When the visual system is confronted with incompatible images in the same part of the visual field, the conscious percept switches back and forth between the rivaling stimuli. Such spontaneous flips provide important clues to the neuronal basis for visual awareness. The general idea is that two representations compete for dominance in a process of mutual inhibition, in which adaptation shifts the balance to and fro. The inherent nonlinear nature of the rivalrous flip-flop and its stochastic behavior, however, made it impossible to disentangle inhibition and adaptation. Here we report a general method to measure the time course, and asymmetries, of mechanisms involved in perceptual rivalry. Supported by model simulations, we show the dynamics of opponent interactions between mutual inhibition and adaptation. The findings not only provide new insight into the mechanism underlying rivalry but also offer new opportunities to study and compare a wide range of bistable processes in the brain and their relation to visual awareness.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1167/6.4.1 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Neurovascular Unit Research Group, Korea Brain Research Institute, Daegu 41062, Republic of Korea.
In ephaptic coupling, physically adjacent neurons influence one another's activity via the electric fields they generate. To date, the molecular mechanisms that mediate and modulate ephaptic coupling's effects remain poorly understood. Here, we show that the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel lateralizes the potentially mutual ephaptic inhibition between gustatory receptor neurons (GRNs).
View Article and Find Full Text PDFCancer Discov
January 2025
Memorial Sloan Kettering Cancer Center, New York, NY, United States.
The role of ubiquitin-mediated degradation mechanisms in the pathogenesis of diffuse large B cell (DLBCL) and follicular lymphoma (FL) is not completely understood. We show that conditional deletion of the E3 ubiquitin ligase Fbxo45 in germinal center B-cells results in B-cell lymphomagenesis in homozygous (100%) and heterozygous (48%) mice. Mechanistically, FBXO45 targets the RHO guanine exchange factor ARHGEF2/GEF-H1 for ubiquitin-mediated degradation.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Molecular and Cellular Physiology and Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Injured epithelial organs must rapidly replace damaged cells to restore barrier integrity and physiological function. In response, injury-born stem cell progeny differentiate faster compared to healthy-born counterparts, yet the mechanisms that pace differentiation are unclear. Using the adult Drosophila intestine, we find that injury speeds cell differentiation by altering the lateral inhibition circuit that transduces a fate-determining Notch signal.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Vaccine Innovative Technology ALliance (VITAL)-Korea, Seoul 03722, Republic of Korea.
Aggregation is intricately linked to protein folding, necessitating a precise understanding of their relationship. Traditionally, aggregation has been viewed primarily as a sequential consequence of protein folding and misfolding. However, this conventional paradigm is inherently incomplete and can be deeply misleading.
View Article and Find Full Text PDFJ Food Sci
January 2025
Faculty of Food Science and Engineering, Kunming University of Science and Technology, Kunming, China.
Hypertension is a major risk factor for many cardiovascular diseases, which can lead to kidney and heart disease, stroke, and premature death. Inhibiting angiotensin-converting enzyme (ACE) activity is an effective method to relieve hypertension. Previously, we screened an active peptide KYPHVF (KF6) from Boletus griseus-Hypomyces chrysospermus with excellent ACE inhibitory activity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!