS) in mice could alter neuronal response to acute stress and whether these changes are associated with chronic stress-induced behavioral deficits. More specifically, we assessed neuronal activation indexed by c-Fos+ cell counts in 24 stress- and mood-related brain regions, and determined if changes in acute stress-induced neuronal activation were linked to chronic stress-induced behavioral impairments. Results indicated that CRS and UCMS led to convergent physiological and anxiety-like deficits, whereas cognition was impaired only in UCMS mice. CRS and UCMS exposure exacerbated neuronal activation in response to an acute stressor in anterior cingulate cortex (ACC) area 24b and ventral hippocampal (vHPC) CA1, CA3, and subiculum. In dysregulated brain regions, levels of neuronal activation were positively correlated with principal components capturing variance across widespread behavioral alterations relevant to stress-related disorders. Our data supports an association between a dysregulated stress response, altered corticolimbic excitation/inhibition balance, and the expression of maladaptive behaviors.

10492: The time course of recognition memory impairment and glial pathology in the hAPP-J20 mouse model of Alzheimer's disease.
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Posted to bioRxiv 13 Dec 2018

The time course of recognition memory impairment and glial pathology in the hAPP-J20 mouse model of Alzheimer's disease.
236 downloads neuroscience

Kamar E. Ameen-Ali, Julie E Simpson, Stephen B Wharton, Paul R Heath, Paul Sharp, Gaia Brezzo, Jason Berwick

The role of cellular changes in the neurovascular unit is increasingly being investigated to understand the pathogenesis of Alzheimers disease. The aim of the current study was to determine the time course of recognition memory impairment in the J20 mouse model of AD, in relation to neuroinflammatory responses and the pathology of Aβ. Male hAPP-J20 and wild-type mice were assessed at 3, 6, 9, and 12 months of age. The spontaneous object recognition (SOR) task provided a measure of memory, with assessment of both a short delay (1 min) and a long delay (4 hrs). Immunohistochemistry was used to characterise Aβ-deposition, and quantify astrocyte and microglial responses. At all ages tested J20 mice had impaired long-term, but preserved short-term, recognition memory. Wild-types demonstrated preserved long-term memory up to 9 months of age, and preserved short-term memory at all ages tested. Plaque pathology in the J20 mice was present from 6 months onwards, with co-localisation of reactive microglia and activated astrocytes. Reactive microglia and astrocyte activation in the hippocampus were significantly greater in the J20 mice at 9 months, compared to wild-types. This study contributes to our understanding of the pathological and cognitive mechanisms at play in AD. J20 mice showed impairment in retaining information over longer periods from an early age, preceding the deposition of Aβ and glial activation. Defining early physiological changes in relation to cognitive decline could provide insight into new therapeutic targets early in the disease process, when intervention is most likely to effectively slow disease progression.

10493: A novel virtual plus-maze for studying electrophysiological correlates of spatial reorientation
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Posted to bioRxiv 13 Jul 2018

A novel virtual plus-maze for studying electrophysiological correlates of spatial reorientation
236 downloads neuroscience

Ágoston Török, Andrea Kóbor, Ferenc Honbolygó, Travis Baker

Quick reorientation is an essential part of successful navigation. Despite growing attention to this ability, little is known about how reorientation happens in humans. To this aim, we recorded EEG from 34 participants. Participants were navigating a simple virtual reality plus-maze where at the beginning of each trial they were randomly teleported to either the North or the South alley. Results show that the teleportation event caused a quick reorientation effect over occipito-parietal areas as early as 100 msec; meaning that despite the known stochastic nature of the teleportation, participants built up expectations for their place of arrival. This result has important consequences for the optimal design of virtual reality locomotion.

10494: Genes critical for development and differentiation of dopaminergic neurons are downregulated in Parkinson’s disease
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Posted to bioRxiv 24 Mar 2020

Genes critical for development and differentiation of dopaminergic neurons are downregulated in Parkinson’s disease
236 downloads neuroscience

Aditi Verma, Etienne C. Hirsch, Vijayalakshmi Ravindranath

We performed transcriptome analysis using RNAseq on substantia nigra pars compacta (SNpc) from mice after acute and chronic MPTP treatment and Parkinson’s disease (PD) patients. Acute and chronic exposure to MPTP resulted in decreased expression of genes involved in sodium channel regulation. However, upregulation of pro-inflammatory pathways was seen after single dose but not after chronic MPTP treatment. Dopamine biosynthesis and synaptic vesicle recycling pathways were downregulated in PD patients and only after chronic MPTP treatment in mice. Genes essential for midbrain development and determination of dopaminergic phenotype such as, LMX1B, FOXA1, RSPO2, KLHL1, EBF3, PITX3, RGS4, ALDH1A1, RET, FOXA2, EN1, DLK1, GFRA1, LMX1A, NR4A2, GAP43, SNCA, PBX1 and GRB10 were downregulated in human PD and overexpression of LMX1B rescued MPP+ induced death in SH-SY5Y neurons. Downregulation of ensemble of genes involved in development and differentiation of dopaminergic neurons indicate their critical involvement in pathogenesis and progression of human PD. ### Competing Interest Statement The authors have declared no competing interest.

10495: Altered brain morphology in boys with attention-deficit/hyperactivity disorder with and without comorbid conduct disorder/oppositional defiant disorder
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Posted to bioRxiv 22 Feb 2019

Altered brain morphology in boys with attention-deficit/hyperactivity disorder with and without comorbid conduct disorder/oppositional defiant disorder
236 downloads neuroscience

Nora C. Vetter, Lea L. Backhausen, Judith Buse, Veit Roessner, Michael N. Smolka

About 50% of ADHD patients suffer from comorbidity with oppositional defiant disorder/conduct disorder (ODD/CD). Most previous studies on structural morphology did not differentiate between pure ADHD (ADHD-only) and ADHD with comorbid ODD/CD (ADHD+ODD/CD) and only focused on specific measures (e.g. volumetric differences), leading to inconsistent results. Therefore, we aimed to investigate the structural profile of ADHD-only versus ADHD+ODD/CD spanning different indices, i.e. subcortical and cortical volume, cortical thickness, and surface area. We aimed to disentangle disorder-specific etiological contributions regarding structural brain alterations and expected similar and differential alterations between the patient groups. We acquired structural images from an adolescent sample range (11 to 17 years) matched with regard to age, pubertal status, and IQ - including 36 boys with ADHD-only, 26 boys with ADHD+ODD/CD, and 30 typically developing boys (TD). We analyzed subcortical and cortical volume, cortical thickness, and surface area with FreeSurfer. We found reductions in total gray matter and right cerebellar volume as well as total surface area for both patient groups. For the left cerebellar volume ADHD+ODD/CD, but not ADHD only differed from TD. Boys with ADHD+ODD/CD had a thicker cortex than the other groups in a right rostral middle frontal cluster, which was related to stronger ODD/CD symptoms, even when controlling for ADHD symptoms. No group differences in local cortical volume or surface area emerged. Overall, we found similarities but also differences in brain morphology between the two related disorders. Patients with a double burden seem to be even more affected than patients with pure ADHD.

10496: Apparent Motion Perception in the Praying Mantis: Psychophysics and Modelling
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Posted to bioRxiv 11 May 2018

Apparent Motion Perception in the Praying Mantis: Psychophysics and Modelling
236 downloads neuroscience

Ghaith Tarawneh, Lisa Jones, Vivek Nityananda, Ronny Rosner, Claire Rind, Jenny Read

Apparent motion is the perception of a motion created by rapidly presenting still frames in which objects are displaced in space. Observers can reliably discriminate the direction of apparent motion when inter-frame object displacement is below a certain limit, Dmax. Earlier studies of motion perception in humans found that Dmax scales with spatial element size, interpreting the relationship between the two as linear, and that Dmax appears to be lower-bounded at around 15 arcmin. Here, we run corresponding experiments in the praying mantis Sphodromantis lineola to investigate how Dmax scales with element size. We used moving random chequerboard patterns of varying element and displacement step sizes to elicit the optomotor response, a postural stabilization mechanism that causes mantids to lean in the direction of largefield motion. Subsequently, we calculated Dmax as the displacement step size corresponding to a 50% probability of detecting an optomotor response in the same direction as the stimulus. Our main findings are that mantis Dmax appears to scale as a power-law of element size and that, in contrast to humans, it does not appear to be lower-bounded. We present two models to explain these observations: a simple highlevel model based on motion energy in the Fourier domain and a more detailed one based on the Reichardt Detector. The models present complementary intuitive and physiologically-realistic accounts of how Dmax scales with element size in insects.

10497: Allele-Specific Expression and High-Throughput Reporter Assay Reveal Functional Variants in Human Brains with Alcohol Use Disorders
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Posted to bioRxiv 09 Jan 2019

Allele-Specific Expression and High-Throughput Reporter Assay Reveal Functional Variants in Human Brains with Alcohol Use Disorders
236 downloads neuroscience

Xi Rao, Kriti S Thapa, Andy B Chen, Hai Lin, Hongyu Gao, Jill L Reiter, Katherine A Hargreaves, Joseph Ipe, Dongbing Lai, Xiaoling Xuei, Hongmei Gu, Manav Kapoor, Sean P Farris, Jay Tischfield, Tatiana Foroud, Alison Goate, Todd C Skaar, R. Dayne Mayfield, Howard J Edenberg, Yunlong Liu

Transcriptome studies can identify genes whose expression differs between alcoholics and controls. To test which variants associated with alcohol use disorder (AUDs) may cause expression differences, we integrated deep RNA-seq and GWAS data from four postmortem brain regions of 30 AUDs subjects and 30 controls (social/non-drinkers) and analyzed allele-specific expression (ASE). We identified 90 genes with differential ASE in subjects with AUDs compared to controls. Of these, 61 genes contained 437 single nucleotide polymorphisms (SNPs) in the 3' untranslated regions (3'UTR) with at least one heterozygote among the subjects studied. Using a modified PASSPORT-seq (parallel assessment of polymorphisms in miRNA target-sites by sequencing) assay, we identified 25 SNPs that showed affected RNA levels in a consistent manner in two neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2). Many of these are in binding sites of miRNAs and RNA binding proteins, indicating that these SNPs are likely causal variants of AUD-associated differential ASE.

10498: Breathlessness And The Body: Neuroimaging Evidence For The Inferential Leap
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Posted to bioRxiv 24 Mar 2017

Breathlessness And The Body: Neuroimaging Evidence For The Inferential Leap
236 downloads neuroscience

Olivia K. Faull, Anja Hayen, Kyle T. S. Pattinson

Breathlessness debilitates millions of people with chronic illness. Mismatch between breathlessness severity and objective disease markers is common and poorly understood. Traditionally, sensory perception was conceptualised as a stimulus-response relationship, although this cannot explain how conditioned symptoms may occur in the absence of physiological signals from the lungs or airways. A Bayesian model is now proposed in which the brain generates sensations based on expectations learned from past experiences (priors), which are then checked against incoming afferent signals. In this model, psychological factors may act as moderators. They may either alter priors, or change the relative attention towards incoming sensory information, leading to more variable interpretation of an equivalent afferent input. In the present study we conducted a preliminary test of this model in a supplementary analysis of previously published data (Hayen 2017). We hypothesised that individual differences in psychological traits (anxiety, depression, anxiety sensitivity) would correlate with the variability of subjective evaluation of equivalent breathlessness challenges. To better understand the resulting inferential leap in the brain, we explored whether these behavioural measures correlated with activity in areas governing either prior generation or sensory afferent input. Behaviorally, anxiety sensitivity was found to positively correlate with each subject's variability of intensity and unpleasantness during mild breathlessness, and with unpleasantness during strong breathlessness. In the brain, anxiety sensitivity was found to positively correlate with activity in the anterior insula during mild breathlessness, and negatively correlate with parietal sensorimotor areas during strong breathlessness. Our findings suggest that anxiety sensitivity may reduce the robustness of this Bayesian sensory perception system, increasing the variability of breathlessness perception and possibly susceptibility to symptom misinterpretation. These preliminary findings in healthy individuals demonstrate how differences in psychological function influence the way we experience bodily sensations, which might direct us towards better understanding of symptom mismatch in clinical populations.

10499: The influence of kinesthetic motor imagery and effector specificity on the long-latency stretch response
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Posted to bioRxiv 02 Jan 2019

The influence of kinesthetic motor imagery and effector specificity on the long-latency stretch response
236 downloads neuroscience

Christopher J. Forgaard, Ian M. Franks, Dana Maslovat, Romeo Chua

The long-latency reflexive response (LLR) following an upper-limb mechanical disturbance is generated by neural circuitry shared with voluntary control. This feedback response supports many task-dependent behaviours and permits the expression of goal-directed corrections at latencies shorter than voluntary reaction time. An extensive body of literature has demonstrated that the LLR shows flexibility akin to voluntary control, but it has never been tested whether instruction-dependent LLR changes can also occur in the absence of an overt voluntary response. The present study used kinesthetic motor imagery (Experiment 1) and instructed participants to execute a voluntary response in a non-stretched contralateral muscle (Experiment 2) to explore the relationship between the overt production of a voluntary response and LLR facilitation. Activity in stretched right wrist flexors were compared to standard not-intervene and compensate conditions. Our findings revealed that on ~40% of imagery and ~50% of contralateral trials, a partial voluntary response leaked-out into the stretched right wrist flexor muscle. On these leaked trials, the early portion of the LLR (R2) was facilitated and displayed a similar increase to compensate trials. The latter half of the LLR (R3) showed further modulation, mirroring the patterns of voluntary response activity. By contrast, the LLR on non-leaked imagery and contralateral trials did not modulate. We suggest that even though a hastened voluntary response cannot account for all instruction-dependent LLR modulation, the overt execution of a voluntary response in the same muscle(s) as the LLR is a pre-requisite for facilitation of this rapid feedback response.

10500: Asymmetry of an intracellular scaffold at vertebrate electrical synapses
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Posted to bioRxiv 09 Aug 2017

Asymmetry of an intracellular scaffold at vertebrate electrical synapses
236 downloads neuroscience

Audrey J. Marsh, Jennifer Carlisle Michel, Anisha P. Adke, Emily L. Heckman, Adam C. Miller

Neuronal synaptic connections are electrical or chemical and together are essential to dynamically defining neural circuit function. While chemical synapses are well known for their biochemical complexity, electrical synapses are often viewed as comprised solely of neuronal gap junction channels that allow direct ionic and metabolic communication. However, associated with the gap junction channels are structures observed by electron microscopy called the Electrical Synapse Density (ESD). The ESD has been suggested to be critical for the formation and function of the electrical synapse, yet the biochemical makeup of these structures is poorly understood. Here we find that electrical synapse formation in vivo requires an intracellular scaffold called Tight Junction Protein 1b (Tjp1b). Tjp1b is localized to electrical synapses where it is required for the stabilization of the gap junction channels and for electrical synapse function. Strikingly, we find that Tjp1b protein localizes and functions asymmetrically, exclusively on the postsynaptic side of the synapse. Our findings support a novel model in which there is molecular asymmetry at the level of the intracellular scaffold that is required for building the electrical synapse. ESD molecular asymmetries may be a fundamental motif of all nervous systems and could support functional asymmetry at the electrical synapse.

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