30472 research outputs found
Sort by
Predictions and errors are distinctly represented across V1 layers
Popular accounts of mind and brain propose that the brain continuously forms predictions about future sensory inputs and combines predictions with inputs to determine what we perceive.1–6 Under ‘‘predictive processing’’ schemes, such integration is supported by the hierarchical organization of the cortex, whereby feedback connections communicate predictions from higher-level deep layers to agranular (superficial and deep) lower-level layers.7–10 Predictions are compared with input to compute the ‘‘prediction error,’’ which is transmitted up the hierarchy from superficial layers of lower cortical regions to the middle layers of higher areas, to update higher-level predictions until errors are reconciled.11–15 In the primary visual cortex
(V1), predictions have thereby been proposed to influence representations in deep layers while error signals may be computed in superficial layers. Despite the framework’s popularity, there is little evidence for these functional distinctions because, to our knowledge, unexpected sensory events have not previously been presented in human laminar paradigms to contrast against expected events. To this end, this 7T fMRI study contrasted V1 responses to expected (75% likely) and unexpected (25%) Gabor orientations. Multivariate decoding analyses revealed an interaction between expectation and layer, such that expected events could be decoded with comparable accuracy across layers, while unexpected events could only be decoded in superficial laminae. Although these results are in line with these accounts that have been popular for decades, such distinctions have not previously been demonstrated in humans. We discuss how both prediction and error processes may operate together to shape our unitary perceptual experiences
Can neurofeedback training decrease cognitive bias? An exploratory analysis
Cognitive biases are ubiquitous and finding ways to mitigate them has been an ongoing challenge. Here, we explore the possibility that brain training or neurofeedback could alter a particular bias that presents itself in a card selection task. Specifically, we address the win-stay/lose-shift strategy in the Iowa Gam-bling Task. Data was analyzed from a large neurofeedback study in which par-ticipants were trained to enhance the spectral power in the theta band (4-8Hz) over 10 sessions. An active control group was included whose members were trained to enhance their sensorimotor rhythm (12-15Hz). We show that theta power did increase over the sessions and that strategy use was modulated as a consequence. However, the impact was on the P(shift|loss), but not on P(stay|win) or P(WSLS). This was independent of the training group. The results are discussed in terms of different temporal scales associated with neural modu-lation of P(shift|loss) and P(stay|win). Suggestions for further research are pro-vided in light of challenges during the running of the study
Improving cell type identification with Gaussian noise-augmented single-cell RNA-seq contrastive learning
Cell type identification is an important task for single-cell RNA-sequencing (scRNA-seq) data analysis. Many prediction methods have recently been proposed, but the predictive accuracy of difficult cell type identification tasks is still low. In this work, we proposed a novel Gaussian noise augmentation-based scRNA-seq contrastive learning method (GsRCL) to learn a type of discriminative feature representations for cell type identification tasks. A large-scale computational evaluation suggests that GsRCL successfully outperformed other state-of-the-art predictive methods on difficult cell type identification tasks, while the conventional random genes masking augmentation-based contrastive learning method also improved the accuracy of easy cell type identification tasks in general
Spinoza on the poetic imagination: replies
These eight generous commentaries raise an inspiring array of questions about the relationship between philosophy and poetry as it was viewed by Spinoza and his contemporaries. Taken singly and together, they enrich the argument of my paper [James Citation2023] by embedding it in a sequence of illuminating contexts, testing and contesting some of its claims and refining the conceptions of poetry at issue. I am deeply grateful to Aurelia Armstrong, Sandra Field, Moira Gatens, Russ Leo, Alison Ross, Hasana Sharp, Jack Stetter, and Ericka Tucker for giving so much time and thought to my article. Bringing their own research to bear on it, each of them takes it in a different direction and opens up a new vista
Social media usage to facilitate knowledge creation
Social media usage is a direct result of Internet connectivity and is gaining increased prominence in business-to-consumer (B2C), business-to-business (B2B), and consumer-to-business (C2B) relationship building, which is allowing
marketers to devise and implement digital marketing strategies that are perceived as enhancing a customer’s well-being.
Through the process of utilizing social media (SM) to share information with consumers, marketers are affording
themselves with the concept of value co-creation and ensuring that the development of knowledge is given priority
The impact (or not) of the war in Ukraine on Russian minorities and minorities policy
The European Yearbook of Minority Issues provides a critical and timely review of contemporary developments in minority-majority relations in Europe. It combines analysis, commentary and documentation in relation to conflict management, international legal developments and domestic legislation affecting minorities in Europe
Use of zebrafish to identify host responses specific to type VI secretion system mediated interbacterial antagonism
Interbacterial competition is known to shape the microbial communities found in the host, however the interplay between this competition and host defense are less clear. Here, we use the zebrafish hindbrain ventricle (HBV) as an in vivo platform to investigate host responses to defined bacterial communities with distinct forms of interbacterial competition. We found that antibacterial activity of the type VI secretion system (T6SS) from both Vibrio cholerae and Acinetobacter baylyi can induce host inflammation and sensitize the host to infection independent of any individual effector. Chemical suppression of inflammation could resolve T6SS-dependent differences in host survival, but the mechanism by which this occurred differed between the two bacterial species. By contrast, colicin-mediated antagonism elicited by an avirulent strain of Shigella sonnei induced a negligible host response despite being a more potent bacterial killer, resulting in no impact on A. baylyi or V. cholerae virulence. Altogether, these results provide insight into how different modes of interbacterial competition in vivo affect the host in distinct ways
Structural basis for the rescue of hyperexcitable cells by the amyotrophic lateral sclerosis drug Riluzole
Neuronal hyperexcitability is a key element of many neurodegenerative disorders including the motor neuron disease Amyotrophic Lateral Sclerosis (ALS), where it occurs associated with elevated late sodium current (INaL). INaL results from incomplete inactivation of voltage-gated sodium channels (VGSCs) after their opening and shapes physiological membrane excitability. However, dysfunctional increases can cause hyperexcitability-associated diseases. Here we reveal the atypical binding mechanism which explains how the neuroprotective ALS-treatment drug riluzole stabilises VGSCs in their inactivated state to cause the suppression of INaL that leads to reversed cellular overexcitability. Riluzole accumulates in the membrane and enters VGSCs through openings to their membrane-accessible fenestrations. Riluzole binds within these fenestrations to stabilise the inactivated channel state, allowing for the selective allosteric inhibition of INaL without the physical block of Na+ conduction associated with traditional channel pore binding VGSC drugs. We further demonstrate that riluzole can reproduce these effects on a disease variant of the non-neuronal VGSC isoform Nav1.4, where pathologically increased INaL is caused directly by mutation. Overall, we identify a model for VGSC inhibition that produces effects consistent with the inhibitory action of riluzole observed in models of ALS. Our findings will aid future drug design and supports research directed towards riluzole repurposing